Oral cancer (OC) has become increasingly prevalent in recent years, making it one of the most often occurring types of cancer in patients. The clinical identification of OC is usually a time-consuming procedure, and the outlook for individuals with OC is generally unfavorable, as no particular biomarkers have been established to far. The main risk factors linked to OC are high levels of tobacco and alcohol intake, together with a reduced occurrence of viral infections, such as human papillomavirus. Furthermore, there is evidence suggesting that genetic characteristics that can be passed down from parents to offspring play a role in increasing the likelihood of getting ovarian cancer. MicroRNAs (miRNAs) are brief RNA molecules that do not code for proteins and have the ability to either repress or promote the growth of tumors during cancer development. They have been discovered to control multiple signaling pathways within cells, and their abnormal regulation has been demonstrated to be crucial in initiating and furthering the development of cancer. Additionally, they have the ability to either facilitate or impede the entire multi-stage process of cancer metastasis, including epithelial-mesenchymal transition (EMT), migration, and invasion, by selectively targeting essential genes involved in these pathways. Several microRNAs have the ability to regulate gene expression through various ways. In addition, like other types of cancer, OC has shown alterations in the expression of miRNAs, and certain miRNAs may have the ability to be used for diagnosis and treatment. The investigation of these miRNA could perhaps result in advancements in the specified instances of OC.

MicroRNAs (miRNAs) are short non‑coding RNAs, which perform a key role in cellular differentiation and development. Most human diseases, particularly cancer, are linked to miRNA functional dysregulation implicated in the expression of tumor‑suppressive or oncogenic targets. Cancer hallmarks such as continued proliferative signaling, dodging growth suppressors, invasion and metastasis, triggering angiogenesis, and avoiding cell death have all been demonstrated to be affected by dysregulated miRNAs. Thus, for the treatment of different cancer types, the detection and quantification of this type of RNA is significant. The classical and current methods of RNA detection, including northern blotting, reverse transcription‑quantitative PCR, rolling circle amplification and next‑generation sequencing, may be effective but differ in efficiency and accuracy. Furthermore, these approaches are expensive, and require special instrumentation and expertise. Thus, researchers are constantly looking for more innovative approaches for miRNA detection, which can be advantageous in all aspects. In this regard, an RNA manipulation tool known as the CRISPR and CRISPR‑associated sequence 13 (CRISPR/Cas13) system has been found to be more advantageous in miRNA detection. The Cas13‑based miRNA detection approach is cost effective and requires no special instrumentation or expertise. However, more research and validation are required to confirm the growing body of CRISPR/Cas13‑based research that has identified miRNAs as possible cancer biomarkers for diagnosis and prognosis, and as targets for treatment. In the present review, current updates regarding miRNA biogenesis, structural and functional aspects, and miRNA dysregulation during cancer are described. In addition, novel approaches using the CRISPR/Cas13 system as a next‑generation tool for miRNA detection are discussed. Furthermore, challenges and prospects of CRISPR/Cas13‑based miRNA detection approaches are described.

Alzheimer's disease is a progressive neurodegenerative condition that is the most frequent reason for dementia. Due to the increasing trend of aging in societies, it will place a large social and financial burden on society. Although beta amyloid plaques and the formation of neurofibrillary tangles are mentioned as the main events in this disorder, the exact molecular pathology and inflammatory regulatory networks involved in neuroinflammatory events, as a fundamental pathogenic mechanism remain unknown. Understanding these molecular network pathways in addition to helping to understand the pathogenesis of Alzheimer's disease, can also help in the early diagnosis as well as the control of inflammatory processes that are involved in its progression. So, in this study, we intend to have an overview on the regulatory lncRNAs of Alzheimer's disease and their related miRNA and mRNAs, as well as the relationship of these regulatory pathways with inflammatory processes, so that we can provide a perspective for future studies in the field of diagnosis and possibly treatment of this disorder.

Pemphigus is a group of rare and severe autoimmune blistering diseases (AIBDs). MicroRNA's role in the pathogenesis of pemphigus disease has been previously studied, but MicroRNAmicroRNAs research in dermatology is still at its beginning.

This review was carried out using a systematic search on PubMed, Scopus Embase, and Web of Science from 1990 to February 2025 to explore the role of microRNA in the diagnosis and severity evaluation of pemphigus disease.

A total of 8 studies were identified in the systematic review that indicated the expression level of 18 types of microRNA was significantly different from that of healthy people.

The collective data presented in this review indicate that MicroRNAmicroRNAs may help diagnose and predict the course of pemphigus, while the clinical application of these findings has yet to be verified.

Fruits, vegetables, and plant-based foods contain several bioactive substances such as phenolic compounds (PCs), that are plant secondary metabolites with attributed health properties. The study of the metabolic pathways of PCs, including those related with their synthesis, transport, accumulation, and degradation are essential to advance in this field of research. In this regard, omics tools such as foodomics are gaining relevance due to their versatility and their tremendous potential to generate significant advances in PC research. In this review, we present a comprehensive overview of the applications of omics technologies in PC analysis, including transcriptomics, micromics, proteomics and metabolomics, highlighting their role in metabolic pathways, current limitations, and emerging insights. Omics techniques as well as data analyses are continuously progressing, emerging new opportunities with onset of artificial intelligence and machine learning. However, significant limitations and challenges still remain. The immense diversity of PC chemical structures and their variability across plant species, varieties, and impact of agronomic factors complicate the analyses and limit the extrapolation of findings. Additionally, high data dimensionality, strong correlations among measured variables, and general lack of standardization in the different omics techniques can impact in the results. Addressing these limitations requires integrating multi-omics approaches and developing standardized protocols to enhance comparability and interpretation in PC research. In summary, foodomics approaches arise as essential for the complete mapping of PC biosynthesis.

Particulate matter containing environmentally persistent free radicals (EPFRs) is formed when organic pollutants are incompletely burned and adsorb to the surface of particles containing redox-active metals. Our prior studies showed that in mice, EPFR inhalation impaired vascular relaxation in a dose- and endothelium-dependent manner. We also observed that activation of the aryl hydrocarbon receptor (AhR) in the alveolar type-II (AT-II) cells that form the air-blood interface stimulates the release of systemic factors that promote endothelial dysfunction in vessels peripheral to the lung. AhR is a recognized regulator of microRNA (miRNA) biogenesis, and miRNA control diverse signaling pathways. We thus hypothesized that systemic EPFR-induced vascular endothelial dysfunction is initiated via AhR activation in AT-II cells, resulting in a systemic release of miRNA. Using a combustion reactor, we generated EPFR of two free radical concentrations-EPFRlo (1016-17 radicals/g particles) and EPFR (1018-19 radicals/g)-and exposed mice by inhalation. EFPR inhalation resulted in changes in a distinct array of miRNA in the plasma, and these miRNAs are linked to multiple systemic effects, including cardiovascular diseases and dysregulation of cellular and molecular pathways associated with cardiovascular dysfunction. We identified 17 miRNA in plasma that were altered dependent upon both AhR activation in AT-II cells and ~ 280 ug/m3 EPFR exposure. Using Ingenuity Pathway Analysis, we found that 5 of these miRNAs have roles in modulating endothelin-1 and endothelial nitric oxide signaling, known regulators of endothelial function. Furthermore, EPFR exposure reduced the expression of lung adherens and gap junction proteins in control mice but not AT-II-AhR deficient mice, and reductions in barrier function may facilitate miRNA release from the lungs. In summary, our findings support that miRNA may be systemic mediators promoting endothelial dysfunction mediated via EPFR-induced AhR activation at the air-blood interface.

To investigate the molecular mechanism by which the miRNA let-7a regulates renal tubular epithelial cell apoptosis by influencing the activity of the PI3K/Akt pathway, which is involved in the development of sepsis-associated acute kidney injury (SA-AKI).

A sepsis-associated acute kidney injury model was constructed in vitro and in vivo using LPS, and the expression of the miRNA let-7a and activation of the PI3K/Akt pathway were detected in SA-AKI. Apoptosis marker molecules and inflammatory factor expression were detected by transfecting miRNA let-7a mimics with LPS-stimulated human renal tubular epithelial cells (HKCs) or using the PI3K/Akt pathway inhibitor LY294002. Bioassay analysis elucidated the relationship between miRNA let-7a and the PI3K/Akt signaling pathway. The mechanism was validated in primary renal tubular epithelial cells.

In the in vivo and in vitro models, miRNA let-7a expression was significantly reduced, and the PI3K/Akt pathway was activated. When miRNA let-7a was overexpressed or the PI3K/Akt pathway was inhibited, the inflammatory response of renal tubular epithelial cells was attenuated. Bioassay analysis verified that the miRNA let-7a binds to the PI3K/Akt signaling pathway. The miRNA let-7a-PI3K/Akt regulatory axis regulates the apoptosis of renal tubular epithelial cells in primary tubular epithelial cells.

The miRNA let-7a regulates inflammation and apoptosis in renal tubular epithelial cells by affecting the activity of the PI3K/Akt pathway in the development of sepsis-associated acute kidney injury.

Gastric cancer is a significant contributor to worldwide cancer deaths with limited treatment options and poor patient survival. MicroRNAs play crucial roles as potential oncogenic factors or tumor suppressors in cancers by modulating cell cycle progression, proliferation, migration, invasion, and apoptosis. However, the functional implications of miR-103a-3p in gastric cancer remain poorly known. The current study demonstrates a noteworthy increase in the expression of miR-103a-3p in gastric cancer tissues when compared to neighboring non-cancerous tissues. Our functional investigations indicate that the upregulation of miR-103a-3p contributes to enhanced proliferation, invasion, and migration capabilities in gastric cancer cells. After mechanistic studies, our findings indicate that miR-103a-3p may directly target insulin-like growth factor binding protein 5 (IGFBP5) in gastric cancer. Moreover, rescue experiments reveal that IGFBP5 overexpression can attenuate the progression induced by miR-103a-3p in gastric cancer cells. In summary, our findings suggest that the miR-103a-3p/IGFBP5 axis may play a role in gastric cancer progression, highlighting its potential as a therapeutic target and prognostic marker.

Tumor heterogeneity, characterized by the presence of diverse cell populations within a tumor, is a key feature of the complex nature of cancer. This diversity arises from the emergence of cells with varying genomic, epigenetic, transcriptomic, and phenotypic profiles over the course of the disease. Host factors and the tumor microenvironment play crucial roles in driving both inter-patient and intra-patient heterogeneity. These diverse cell populations can exhibit different behaviors, such as varying rates of proliferation, responses to treatment, and potential for metastasis. Both inter-patient heterogeneity and intra-patient heterogeneity pose significant challenges to cancer therapeutics and management. In retinoblastoma, while heterogeneity at the clinical presentation level has been recognized for some time, recent attention has shifted towards understanding the underlying cellular heterogeneity. This review primarily focuses on retinoblastoma heterogeneity and its implications for therapeutic strategies and disease management, emphasizing the need for further research and exploration in this complex and challenging area.

Diverse CD4+ T cell subsets with specialized functions operate at different phases of the immune response. Among these are phenotypically and functionally characterized naïve, central memory (CM), effector memory (EM), and regulatory (Treg) cells. Using small RNA-sequencing, we have profiled miRNAs in these cell subsets from healthy subjects and untreated patients with relapsing-remitting multiple sclerosis (RRMS). MiRNA genomic clustering and abundance were also investigated. From the 60 most differentially expressed miRNAs, broad and highly selective core signatures were determined for naïve and memory cells at homeostasis, while miR-146a-5p was strongly upregulated in Treg cells. In line with other studies, a 5-miRNA core was identified for naïve cells (miR-125b-5p, miR-99a-5p, miR-365a-3p, miR-365b-3p, miR-193b-3p). In memory cells, a number of identical miRNAs were more expressed in EM than CM cells, supporting the progressive T cell differentiation model. This was particularly the case for an 8-miRNA core (members from miR-23a∼27a∼24-2, miR-23b∼27b∼24-1, miR-221∼222 clusters, miR-22-3p, miR-181c-5p) and for the large ChrXq27.3 miR-506∼514 cluster. Interestingly, most of these miRNAs were reported to negatively regulate cell proliferation and survival. Finally, we found that the miRNA core signatures of naïve and memory CD4+ T cells were conserved in RRMS patients. Only few miRNAs were quantitatively modified and, among these, miR-1248 was validated to be downregulated in EM cells. Overall, this study expands and provides novel insights into miRNA profiling of CD4+ T cell subsets that may be useful for further investigations.

Recently, the regulatory effects of microRNAs (miRNAs) on gene expression have been exploited for applications in the diagnosis and treatment of cancer, neurological diseases, and cardiovascular diseases. However, the susceptibility of miRNAs to degradation during somatic circulation and the challenges associated with their delivery to target tissues and cells have limited the clinical application of miRNAs. For application in tumor therapy, it is essential for miRNAs to specifically target cancer cells. Therefore, various novel miRNA delivery systems that protect miRNA against the activity of serum nuclease and deliver miRNA to target cells have been developed and optimized. This review introduces the passive and active targeting strategies of nanoparticles, summarizes the recent progress of miRNA nanocarriers with tumor-targeting ability, and discusses various nanoparticle delivery systems and their antitumor applications. Additionally, this review focuses on the translational challenges and potential strategies for advancing miRNA-based therapies into the clinic.

Alzheimer's disease (AD) is a prevalent neurodegenerative disorder marked by a gradual decline in memory and cognitive functions. It is characterized by the presence of senile plaques, neurofibrillary tangles, and neuronal degeneration, affecting a significant portion of the human population. A key feature of various nervous system disorders, including AD, is extensive cellular death caused by apoptosis, which affects not only neurons but also glial cells. While apoptosis plays a vital role in eliminating certain cells and supporting normal development, alterations or disruptions in apoptotic pathways can lead to harmful neurodegenerative conditions such as AD. Thus, targeting apoptosis presents a promising therapeutic approach for these diseases. MicroRNAs (miRNAs), a class of non-coding RNA, play diverse roles in cellular functions, including proliferation, gene expression regulation, programmed cell death, intercellular communication, and angiogenesis. By modulating regulatory genes, miRNAs can influence apoptosis, either promoting or inhibiting it. Aberrant expression of miRNAs can impact multiple apoptotic pathways, potentially driving the progression of AD and related health issues. This review summarizes recent research on miRNAs and their dual role in exacerbating or protecting against neural cell damage in AD by altering apoptotic pathways. The regulation of apoptosis by miRNAs offers a prospective therapeutic strategy for Alzheimer's disease.

Construct a prediction model for lymph node metastasis (LNM) in papillary thyroid carcinoma (PTC) using Probe Electrospray Ionization Mass Spectrometry (PESI - MS) combined with artificial intelligence (AI), to assist in the preoperative prediction of lymph node metastasis in thyroid carcinoma by intraoperative frozen pathology.

A total of 78 fresh tissue samples of PTC and their adjacent normal tissues were collected. After proper processing, these samples were subjected to detection and analysis using PESI - MS. Subsequently, a classification prediction model was established based on the mass spectrometry test results integrated with AI algorithms. Support vector machine (SVM), random forest (RF), multi - layer perceptron (MLP), and Gradient boosting classifier (GBC) were employed for model building. Employing Support Vector Machine (SVM), Random Forest (RF), and Multilayer Perceptron (MLP) to conduct a single-blinded test on 10 independent PTC samples with unknown lymph node metastasis status.

The SVM, and MLP algorithms achieved an accuracy of 100 % in differentiating PTC with or without LNM, while the RF and GBC algorithm reached an accuracy of 92 %. All four algorithms demonstrated an accuracy of 100 % in distinguishing PTC from adjacent normal tissues.

The combination of PESI - MS and AI exhibits high accuracy in predicting LNM in PTC and performs remarkably well in the rapid diagnosis of PTC. This approach can effectively assist in the rapid diagnosis of intraoperative pathology, assist in determining the surgical scope of thyroid lymph node dissection, and offer more precise treatment for patients.

Pancreatic cancer is one of the most aggressive malignancies with poor prognostic outcomes, necessitating the exploration of novel biomarkers and therapeutic targets for early detection and effective treatment. Small extracellular vesicles (sEVs) secreted by cells, have gained considerable attention in cancer research due to their role in intercellular communication and their potential as non-invasive biomarkers. This review focuses on the role of sEVs in the progression of pancreatic cancer and their application as biomarkers. We delve into the biogenesis, composition, and functional implications of sEVs in pancreatic tumor biology, emphasizing their involvement in processes such as tumor growth, metastasis, immune modulation, and chemotherapy resistance. In addition, we discuss the challenges in isolating and characterizing sEVs. The review also highlights recent advances in the utilization of sEV-derived biomarkers for the early diagnosis, prognosis, and monitoring of pancreatic cancer. By synthesizing the latest findings, we aim to underscore the significance of sEVs in pancreatic cancer and their potential to revolutionize patient management through improved diagnostics and targeted therapies.

Vitiligo is an autoimmune depigmenting skin disorder and can affect the mental health of the patients. Current research suggests that the development of vitiligo involves a combination of genetic susceptibility, immune imbalance, and oxidative stress. However, its pathogenesis has not been fully elucidated. Epigenetic modification has gained increasing attention as an emerging way to regulate gene expression at the transcriptional or post-transcriptional level. Currently known modes of epigenetic modification include the regulation of non-coding RNAs, DNA methylation, and histone modification. Studies suggest they play important roles in tumors, immune disorders, and inflammatory diseases. In recent years, the value of epigenetics in the diagnosis, treatment, and prognosis of vitiligo has been explored. They showed the potential to serve as biomarkers and play a therapeutic role. In this review, we summarize the epigenetic modification mechanisms involved in the pathogenesis of vitiligo, including physiological processes such as immune homeostasis, melanocyte survival, cell adhesion and migration, and metabolism. This will help us fully understand the progress of epigenetic research in vitiligo and lay the foundation for targeted therapeutic-related research.

In order to investigate the gene expression patterns and molecular regulatory mechanisms of obstructive sleep apnea hypopnea syndrome (OSAHS), the global transcriptome expression profiles of OSAHS patients and healthy people were analyzed using transcriptome sequencing technology. Differential expression of circular RNA, microRNA, long noncoding RNA, and messenger RNA was investigated between the two groups. To further explore the role of differentially expressed genes in OSAHS, we functionally annotated the differentially expressed genes using enrichment analysis of GO and KEGG pathways. Finally, the ceRNA regulatory network of OSAHS was constructed. And validate the differentially expressed mRNA through qRT-PCR analysis. The results showed that 349 circRNAs,552 lncRNAs,205 miRNAs, 502 mRNAs were differentially expressed in patients with OSAHS compared with the healthy population. Terms such as centrosome, positive regulation of execution phase of apoptosis, oxidoreductase activity, regulation of Th 17 cell differentiation and immune response, neutrophil mediated cytotoxicity were enriched in the GO list, suggesting a potential correlation with OSAHS. Pathway analysis showed that Ferroptosis, Herpes simplex virus 1 infection, Pathways in cancer, Hematopoietic cell lineage and other pathways play an important role in OSAHS. By constructing a ternary network, two circRNAs and four lncRNAs were screened as ceRNAs to compete with miRNAs in the co-expression network, and associated with OSAHS by regulating the function of mRNAs in the network. By constructing a quaternary network miR-8485 and miR-6089 were found to be the top two ranked miRNAs most closely associated with OSAHS. Both qRT-PCR and transcriptome sequencing analysis showed similar trends. This provides more theoretical basis for exploring the complex molecular mechanisms of global transcriptome in the development of OSAHS.

Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by the progressive destruction of pancreatic β-cells, leading to insulin deficiency. The primary drivers of β-cell destruction in T1D involve autoimmune-mediated processes that trigger chronic inflammation and ultimately β-cell loss. Regulatory microRNAs (miRNAs) play a crucial role in modulating these processes by regulating gene expression through post-transcriptional suppression of target mRNAs. Dysregulated miRNAs have been implicated in T1D pathogenesis, serving as both potential diagnostic biomarkers and therapeutic targets. This review explores the role of miRNAs in T1D, highlighting their involvement in disease mechanisms across both rodent models and human patients. While current antidiabetic therapies manage T1D symptoms, they do not prevent β-cell destruction, leaving patients reliant on lifelong insulin therapy. By summarizing key miRNA expression profiles in diabetic animal models and patients, this review explores the potential of miRNA-based therapies to restore β-cell function and halt or slow the progression of the disease.

MicroRNAs (miRNAs) are small, yet profoundly influential, non-coding RNAs that base-pair with mRNAs to induce RNA silencing. Although the basic principles of miRNA biogenesis and function have been established, recent breakthroughs have yielded important new insights into the molecular mechanisms of miRNA biogenesis. In this Review, we discuss the metazoan miRNA biogenesis pathway step-by-step, focusing on the key biogenesis machinery, including the Drosha-DGCR8 complex (Microprocessor), exportin-5, Dicer and Argonaute. We also highlight newly identified cis-acting elements and their impact on miRNA maturation, informed by advanced high-throughput and structural studies, and discuss recently discovered mechanisms of clustered miRNA processing, target recognition and target-directed miRNA decay (TDMD). Lastly, we explore multiple regulatory layers of miRNA biogenesis, mediated by RNA-protein interactions, miRNA tailing (uridylation or adenylation) and RNA modifications.

The enteric nervous system (ENS), an elaborate network of neurons and glia woven through the gastrointestinal tract, is integral for digestive physiology and broader human health. Commensurate with its importance, ENS dysfunction is linked to a range of debilitating gastrointestinal disorders. MicroRNAs (miRNAs), with their pleiotropic roles in post-transcriptional gene regulation, serve as key developmental effectors within the ENS. Herein, we review the regulatory dynamics of miRNAs in ENS ontogeny, showcasing specific miRNAs implicated in both congenital and acquired enteric neuropathies, such as Hirschsprung's disease (HSCR), achalasia, intestinal neuronal dysplasia (IND), chronic intestinal pseudo-obstruction (CIPO), and slow transit constipation (STC). By delineating miRNA-mediated mechanisms in these diseases, we underscore their importance for ENS homeostasis and highlight their potential as therapeutic targets.

Liver cancer or hepatocellular carcinoma (HCC) remains the most common cancer in global epidemiology. Both the frequency and fatality of this malignancy have shown an upward trend over recent decades. Liver cancer is a significant concern due to its propensity for both intrahepatic and extrahepatic metastasis. Liver cancer metastasis is a multifaceted process characterized by cell detachment from the bulk tumor, modulation of cellular motility and invasiveness, enhanced proliferation, avoidance of the immune system, and spread either via lymphatic or blood vessels. MicroRNAs (miRNAs) are small non-coding ribonucleic acids (RNAs) playing a crucial function in the intricate mechanisms of tumor metastasis. A number of miRNAs can either increase or reduce metastasis via several mechanisms, such as control of motility, proliferation, attack by the immune system, cancer stem cell properties, altering the microenvironment, and the epithelial-mesenchymal transition (EMT). Besides, two other types of non-coding RNAs, such as long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) can competitively bind to endogenous miRNAs. This competition results in the impaired ability of the miRNAs to inhibit the expression of the specific messenger RNAs (mRNAs) that are targeted. Increasing evidence has shown that the regulatory axis comprising circRNA/lncRNA-miRNA-mRNA is correlated with the regulation of HCC metastasis. This review seeks to present a thorough summary of recent research on miRNAs in HCC, and their roles in the cellular processes of EMT, invasion and migration, as well as the metastasis of malignant cells. Finally, we discuss the function of the lncRNA/circRNA-miRNA-mRNA network as a crucial modulator of carcinogenesis and the regulation of signaling pathways or genes that are relevant to the metastasis of HCC. These findings have the potential to offer valuable insight into the discovery of novel therapeutic approaches for management of liver cancer metastasis.

Bone healing is a well-orchestrated process involving various bone cells and signaling pathways, where disruptions can result in delayed or incomplete healing. MicroRNAs (miRNAs) are small non-coding RNAs capable of influencing various cellular processes, including bone remodeling. Due to their biological relevance and stable presence in biofluids, miRNAs may serve as candidates for diagnosis and prognosis of delayed bone healing. The aim of the study was to investigate changes in miRNAs circulating in the blood during the healing of rat calvaria defects as biomarkers of successful bone regeneration.

Standardized calvaria defects were created in 36 Wistar rats with a trephine drill and treated with collagen hydroxyapatite (CHA) scaffolds. The treatment groups included CHA scaffolds only, CHA scaffolds containing a plasmid coding for bone morphogenetic protein 2 (BMP2) and miR-590-5p, CHA scaffolds containing mesenchymal stromal cell-derived extracellular vesicles, and empty defects as a control group. After 1, 4 and 8 weeks of healing, the animals were evaluated by microcomputed tomography (microCT), as well as subjected to histological analyses. Blood was sampled from the tail vein prior to surgeries and after 1, 4, and 8 weeks of healing. miRNAs circulating in the plasma were determined using next-generation sequencing.

Variability of bone regeneration within the four groups was unexpectedly high and did not result in significant differences between the groups, as indicated by the microCT and histological analyses of the newly formed bone tissue. However, irrespective of the treatment group and regenerative activity, we identified miRNAs with distinct expression patterns of up- and downregulation at different time points. Furthermore, rats with high and low regenerative activity were characterized by distinct circulating miRNA profiles. miR-133-3p was identified as the top upregulated miRNA and miR-375-3p was identified as the top downregulated miRNA in animals exhibiting strong regeneration over all time points evaluated.

Our study indicates that regardless of the treatment group, success or lack of bone regeneration is associated with a distinct expression pattern of circulating microRNAs. Further research is needed to determine whether their levels in the blood can be used as predictive factors of successful bone regeneration.

MicroRNAs (miRNAs) have emerged as promising biomarkers for diagnosis and prognosis in laryngeal squamous cell carcinoma (LSCC). This study investigates the expression patterns of specific cancer-associated miRNAs in early and advanced stage LSCC to evaluate their potential role in disease progression.

The expression levels of miRNA-21, miRNA-802, miRNA-29 and miRNA-9 were analysed in formalin-fixed paraffin-embedded (FFPE) tissues from 44 LSCC patients (20 early stage, 24 advanced stage) using quantitative multiplex RT-PCR. Tissue samples were analysed retrospectively.

The expression level of hsa-miR-9a expression was significantly upregulated (5.2-fold) in advanced stage patients compared to the early stage group (p = 0.0088). Similarly, hsa-miR-802a showed significantly higher expression (9.2-fold) in advanced stage patients compared to early stage patients (p = 0.005). No significant differences in miRNA-21 and miRNA-29 expression levels were observed between the groups.

As a result of the study, elevated miRNA levels in advanced stage patients can be used in targeted therapy and evaluated as a treatment option in LSCC patients.

MicroRNAs (miRNAs) are a class of non-coding RNA sequences that regulate gene expression post-transcriptionally. The miR-99 family, which is highly evolutionarily conserved, comprises three homologs: miR-99a, miR-99b, and miR-100. Its members are under-expressed in most cancerous tissues, suggesting their cancer-repressing properties in multiple cancers; however, in some contexts, they also promote malignant lesion progression. MiR-99 family members target numerous genes involved in various tumor-related processes such as tumorigenesis, proliferation, cell-cycle regulation, apoptosis, invasion, and metastasis. We review the recent research on this family, summarize its implications in cancer, and explore its potential as a biomarker and cancer therapeutic target. This review contributes to the clinical translation of the miR-99 family members.

Postoperative delirium (POD) is a serious neuropsychiatric complication in elderly surgical patients, yet its pathogenesis remains incompletely understood. Transfer RNA-derived small RNAs (tsRNAs) have emerged as crucial regulators in neurological disorders. We investigated whether specific tsRNAs could serve as predictive biomarkers for POD.

This study conducted a prospective case-control study of 158 elderly patients (≥60 years) undergoing orthopedic surgery. Plasma samples were collected preoperatively and on postoperative day 3.tsRNA expression profiles were analyzed using RNA sequencing and validated by RT-qPCR. Propensity score matching was performed to balance demographic and clinical variables. The predictive value of candidate tsRNAs was assessed using ROC analysis, and their potential functions were explored through bioinformatic analyses.

Among 128 non-POD and 30 POD patients, two tsRNAs (Other-14: 31-tRNA-Gly-CCC-3 and Other-39: 73-tRNA-Arg-TCG-5) showed significantly elevated preoperative levels in POD patients (p<0.001).ROC analysis revealed strong predictive performance (AUC=0.868 and 0.956, respectively).These differences persisted in the propensity-matched cohort (29 pairs).Bioinformatic analyses indicated enrichment in pathways related to neurotransmission, inflammation, and metabolism.

This study identified novel tsRNA biomarkers that robustly predict POD risk and provide insights into its molecular pathogenesis. These findings may facilitate early risk stratification and preventive interventions.

RNAs are a vast reservoir of untapped drug targets. Structure-based virtual screening (VS) identifies candidate molecules by leveraging binding site information, traditionally using molecular docking simulations. However, docking struggles to scale with large compound libraries and RNA targets. Machine learning offers a solution but remains underdeveloped for RNA due to limited data and practical evaluations. We introduce a data-driven VS pipeline tailored for RNA, utilizing coarse-grained 3D modeling, synthetic data augmentation, and RNA-specific self-supervision. Our model achieves a 10,000x speedup over docking while ranking active compounds in the top 2.8% on structurally distinct test sets. It is robust to binding site variations and successfully screens unseen RNA riboswitches in a 20,000-compound in-vitro microarray, with a mean enrichment factor of 2.93 at 1%. This marks the first experimentally validated success of structure-based deep learning for RNA VS.

This study aims to screen common immunological markers of lung tissues and blood for diagnosis of tuberculosis (TB).

Differentially expressed miRNAs (DEmRs) and mRNAs (DEGs) were obtained by whole-transcriptome sequencing profiles on 18F-FDG PET/CT high and low metabolic active regions in lung tissues of nine TB patients. Common miRNAs were screened by intersecting with DEmRs, four miRNA GEO datasets, and their target mRNAs were predicted through the miRTarbase and Tarbase databases. Then these mRNAs were intersected with DEGs, mRNAs from blood samples and immune-related genes, to construct a miRNA-mRNA interaction network, and the hub genes were identified by Cytoscape. The relationship between immune infiltration and hub genes were evaluated using Cibersort. Finally, a diagnostic model based on Lasso regression analysis was established and validated by qRT-PCR.

Five common miRNAs were obtained in both blood and tissues. Six immune-related mRNAs (NEDD4, PLTP, RNASEL, SEMA7A, TAPBP, and THBS1) were screened out. A diagnostic model was established and validated in the blood samples of 30 pairs (TB/health volunteers). The AUC for the 6-mRNA combination was 0.79.

We screened six mRNAs as a combination for diagnosing tuberculosis.

Silencing by the miRNA-guided RNA induced silencing complex (miRISC) is dependent on Ago2-chaperoned base pairing between the miRNA 5' seed (5'S) and a complementary sequence in the 3' untranslated region of an mRNA. Prevailing mechanistic understanding posits that initial 5'S pairing can further allow functional base pair expansion into the 3' non-seed (3'NS), while functionally distinct non-canonical pairing was reported between only the 3'NS and the mRNA coding sequence. We developed single-molecule kinetics through equilibrium Poisson sampling (SiMKEPS) to measure highly precise binding and dissociation rate constants of varying-length target sequences to 5'S and 3'NS in a paradigmatic miRISC isolated from human cells, revealing distinct stable states of miRISC with mutually exclusive 5'S and 3'NS pairing. Our data suggest conformational rearrangements of the Ago2-bound miRNA that regulate alternative 5'S- and 3'NS-driven target recognition. The resulting model reconciles previously disparate observations and deepens our acumen for successfully marshaling RNA silencing therapies.

Mitochondrial oxidative stress (MOS) is a key contributor to poor cardiac function and a major driver of myocardial ischemia-reperfusion injury (MIRI). Our previous research demonstrated that stem cell-derived nanovesicles (NVs) enhanced cardiac function following ischemia-reperfusion (I/R) injury, although the underlying mechanisms remain unclear. We constructed and characterized miR-222-3p-loaded NVs.

An in vitro hypoxia-reoxygenation (H/R) model was established using H9C2 cardiomyocytes. Mitochondrial oxidative respiratory function was assessed using Seahorse XF technology, while mitochondrial reactive oxygen species (mtROS) levels were quantified via flow cytometry. Additional assessments included mitochondrial permeability transition pore (mPTP) status, mitochondrial membrane potential, and mitochondrial DNA (mtDNA) integrity. An in vivo H/R model was developed using C57BL/6 mice. The therapeutic effects of NVs on MOS reduction and cardiac function improvement were evaluated through Masson's staining, immunofluorescence, echocardiography, transmission electron microscopy (TEM), and positron emission tomography/computed tomography (PET/CT).

RNA immunoprecipitation (RIP) confirmed that miR-222-3p directly targets cyp1a1. Overexpression of miR-222-3p or knockdown of cyp1a1 significantly improved mitochondrial activity in cardiomyocytes and conferred protection against I/R injury. Conversely, overexpression of cyp1a1 abrogated the protective effects of miR-222-3p. In vivo, NV treatment enhanced cardiac function, reduced MOS, and improved mitochondrial respiratory capacity in MIRI model mice. NV treatment, via miR-222-3p-mediated suppression of cyp1a1, mitigates MOS, enhances mitochondrial respiratory function, and improves cardiac outcomes in MIRI models.

These findings provide a foundational basis for the clinical translation of NV-based therapies.

The increasing efficacy of cancer therapies has significantly improved survival rates, but it has also highlighted the prevalence of cancer-therapy-related cardiac dysfunction (CTRCD). This review provides a comprehensive overview of the identification, monitoring, and management of CTRCD, a condition resulting from several treatments, such as anthracyclines, HER2-targeted therapies, target therapies, and radiotherapy. The paper includes a discussion of the mechanisms of CTRCD associated with various cancer treatments. Early detection through serum biomarkers and advanced imaging techniques is crucial for effective monitoring and risk stratification. Preventive strategies include pharmacological interventions such as ACE inhibitors/angiotensin receptor blockers, beta-blockers, and statins. Additionally, novel agents like sacubitril/valsartan, sodium-glucose co-transporter type 2 inhibitors, and vericiguat show promise in managing left ventricular dysfunction. Lifestyle modifications, including structured exercise programs and optimized nutritional strategies, further contribute to cardioprotection. The latest treatments for both asymptomatic and symptomatic CTRCD across its various stages are also discussed. Emerging technologies, including genomics, artificial intelligence, novel biomarkers, and gene therapy, are paving the way for personalized approaches to CTRCD prevention and treatment. These advancements hold great promise for improving long-term outcomes in cancer patients by minimizing cardiovascular complications.

Coronary artery disease (CAD) is a leading cause of morbidity and mortality worldwide, with platelet reactivity playing a central role in its pathogenesis. Recent research has identified microRNAs (miRNAs; miRs) as potential biomarkers for CAD, due to their ability to regulate platelet function and reactivity. This review focuses on four key miRNAs-miR-223, miR-126, miR-21, and miR-150-known to influence platelet reactivity and their implications in CAD. miR-223, which is highly expressed in platelets, has shown associations with CAD and myocardial infarction, while miR-126 has been linked to thrombus formation and vascular health. Additionally, miR-21 and miR-150 have also emerged as important players, with roles in platelet reactivity and cardiovascular outcomes. However, despite their potential, the use of miRNAs as clinical biomarkers faces several challenges, including variability in reported results across studies. These inconsistencies often arise from differences in sample material, preanalytical conditions, and normalization strategies. Furthermore, the influence of antiplatelet therapy on miRNA expression adds another layer of complexity, making it difficult to determine whether observed changes in miRNA levels are due to disease states or therapeutic interventions. This review therefore highlights the need for standardization in miRNA research to enhance the reliability of findings. By addressing these methodological challenges, miRNAs could become powerful tools in personalized medicine, aiding in the development of tailored therapeutic strategies for CAD patients and ultimately improving clinical outcomes.

Platelets are highly enriched in microRNAs (miRNAs), which are genomically encoded 19-25 nucleotide non-coding RNAs that target complementary mRNAs through total or near-total base pairing. MiR-223 is among the most abundant miRNAs in human and murine platelets, but despite ongoing investigations in recent years, miR-223 roles in platelet physiology and its putative roles in high on-treatment platelet reactivity (HTPR) remain controversial, as studies showed varying findings.

In the current hybrid review/report, we aim to compare studies that investigated miR-223 in platelet function and HTPR. Additionally, we briefly report our own findings on murine miR-223-deficient platelets.

We have thoroughly searched the literature and found three studies that investigated the roles of miR-223 in platelet function by utilizing miR-223 global knockout mice, and three studies that explored the association between miR-223 and residual platelet reactivity by measuring miR-223 levels in platelets of patients treated with clopidogrel for cardiac artery disease. We assessed platelet function in response to different agonists and evaluated P2y12 levels in male and female miR-223-deficient platelets.

Integrin activation and α granule secretion were similar between WT and KO platelets in response to all agonists in platelets from both female and male mice, although both genotypes showed elevated thrombin response in females compared to males.

In all studies, including ours, taken together, miR-233 appears to play a modest role in platelet function and development of HTPR.

MicroRNAs (miRNAs) regulate biological processes by inhibiting translation and causing mRNA degradation. In this study, we identified the miRNAs involved in the development and progression of lupus nephritis (LNs) and verified their roles.

Total RNA, extracted from PBMCs collected from patients with LNs before and after treatment, was used for miRNA array analysis to identify miRNAs whose expression was significantly altered. The results of this analysis were confirmed using qRT-PCR. The identified miRNAs were transfected into normal human mesangial cells (NHMCs), human renal proximal tubule epithelial cells (RPTECs), human umbilical vein endothelial cells (HUVECs), and THP-1-derived macrophages (THP1-Mφ) to investigate their biological functions.

Three miRNAs were altered in PBMCs before and after treatment of LNs. Among these miRNAs, hsa-miR-6516-3p promoted TNF-α-induced expression of MMP-9 in NHMCs. Moreover, hsa-miR-6516-3p downregulated the expression of RECK, an endogenous inhibitor of MMP-9. However, in NHMCs, endogenous hsa-miR-6516-3p was not present in functional amounts under inflammatory environment; therefore, we performed analysis using an experimental system considering extracellular influences of mesangial cells under LNs. The expression of hsa-miR-6516-3p was increased in HUVECs under inflammatory conditions and in activated macrophages.

hsa-miR-6516-3p increases MMP9 expression by suppressing RECK, and might, thereby, exacerbate LNs.

The post-transcriptional regulation of epigenetic modification is a hot topic in skeletal muscle development research. Both m6A modifications and miRNAs have been well-established as crucial regulators in skeletal muscle development. However, the interacting regulatory mechanisms between m6A modifications and miRNAs in skeletal muscle development remain unclear. In this study, miRNA sequencing analysis of goat primary myoblasts (GPMs) pre- and post-differentiation revealed that miR-503-5p was upregulated during myogenic differentiation, and its precursor was identified to contain m6A modification sites. Combined analysis of RIP, qRT-PCR and mRNA stability assay showed that Ythdf2 could recognize and bind the m6A site on pre-miR-503-5p, thereby facilitating the maturation of pre-miR-503-5p in an m6A-dependent manner. Moreover, the overexpression of miR-503-5p significantly inhibits the proliferation of GPMs, promotes myogenic differentiation, and enhances mitochondrial biogenesis while activating the mTOR pathway. However, the suppression of mTOR activity can effectively counteract the accelerated myogenic differentiation induced by miR-503-5p overexpression. Collectively, our results indicate that Ythdf2-dependent m6A modification facilitates the maturation of pre-miR-503-5p, thereby promoting skeletal muscle differentiation through the activation of the mTOR pathway. These insights lay a valuable foundation for further investigation into the complexities of skeletal muscle development and the potential implications of epigenetic regulation in this process.

MicroRNAs (miRNAs) are regulators of mRNA translation and play crucial roles in various physiological and pathological processes. In this study, we profiled miRNAs in umbilical cord plasma (UCP) to explore the association of neonatal circulating miRNAs with maternal metabolic parameters and neonatal anthropometric, metabolic and inflammatory characteristics in healthy pregnancies. Data and UCP samples were collected from 16 pregnancies, equally divided between normal-weight and overweight mothers and between male and female newborns. Using next-generation sequencing, we identified and quantified miRNAs in UCP, alongside the analysis of metabolic and inflammatory parameters. Our results revealed that the majority of UCP miRNAs are sensitive to maternal and neonatal characteristics, particularly maternal body mass index, gestational weight gain, placental weight, UCP leptin, UCP C-reactive protein and UCP insulin levels. Notably, we identified a strong association between the placenta-derived chromosome 19 microRNA cluster (C19MC) and placental weight, gestational weight gain, UCP insulin and neonatal weight. Likewise, the pregnancy-specific chromosome 14 microRNA cluster (C14MC) was associated with maternal body mass index and UCP leptin. Our study highlights the sensitivity of UCP miRNAs to maternal metabolic conditions, demonstrates their association with neonatal metabolic and inflammatory traits, and underscores the potential role of circulating cord blood miRNAs in fetal metabolism and development. KEY POINTS: MicroRNAs (miRNAs) are regulatory RNA molecules that modulate protein expression. They are present in all body fluids and umbilical cord plasma and are affected by metabolic changes. Pregnancy is a state of metabolic change in the mother, and maternal metabolism affects fetal development. We found that the composition of umbilical cord blood miRNAs is associated with maternal and neonatal metabolism. Pregnancy-specific groups of miRNAs showed particular patterns, with miRNAs encoded by a region of chromosome 14 associated with maternal body mass index and with miRNAs encoded by a specific region of chromosome 19 associated with umbilical cord plasma insulin. MicroRNAs represent a separate dimension through which maternal metabolism can influence fetal development.

Understanding the epigenetic molecular mechanisms (EMMs) of reproduction is crucial for developing advanced and targeted control strategies for Spodoptera frugiperda. Differential expression analysis revealed 11 known miRNAs with varying expression levels, including nine upregulated and two downregulated miRNAs, in virgin females compared with males. The predictive analysis identified 426 target genes for these miRNAs, with ribogenesis highlighted as a key process in oogenesis and egg fertilization. This study also investigated the expression of miRNAs in both virgin and mated male and female S. frugiperda, with a focus on their roles in reproduction. A strong negative correlation was observed between miRNA expression levels and their target hub genes, confirming the transcriptional regulation by miRNAs. Additionally, protein-protein interaction (PPI) network identified the gene CG5033 (BOP1), as a central hub, was also predicted to be the target of miR-92a-3p in S. frugiperda, is involved in the maturation of large ribosomal RNA subunits. This study further provided experimental evidence that either the depletion of miR-92a-3p in virgin females or the knockdown of BOP1 in virgin males led to the production of infertile eggs post-mating. These findings validate the regulatory role of the miR-92a-3p - BOP1 interaction and underscore its importance in oogenesis and fertilization.

Supplementing choline and DHA to pregnant gilts modified fetal pig hepatic global DNA methylation induced by gestational malnutrition, suggesting that gene expression and regulation and its associated metabolic pathways are affected in the liver of offspring during growth and development.

This study aimed to investigate the effect of maternal supplementation of choline, DHA, and their interaction on hepatic mRNA expression, miRNA regulation, and metabolic pathways in the fetal pigs born to malnourished mothers.

The abundance of mRNA and miRNA was profiled in fetal liver from sows with undernutrition supplemented with choline and DHA in a 2 × 2 factorial design. The effects of choline, DHA, and their interaction on mRNA and miRNA expression were evaluated. Identification of the Biological Processes from the Gene Ontology database and miRNA Target Prediction Analysis were performed using the DAVID Functional Annotation Tool and Ingenuity Pathway Analysis. The identified miRNA-mRNA pairings were validated using RT-qPCR.

In total, 144 mRNA and 1 miRNA were altered by supplementation of choline, and the alterations were associated with the inhibitions of cardiac hypertrophy signaling, IL-6 signaling, IL-3 signaling, the Th1 pathway, and the acute phase response signaling pathway. Further, 151 mRNAs and 6 miRNAs were altered by maternal supplementation DHA and were associated with inhibition of 5 inositol-related pathways, 5 immune-related pathways, and 7 other pathways and the stimulation of peroxisome proliferator-activated receptor signaling and RhoGDI signaling pathways. In addition, 383 mRNAs and 25 miRNAs displayed choline × DHA interactions including synergistic effects on acute phase response signaling, and antagonistic effects on tRNA splicing, peroxisome proliferator-activated receptor α/retinoid X receptor α activation, and sirtuin signaling, NAD signaling, and RNA polymerase I transcription pathways. Ten of the identified 20 miRNA-mRNA pairings were validated using RT-qPCR.

The supplementation of choline, DHA, or choline plus DHA to pregnant gilts modifies liver mRNA, miRNA, and pathways in fetal pigs during gestational undernutrition.

Colorectal cancer (CRC) remains a leading cause of cancer-related mortality globally, necessitating the development of innovative treatment strategies. Recent research has underscored the significant role of non-coding RNAs (ncRNAs) in CRC pathogenesis, offering new avenues for diagnosis and therapy. In this review, we delve into the intricate roles of various ncRNAs, including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), in CRC progression, epithelial-mesenchymal transition (EMT), metastasis, and drug resistance. We highlight the interaction of these ncRNAs with and regulation of key signaling pathways, such as Wnt/β-catenin, Notch, JAK-STAT, EGFR, and TGF-β, and the functional relevance of these interactions in CRC progression. Additionally, the review highlights the emerging applications of nanotechnology in enhancing the delivery and efficacy of ncRNA-based therapeutics, which could address existing challenges related to specificity and side effects. Future research directions, including advanced diagnostic tools, targeted therapeutics, strategies to overcome drug resistance, and the integration of personalized medicine approaches are discussed. Integrating nanotechnology with a deeper understanding of CRC biology offers the potential for more effective, targeted, and personalized strategies, though further research is essential to validate these approaches.

MicroRNAs play a crucial role in regulating tumor progression and invasion. Nevertheless, the expression of miRNA-335 in prostate cancer (PCa) and its clinical significance remain unelucidated. Here, we report that miRNA-335 functions as a tumor suppressor by regulating expression of glutaminase 1 (GLS1), a key enzyme of glutamine metabolism pathway, in PCa. In this study, we show that the expression of miRNA-335 is downregulated in PCa tissues. The level of miRNA-335 is even lower in highly invasive PCa cell lines. Furthermore, enhancing the expression of miRNA-335 inhibits PCa cell migration and invasion in vitro. Additionally, we identify GLS1 as the downstream effector, governed by miRNA-335 via 3'-untranslated region, and the direct regulation is verified by dual luciferase reporter assay. MiRNA-335 interrupts glutamine catabolism by inhibiting GLS1 enzymatic activity. Overexpression of miRNA-335 markedly suppresses tumor growth of PCa in vivo. To sum up, our results indicate that miRNA-335 acts as a tumor suppressor and has an important role in restraining the metastasis of PCa cells by targeting GLS1. These discoveries indicate that miRNA-335 could serve as a new prospective therapeutic target for PCa. SIGNIFICANCE STATEMENT: miRNA-335, a metabolism-related microRNA, is a potential therapeutic target for prostate cancer by interfering with glutaminase 1 activity.

Puberty is a crucial developmental stage marked by the transition from childhood to adulthood, organized by complex hormonal signaling within the neuroendocrine system. The hypothalamus, a central region in this system, regulates pubertal functions through the hypothalamic-pituitary-gonadal (HPG) axis. Gonadotropin-releasing hormone (GnRH) neurons, essential in puberty control, release GnRH in a pulsatile manner, initiating the production of sex hormones. Major influence in pubertal timing has been attributed to genetic predisposition, environmental factors, and nutritional status. MicroRNAs (miRNAs), small non-coding RNA molecules, have emerged as key regulators in various cellular processes by either repressing genes or activating them by inhibiting their repressors. The present study aims to investigate the involvement of miRNAs in the control of puberty.

Small RNA sequencing was used to identify and compare the total population of miRNAs in the hypothalamus of female mice before, during and after puberty. Bioinformatic analysis was applied to analyse the expression profile of miRNAs with altered levels followed by pathway enrichment analysis.

Expression levels of several miRNAs were found up- or down-regulated from pre-pubertal to pubertal stage. Furthermore, monitoring the levels of these miRNAs at the post-pubertal stage revealed four expression patterns, in which pathway analysis displayed the associations of these miRNAs with developmental processes, cell cycle regulation, metabolic biosynthesis and epigenetic regulation.

The findings of the present study improve our understanding of the molecular pathways underlying puberty and stress the significance of miRNAs in fine-tuning gene expression within the hypothalamus during this critical developmental stage.

Psoriasis is a sustainable skin disease characterized by inflammation resulting from the interaction between immune cells and keratinocytes. Significant advancements have been achieved in studying the molecular process behind noncoding and coding genes, leading to valuable insights for clinical therapy. Nevertheless, our comprehension of this intricate ailment remains ambiguous. Natural products such as curcumin, vitamin D, omega-3, vitamin E, psoralen, gallic acid (GA), and resveratrol offer a promising alternative or adjunct therapy for psoriasis by modulating multiple pathways and exhibiting fewer side effects compared to conventional treatments. MicroRNAs (miRNAs) are short RNAs that are involved in regulating gene expression after transcription, namely by suppressing gene activity. Recent research on miRNAs has uncovered their significant significance in the development of psoriasis. In this review, we examined the latest developments in the investigation of miRNAs in psoriasis. Previous studies have revealed that imbalanced miRNAs in psoriasis have a significant impact on the processes of keratinocyte differentiation, proliferation, and the progression of inflammation. Furthermore, miRNAs exert an impact on the activity of immune cells involved in psoriasis, such as Langerhans cells, dendritic cells, and CD4+ T cells. Furthermore, we explore potential miRNA-focused treatment options for psoriasis, including the localized administration of external miRNA mimics, and miRNA inhibitors. The effectiveness of natural products and miRNAs in treating psoriasis, as well as the signaling pathways that may be involved, are summarized in this article.