Donate-Correa J, González-Luis A, Díaz-Vera J, Hernandez-Fernaud JR. MicroRNA-630: A promising avenue for alleviating inflammation in diabetic kidney disease. World J Diabetes 2024; 15(7): 1398-1403 [DOI: 10.4239/wjd.v15.i7.1398]
Corresponding Author of This Article
Javier Donate-Correa, PhD, Research Scientist, Teacher, Research Unit, University Hospital Nuestra Señora de Candelaria (UHNSC), Carretera del Rosario S/N, Santa Cruz de Tenerife 38010, Spain. jdonatecorrea@gmail.com
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Diabetes. Jul 15, 2024; 15(7): 1398-1403 Published online Jul 15, 2024. doi: 10.4239/wjd.v15.i7.1398
MicroRNA-630: A promising avenue for alleviating inflammation in diabetic kidney disease
Javier Donate-Correa, Ainhoa González-Luis, Jésica Díaz-Vera, Juan Ramón Hernandez-Fernaud
Javier Donate-Correa, Ainhoa González-Luis, Jésica Díaz-Vera, Research Unit, University Hospital Nuestra Señora de Candelaria (UHNSC), Santa Cruz de Tenerife 38010, Spain
Juan Ramón Hernandez-Fernaud, Department of Biochemistry, Microbiology, Cell Biology and Genetics, Instituto de Tecnologías Biomédicas, Universidad de La Laguna, Santa Cruz de Tenerife 38000, Spain
Author contributions: Donate-Correa J, González-Luis A, Díaz-Vera J and Hernandez-Fernaud JR designed this editorial; González-Luis A, Díaz-Vera J and Hernandez-Fernaud JR contributed to the data collection and editing of the manuscript; Donate-Correa J wrote the paper; All the authors have read and approved the final version of the present manuscript.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Javier Donate-Correa, PhD, Research Scientist, Teacher, Research Unit, University Hospital Nuestra Señora de Candelaria (UHNSC), Carretera del Rosario S/N, Santa Cruz de Tenerife 38010, Spain. jdonatecorrea@gmail.com
Received: February 10, 2024 Revised: March 18, 2024 Accepted: April 22, 2024 Published online: July 15, 2024 Processing time: 148 Days and 15.3 Hours
Abstract
Diabetic kidney disease (DKD) is one of the complications of diabetes, affecting millions of people worldwide. The relentless progression of this condition can lead to kidney failure, requiring life-altering interventions such as dialysis or transplants. Accumulating evidence suggests that immunologic and inflammatory elements play an important role in initiating and perpetuating the damage inflicted on renal tissues, exacerbating the decline in organ function. Toll-like receptors (TLRs) are a family of receptors that play a role in the activation of the innate immune system by the recognition of pathogen-associated molecular patterns. Recent data from in vitro and in vivo studies have highlighted the critical role of TLRs, mainly TLR2 and TLR4, in the pathogenesis of DKD. In the diabetic milieu, these TLRs recognize diabetic-associated molecular signals, triggering a proinflammatory cascade that initiates and perpetuates inflammation and fibrogenesis in the diabetic kidney. Emerging non-traditional strategies targeting TLR signaling with potential therapeutic implications in DKD have been pro-posed. One of these approaches is the use of microRNAs, small non-coding RNAs that can regulate gene expression. This editorial comments on the results of this approach carried out in a rat model of diabetes by Wu et al, published in this issue of the World Journal of Diabetes. The results of the experimental study by Wu et al shows that microRNA-630 decreased levels compared to non-diabetic rats. Additionally, microRNA-630 exerted anti-inflammatory effects in the kidneys of diabetic rats through the modulation of TLR4. These findings indicate that the microRNA-630/TLR4 axis might represent a pathological mechanism of DKD and a potential therapeutic target capable of curbing the destructive inflammation characteristic of DKD.
Core Tip: Targeting Toll-like receptors (TLRs) via microRNAs is a promising therapeutic approach for reducing inflammation and slowing the progression of diabetic kidney disease (DKD). Understanding how TLR4 expression and signaling are linked to microRNAs regulation, may pave the path for future targeted clinical interventions in DKD.
