• Psoriasis
• macrophage
• oxidative stress
• withaferin A

• DNA nanostructure
• Microneedles
• Psoriasis
• Reactive oxygen species
• siRNA

• adipokines
• cardiometabolic risk
• dyslipidemia
• insulin resistance
• oxidative stress
• psoriatic arthritis
• systemic inflammation

• Keratinocytes/drug effects
• Humans
• Polysaccharides/pharmacology
• Polysaccharides/chemistry
• Antioxidants/pharmacology
• Antioxidants/chemistry
• Skin Aging/drug effects
• Anti-Inflammatory Agents/pharmacology
• Anti-Inflammatory Agents/chemistry
• Cell Line
• HaCaT Cells
• Tumor Necrosis Factor-alpha/metabolism
• Chemokine CCL2/metabolism

• ROS
• nano-antioxidants
• nanomedicine
• skin

• 81872520 National Natural Science Foundation of China

• Alcohol
• Biologic therapy
• IL-17 receptor A inhibitor
• Obesity
• Plaque psoriasis
• Tobacco

• Ortho Dermatologics

• GGT
• Gamma-glutamyltransferase
• cohort study
• psoriasis
• risk factor

• Erectile dysfunction (ED)
• bidirectional Mendelian randomization (bidirectional MR)
• causality
• genome-wide association study (GWAS)
• psoriasis

• TYK2 inhibitor
• psoriasis
• reactive oxygen species
• supramolecular polymers micelle
• transdermal delivery

• Reactive Oxygen Species/metabolism
• Psoriasis/drug therapy
• Psoriasis/metabolism
• Humans
• Oxidative Stress/drug effects
• Mitochondria/metabolism
• Mitochondria/drug effects
• Micelles
• Animals
• Mice
• Skin/metabolism
• Skin/drug effects
• Skin/pathology
• Polymers/chemistry
• HaCaT Cells
• Administration, Cutaneous
• Male

• Autoimmunity
• dysbiosis
• microbiota
• oxidative stress
• psoriasis

• arecoline
• interleukin-6
• keratin 6
• reactive oxygen species
• tumor necrosis factor-α

• CMU112-ASIA-12, CMU112-MF-41, and CMU112-S-51 CMU112-ASIA-12, CMU112-MF-41, and CMU112-S-51
• IRD-111002, IRD-111003, and IRD-111004 Show Chwan Memorial Hospital
• MOST 111-2314-B-039-027-MY3 Ministry of Science and Technology

• Dynamic cross-correlation matrix
• NF-kB
• free-energy landscape
• molecular dynamics simulation
• principal component analysis
• quantum mechanics

• Humans
• NF-kappa B/chemistry
• Molecular Docking Simulation
• Hesperidin
• Molecular Dynamics Simulation
• Signal Transduction

• 3,4,5-tri-O-caffeoylquinic acid (TCQA)
• AP-1
• MAPK
• MMP-1
• NF-κB
• Nrf2
• Nymphoides peltata
• anti-wrinkle
• antioxidant

• NRF-2019M3A9I3080265, NRF-2019M3A9I3080266, and NRF-2022R1A2C1003088 National Research Foundation of Korea
• KGM4582221 Korea Research Institute of Bioscience and Biotechnology

• Caspase-3
• NEAT
• Psoriasis
• ROS
• TNF-α
• VEGF

• Humans
• Up-Regulation/genetics
• Caspase 3/metabolism
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• Tumor Necrosis Factor-alpha/metabolism
• Reactive Oxygen Species/metabolism
• Vascular Endothelial Growth Factor A/genetics
• Vascular Endothelial Growth Factor A/metabolism
• Psoriasis/genetics
• Psoriasis/metabolism
• Inflammation/metabolism
• Keratinocytes/metabolism
• Cell Proliferation/genetics
• Dyslipidemias/metabolism

• Cairo University

• Humans
• Complex Regional Pain Syndromes
• Cytokines/genetics
• Cytokines/metabolism
• Inflammation/metabolism
• Interleukin-6/metabolism
• Keratinocytes/metabolism
• Keratinocytes/pathology
• Phenylephrine/pharmacology
• Receptors, Adrenergic/metabolism
• Tumor Necrosis Factor-alpha/metabolism
• Receptors, Adrenergic, alpha-1/metabolism

Oxidative stress due to excessive reactive oxygen species (ROS) production in the skin microenvironment is one of the main mechanisms in psoriasis pathogenesis. A nano drug delivery system based on ROS-responsive release can enhance drug release at the target site. In this study, a ROS-sensitive material methoxypolyethylene glycol-thioether-thiol (mPEG-SS) was synthesized using mPEG as the parent structure with sulfide structural modification. An mPEG-SS-calcipotriol (mPEG-SS-CPT, PSC) nano-micelle percutaneous delivery system was prepared by encapsulating CPT. A small animal imaging system was used to study PSC’s the ROS-sensitive drug release process. It is shown that endogenous ROS mainly affects PSC and releases drugs. Finally, the therapeutic effect of PSC on psoriasis was explored by animal experiments. Ultimately, it ameliorates imiquimod-induced psoriasis-like inflammation. Overall, PSC is an effective ROS-sensitive transdermal drug delivery system that is expected to provide a new strategy for treating psoriasis.

• Psoriasis
• calcipotriol
• nano-micelle
• reactive oxygen species sensitive
• transdermal drug delivery

• cardamonin
• chalcone
• fruits
• gastric secretion
• gastric ulcer

Reactive oxygen species (ROS) at supraphysiological concentration have a determinate role in contributing to immuno-metabolic disorders in the epithelial immune microenvironment (EIME) of psoriatic lesions. With an exclusive focus on the gene-oxidative stress environment interaction in the EIME, a comprehensive strategy based on ROS-regulating nanomedicines is greatly anticipated to become the mainstay of anti-psoriasis treatment. This potential therapeutic modality could inhibit the acceleration of psoriasis via remodeling the redox equilibrium and reshaping the EIME. Herein, we present a marked overview of the current progress in the pathomechanisms of psoriasis, with particular concerns on the potential pathogenic role of ROS, which significantly dysregulates redox metabolism of keratinocytes (KCs) and skin-resident or -infiltrating cells. Meanwhile, the emergence of versatile nanomaterial-guided evolution for transdermal drug delivery has been attractive for the percutaneous administration of antipsoriatic therapies in recent years. We emphasize the underlying molecular mechanism of ROS-based nanoreactors for improved therapeutic outcomes against psoriasis and summarize up-to-date progress relating to the advantages and limitations of nanotherapeutic application for transdermal administration, as well as update an insight into potential future directions for nanotherapies in ROS-related skin diseases.

• Epithelial immune microenvironment
• Psoriasis
• Reactive oxygen species
• Transdermal drug delivery

• Chronic toxicity
• Development
• Marine copepod
• Microplastics
• Reproduction

• Animals
• Copepoda
• Microplastics
• Plastics
• Polystyrenes/toxicity
• Reproduction
• Water Pollutants, Chemical/toxicity

• Acetylcholinesterase/metabolism
• Alzheimer Disease/chemically induced
• Alzheimer Disease/drug therapy
• Alzheimer Disease/metabolism
• Animals
• Antioxidants/metabolism
• Cholinergic Agents/pharmacology
• Cognition
• Maze Learning
• Memory Disorders/drug therapy
• Mice
• Mycelium/metabolism
• NF-E2-Related Factor 2/metabolism
• Oxidative Stress
• Phenylethyl Alcohol/analogs & derivatives
• Plant Extracts/pharmacology
• Plant Extracts/therapeutic use
• Rhodiola/metabolism
• Scopolamine/pharmacology

Although oxidative stress is recognized as an important effector mechanism of the immune system, uncontrolled formation of reactive oxygen and nitrogen species promotes excessive tissue damage and leads to disease development. In view of this, increased dietary salt intake has been found to damage redox systems in the vessel wall, resulting in endothelial dysfunction associated with NO uncoupling, inflammation, vascular wall remodeling and, eventually, atherosclerosis. Several studies have reported increased systemic oxidative stress accompanied by reduced antioxidant capacity following a high salt diet. In addition, vigorous ionic effects on the immune mechanisms, such as (trans)differentiation of T lymphocytes are emerging, which together with the evidence of NaCl accumulation in certain tissues warrants a re-examination of the data derived from in vitro research, in which the ionic influence was excluded. Psoriasis vulgaris (PV), as a primarily Th17-driven inflammatory skin disease with proven inflammation-induced accumulation of sodium chloride in the skin, merits our interest in the role of oxidative stress in the pathogenesis of PV, as well as in the possible beneficial effects that could be achieved through modulation of dietary salt intake and antioxidant supplementation.

• EGFR
• TXNIP
• differentiation
• keratinocyte
• psoriasis

Psoriasis is a chronic relapsing immunological skin disease characterized by multiple cross-talk inflammatory circuits which are relevantly associated with abnormal cross-reactivity between immune cells and keratinocytes (KCs). It may be inadequate to eradicate complicated pathogenesis only via single-mode therapy. To provide optimal combinatory therapeutics, a nanocomposite-based hydrogel was constructed by loading methotrexate (MTX) into ZnO/Ag to realize combined multiple target therapy of psoriasis.

In this composite hydrogel, ZnO hybrid mesoporous microspheres were utilized both as drug carriers and reactive oxygen species (ROS)-scavenging nanoparticles. A proper amount of Ag nanoparticle-anchored ZnO nanoparticles (ZnO/Ag) was functionalized with inherent immunoregulatory property. The experiments showed that ZnO/Ag nanoparticles could exhibit a self-therapeutic effect that was attributed to reducing innate cytokine profiles by inactivating p65 in proinflammatory macrophages and abrogating secretion of adaptive cytokines in KCs by downregulating ROS-mediated STAT3-cyclin D1 signaling. A preferable antipsoriatic efficacy was achieved via topical administration of this hydrogel on the imiquimod (IMQ)-induced psoriasis mice model, demonstrating the superior transdermal delivery and combined enhancement of therapeutic efficacy caused by intrinsic nanoparticles and extrinsic MTX.

This composite hydrogel could serve as a multifunctional, nonirritating, noninvasive and effective transcutaneous nanoagent against psoriasis.

The online version contains supplementary material available at 10.1186/s12951-022-01368-y.

• Hydrogel
• Immunoregulation
• Methotrexate
• Psoriasis
• Transdermal delivery

• ROS
• diagnostics
• inflammatory skin diseases
• microneedles
• tattoos

Psoriasis is a common, chronic systemic inflammatory disease affecting 125 million people worldwide. It is associated with several important conditions, including psoriatic arthritis, cardiometabolic syndrome, and depression, leading to a significant reduction in patients’ quality of life. Current treatments only reduce symptoms, not cure. This review discusses the mechanisms involved in the initiation and development of the disease, the role of oxidative stress in this autoimmune disease, as well as potential therapeutic options with substances of natural origin. The main aim of the study is intended to offer a review of the literature to present plants and phytochemicals that can represent potential remedies in the fight against psoriasis. We identified many in vitro, in vivo, and clinical trials studies that evaluated the relationship between chosen natural substances and immune system response in the course of psoriasis. We sought to find articles about the efficacy of potential natural-derived drugs in controlling symptoms and their ability to maintain long-term disease inactivity without side effects, and the result of our work is a review, which highlights the effectiveness of plant-derived drugs in controlling the inflammatory burden on psoriatic patients by decreasing the oxidative stress conditions.

• antioxidants
• medicinal plants
• natural substances
• psoriasis

Acne vulgaris (AV) is a chronic skin disease of the pilosebaceous unit affecting both adolescents and adults. Its pathophysiology includes processes of inflammation, increased keratinization, sebum production, hormonal dysregulation, and bacterial Cutibacterium acnes proliferation. Common AV has been treated with antibiotics since the 1960s, but strain resistance has emerged and is of paramount concern. Macroalgae are known producers of substances with bioactive properties, including anti-viral, antibacterial, antioxidant, and anti-inflammatory properties, among several others. In particular, red algae are rich in bioactive compounds such as polysaccharides, phenolic compounds, lipids, sterols, alkaloids, and terpenoids, conferring them antioxidant, antimicrobial, and anti-inflammatory activities, among others. Thus, the exploration of compounds from marine resources can be an appealing approach to discover new treatment options against AV. The aim of this work is to provide an overview of the current knowledge of the potentialities of red macroalgae in the treatment of AV by reviewing the main therapeutic targets of this disease, and then the existence of compounds or extracts with bioactive properties against them.

• Cutibacterium acnes
• Rhodophyta
• acne pathophysiology
• antibacterial
• bioactive compounds
• inflammation
• seaweed extracts

Rapamycin (Rapa) is an immunosuppressive macrolide that inhibits the mechanistic target of rapamycin (mTOR) activity. Thanks to its anti-proliferative effects towards different cell types, including keratinocytes and T cells, Rapa shows promise in the treatment of skin diseases characterized by cell hyperproliferation. However, Rapa skin penetration is limited due to its lipophilic nature (log P = 4.3) and high molecular weight (MW = 914 g/mol). In previous studies, new microenvironment-sensitive core multishell (CMS) nanocarriers capable of sensing the redox state of inflamed skin were developed as more efficient and selective vehicles for macrolide delivery to inflamed skin.

In this study, we tested such redox-sensitive CMS nanocarriers using an inflammatory skin model based on human skin explants co-cultured with Jurkat T cells. Serine protease (SP) was applied on skin surface to induce skin barrier impairment and oxidative stress, whereas phytohaemagglutinin (PHA), IL-17A, and IL-22 were used to activate Jurkat cells. Activation markers, such as CD45 and CD69, phosphorylated ribosomal protein S6 (pRP-S6), and IL-2 release were monitored in activated T cells, whereas pro-inflammatory cytokines were measured in skin extracts and culture medium.

We found that alteration of skin barrier proteins corneodesmosin (CDSN), occludin (Occl), and zonula occludens-1 (ZO-1) as well as oxidation-induced decrease of free thiol groups occurred upon SP-treatment. All Rapa formulations exerted inhibitory effects on T cells after penetration across ex vivo skin. No effects on skin inflammatory markers were detected. The superiority of the oxidative-sensitive CMS nanocarriers over the other formulations was observed with regard to drug delivery as well as downregulation of IL-2 release.

Overall, our results demonstrate that nanocarriers addressing features of diseased skin are promising approaches to improve the topical delivery of macrolide drugs.

• dermatology
• drug release
• psoriasis
• redox-sensitive nanoparticles
• sirolimus
• stratum corneum barrier

• HMC-1 cells
• Manoalide
• allergic inflammation
• caspase-1
• nuclear factor-κB

The development of psoriasis is associated with the consequences of oxidative stress and inflammation leading to metabolic changes locally, in the skin cells, and systemically, in the blood. Therefore, the aim of this study was to analyze the effect of psoriasis vulgaris (PsV) and psoriatic arthritis (PsA) on the basal plasma/keratinocyte levels of matrix metalloproteinases (MMPs), tissue inhibitors of matrix metalloproteinases (TIMPs), and angiogenesis factors, as well as to evaluate the effect of CBD on these parameters in keratinocytes isolated from psoriatic/healthy individuals with and without in vitro irradiation by UVB. A quantitative chemiluminescent method of detection based on an ELISA protocol and zymography technique was used during analysis. It was shown that activity levels of MMP-9 and TIMP-2 in PsA plasma were higher than in PsV. Changes in the proteolytic activity were accompanied by an increase in markers of angiogenesis (angiopoietin-2, HGF, VEGF, TNFα, PDGF, FGF), where in the specific case of angiopoietin-2 and TNFα, the overexpression in PsV was significantly stronger than in PsA. CBD application to keratinocytes partially restored levels of MMP-1/2/3/7 and TIMP-1/2 (in an effect which was particularly enhanced by UVB irradiation), as well as levels of the examined angiogenic factors except TNFα (levels of which were increased in psoriatic keratinocytes and decreased in healthy keratinocytes). Presented results indicate that CBD may be suggested as an antiangiogenic factor that reduces the proinflammatory action of UVB in psoriatic keratinocytes and partially has a protective effect for healthy keratinocytes.

• Lipidomics
• MS based analysis
• Proteomics
• Psoriasis
• Samples preparation
• Signaling pathways

• Chromatography, Liquid
• Humans
• Proteomics
• Psoriasis
• Skin
• Tandem Mass Spectrometry

• anti-inflammatory substances
• nanostructured lipid carriers
• natural products
• topical nanomedicines

• Colorectal cancer
• Crohn's disease
• HMGCS2
• Inflammatory bowel disease
• Intestinal cells
• Ketogenesis
• TNFα
• Ulcerative colitis

• Animals
• Apoptosis
• Caco-2 Cells
• Humans
• Hydroxymethylglutaryl-CoA Synthase
• Intestinal Mucosa
• Ketone Bodies
• Mice
• Tumor Necrosis Factor-alpha/genetics

• P30 CA177558 NCI NIH HHS
• R01 DK048498 NIDDK NIH HHS

Psoriasis (PsO) is a common T cell-mediated inflammatory disorder of the skin with an estimated prevalence of 2%. The condition manifests most commonly as erythematous plaques covered with scales. The aetiology of PsO is multifactorial and disease initiation involves interactions between environmental factors, susceptibility genes, and innate and adaptive immune responses. The underlying pathology is mainly driven by interleukin-17. In addition, various inflammatory mediators from specific T helper (T_H) cell subsets, namely T_H1, T_H17, and T_H22, are overexpressed in cutaneous lesions and may also be detected in the peripheral blood of psoriatic patients. Moreover, these individuals are also at greater risk, compared to the general population, of developing multiple comorbid conditions. Cardiovascular disease (CVD) has been recognised as a prominent comorbidity of PsO. A potential mechanism contributing to this association may be the presence of a hypercoagulable state in these individuals. Inflammation and coagulation are closely related. The presence of chronic, low-grade systemic inflammation may promote thrombosis – one of the major determinants of CVD. A pro-inflammatory milieu may induce the expression of tissue factor, augment platelet activity, and perturb the vascular endothelium. Altogether, these changes will result in a prothrombotic state. In this review, we describe the aetiology of PsO, as well as the pathophysiology of the condition. We also consider its relationship to CVD. Given the systemic inflammatory nature of PsO, we evaluate the potential contribution of prominent inflammatory mediators (implicated in PsO pathogenesis) to establishing a prothrombotic state in psoriatic patients.

• cardiovascular disease
• endothelium
• hypercoagulability
• platelets
• psoriasis
• systemic inflammation

• Brain targeting
• Catalase
• Extracellular vesicle
• Intranasal delivery
• Toxicity

Alcohol affects the symptoms, compliance and comorbidities as well as the safety and efficacy of treatments in psoriatic patients. In this review, we aim to summarize and link clinical observations with a molecular background, such as signaling pathways at the cellular level and genetic variations, and to provide an overview of how this knowledge could influence our treatment selection and patient management.

• addiction
• alcohol
• compliance
• genetic factors
• immune cells
• keratinocytes
• psoriasis

• Animals
• Ethanol/adverse effects
• Genetic Predisposition to Disease
• Humans
• Models, Biological
• Patient Compliance
• Psoriasis/genetics
• Psoriasis/pathology
• Psoriasis/therapy
• Translational Research, Biomedical

• hydrogen peroxide
• oxidative stress
• tumor necrosis factor-α

• Acne Vulgaris/diet therapy
• Acne Vulgaris/etiology
• Acne Vulgaris/prevention & control
• Dairy Products/adverse effects
• Fatty Acids, Omega-3/administration & dosage
• Feeding Behavior
• Glycemic Index
• Humans
• Linoleic Acid/administration & dosage
• Probiotics/administration & dosage
• United States

• Sun Pharmaceutical Industries, Inc.

Psoriasis is caused by a complex interplay among the immune system, genetic background, autoantigens, and environmental factors. Recent studies have demonstrated that patients with psoriasis have a significantly higher serum homocysteine (Hcy) level and a higher prevalence of hyperhomocysteinaemia (HHcy). Insufficiency of folic acid and vitamin B₁₂ can be a cause of HHcy in psoriasis. Hcy may promote the immuno-inflammatory process in the pathogenesis of psoriasis by activating Th1 and Th17 cells and neutrophils, while suppressing regulatory T cells. Moreover, Hcy can drive the immuno-inflammatory process by enhancing the production of the pro-inflammatory cytokines in related to psoriasis. Hcy can induce nuclear factor kappa B activation, which is critical in the immunopathogenesis of psoriasis. There may be a link between the oxidative stress state in psoriasis and the effect of HHcy. Hydrogen sulfide (H₂S) may play a protective role in the pathogenesis of psoriasis and the deficiency of H₂S in psoriasis may be caused by HHcy. As the role of Hcy in the pathogenesis of psoriasis is most likely established, Hcy can be a potential therapeutic target for the treatment of psoriasis. Systemic folinate calcium, a folic acid derivative, and topical vitamin B12 have found to be effective in treating psoriasis.

• folic acid
• homocysteine
• hydrogen sulfide
• psoriasis
• vitamin B12

• Rosacea
• assessor-blinded
• clinical trial
• modified glutathione

• antioxidants
• oxidative stress
• psoriasis
• reactive oxygen species/reactive nitrogen species

• Animals
• Apoptosis
• Autophagy
• Gene Expression Regulation
• Humans
• Oxidative Stress
• Psoriasis/metabolism
• Reactive Nitrogen Species/metabolism
• Reactive Oxygen Species/metabolism
• Transcription Factors/metabolism

• UMO-2017/27/B/NZ3/02212 National Science Centre
• T-32.1 Institute of Biochemistry and Biophysics of the Polish Academy of Sciences

Traditional medicine is still widely practiced in Iraqi Kurdistan, especially by people living in villages on mountainous regions; medicinal plants are also sold in the markets of the large towns, such as at Erbil, the capital of the Kurdistan Autonomous Region. About a dozen of Verbascum species (Scrophulariaceae) are commonly employed in the Kurdish traditional medicine, especially for treating burns and other skin diseases. However, the isolation of bioactive secondary metabolites from these plants has not been the subject of intense scientific investigations in Iraq. Therefore, the information reported in the literature about the species growing in Kurdistan has been summarized in the first part of this paper, although investigations have been performed on vegetable samples collected in neighbouring countries, such as Turkey and Iran. In the second part of the work, we have investigated, for the first time, the contents of a methanol and a hydromethanol extract of V. calvum flowers. The extracts exhibited weak antimicrobial activities, whereas the methanol extract showed significant antiproliferative effects against an A549 lung cancer cell line. Moreover, both extracts exhibited a significant dose-dependent free radical scavenging action against the 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical, comparable to that of ascorbic acid. In the subsequent phytochemical study, a high phenolic content was determined in both extracts by the Folin–Ciocalteu assay and medium-pressure liquid chromatographic (MPLC) separation led to the isolation of iridoid glucosides ajugol and aucubin from the methanol extract. In conclusion, the high anti-inflammatory effects of aucubin and the remarkable antioxidant (antiradical) properties of the extracts give scientific support to the traditional use of V. calvum flowers for the preparation in Kurdistan of remedies to cure skin burns and inflammations.

• Kurdish traditional medicine
• Verbascum
• ajugol
• antiradical activity
• aucubin
• iridoid
• phenolics
• terpenoids

• Calendula officinalis
• Epidermal thickness
• PSI
• Phlebodium decumanum
• correlation
• psoriasis

Monocyte extravasation through the endothelial layer is a hallmark of atherosclerotic plaque development and is mediated by heavily N-glycosylated surface adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1). N-glycosylation is a key co- and post-translational modification that adds sugar molecules to Asparagine residues of surface and secreted proteins. While it has been suggested that surface and secreted proteins will not be expressed unless fully processed to a complex N-glycoform, emerging data has suggested that multiple N-glycoforms can exist on the cell surface. Previous data from our lab has shown that endothelial inflammation produces multiple N-glycoforms of ICAM-1, and that a hypoglycosylated, or high-mannose (HM), form of ICAM-1 enhances adhesion of pro-inflammatory monocytes associated with more severe atherosclerosis and adverse cardiac events. Despite these findings, little is understood about the regulation of N-glycans during disease. In this study, we focus on the α-mannosidases; an understudied class of enzymes for early N-glycan processing. We show that α-mannosidase activity decreases with TNFα treatment in endothelial cells, and this decrease correlates with HM N-glycan formation on the cell surface. Further, we demonstrate that this inhibition is class-I dependent, and is independent of NF-κB upregulation of ICAM-1. Finally, we show that this inhibition is due in part to hydrogen peroxide (H₂O₂), generated by Endoplasmic Reticulum oxidoreductase 1-α (ERO1α). These data provide insights into the regulation of surface N-glycans during inflammation and demonstrate a novel role for reactive species in N-glycan biosynthesis.

• Catalase
• Endoplasmic reticulum redox
• ICAM-1
• Inflammation
• Mannose
• Mannosidase
• N-glycosylation