EndMT Regulation by Small RNAs in Diabetes-Associated Fibrotic Conditions: Potential Link With Oxidative Stress

نویسندگان

چکیده

Diabetes-associated complications, such as retinopathy, nephropathy, cardiomyopathy, and atherosclerosis, the main consequences of long-term hyperglycemia, often lead to organ dysfunction, disability, increased mortality. A common denominator these complications is myofibroblast-driven excessive deposition extracellular matrix proteins. Although fibroblast appears be primary source myofibroblasts, other cells, including endothelial can generate myofibroblasts through a process known mesenchymal transition (EndMT). During EndMT, cells lose their typical phenotype acquire features, characterized by development invasive migratory abilities well expression products ?-smooth muscle actin type I collagen. EndMT involved in many chronic fibrotic diseases regulated complex molecular mechanisms different signaling pathways. Recent evidence suggests that small RNAs, particular microRNAs (miRNAs) long non-coding RNAs (lncRNAs), are crucial mediators EndMT. Furthermore, miRNAs both affected oxidative stress, another key player pathophysiology diabetic complications. In this review, we provide an overview redox signals underpinning diabetic-associated process. Then, discuss current knowledge on role regulation atherosclerosis highlight potential links between stress dyad RNAs-EndMT driving pathological states.

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ژورنال

عنوان ژورنال: Frontiers in Cell and Developmental Biology

سال: 2021

ISSN: ['2296-634X']

DOI: https://doi.org/10.3389/fcell.2021.683594