Stress-related long non-coding RNAs (lncRNAs) regulate the pathogenesis of diabetes and its complications by modulating pathways involved in cell death, proliferation, inflammation, and fibrosis.
Diabetes mellitus (DM) is a chronic metabolic disorder and one of the most significant global health burdens worldwide. Key pathophysiological mechanisms underlying its onset and associated complications include hyperglycemia-related stresses, such as oxidative stress and endoplasmic reticulum stress (ER stress). Long non-coding RNAs (lncRNAs), defined as RNA transcripts longer than 200 nucleotides and lacking protein-coding capacity, play crucial roles in various biological processes and have emerged as crucial regulators in the pathogenesis of diabetes. This review provides a comprehensive overview of lncRNA biogenesis and its functional roles, emphasizing recent findings that link stress-related lncRNAs to diabetic pathology and complications. Also, we discuss how lncRNAs influence diabetes and its complications by modulating pathways involved in cell death, proliferation, inflammation, and fibrosis, which contribute to pancreatic β cell dysfunction, insulin resistance, diabetic nephropathy, and retinopathy. By analyzing current research, we aim to enhance understanding of lncRNA involvement in diabetes while identifying potential therapeutic targets and guiding future research directions to elucidate the complex mechanisms underlying this pervasive condition.
Li et al. (Fri,) conducted a review in Diabetes mellitus and diabetic complications. Stress-related lncRNAs was evaluated. Stress-related long non-coding RNAs (lncRNAs) regulate the pathogenesis of diabetes and its complications by modulating pathways involved in cell death, proliferation, inflammation, and fibrosis.