Abstract
Diabetes mellitus is a well-known metabolic disorder with numerous complications, such as macrovascular diseases (e.g., coronary heart disease, diabetic cardiomyopathy, stroke, and peripheral vascular disease), microvascular diseases (e.g., diabetic nephropathy, retinopathy, and diabetic cataract), and neuropathy. Multiple contributing factors are implicated in these complications, and the accumulation of oxidative stress is one of the critical ones. Several lines of evidence have suggested that oxidative stress may induce epigenetic modifications that eventually contribute to diabetic vascular complications. As one kind of epigenetic regulator involved in various disorders, non-coding RNAs have received great attention over the past few years. Non-coding RNAs can be roughly divided into short (such as microRNAs; ~21–25 nucleotides) or long non-coding RNAs (lncRNAs; >200 nucleotides). In this review, we briefly discussed the research regarding the roles of various lncRNAs, such as MALAT1, MEG3, GAS5, SNHG16, CASC2, HOTAIR, in the development of diabetic vascular complications in response to the stimulation of oxidative stress.
Highlights
Diabetes mellitus (DM) is a chronic metabolic disorder with an increasing risk of cardiovascular diseases
The hyperglycemia-induced tissue injury has been shown to be mediated by the following mechanisms, including the increased flux of glucose and other sugars through the polyol pathway, the increased production of advanced glycation end products (AGEs), activation of protein kinase C (PKC) isoforms, increased hexosamine pathway flux and consequent over-modification of proteins by N-acetylglucosamine, and these pathways are all activated by the hyperglycemia-induced mitochondrial superoxide production by inhibiting GAPDH [6]
Unlike microRNAs which exert their regulatory capacity through binding to the 3 untranslated region (UTR) of their target genes, the embodiment of the long non-coding RNAs (lncRNAs) function includes a variety of ways, such as serving as scaffolds, molecular signals, guides, or decoys [8]
Summary
Diabetes mellitus (DM) is a chronic metabolic disorder with an increasing risk of cardiovascular diseases. DM has a well-established association with an increase in the likelihood of developing various complications, such as macrovascular and microvascular diseases. Macrovascular disorders include coronary heart disease, diabetic cardiomyopathy, stroke, and peripheral vascular disease, and microvascular disorders comprise diabetic nephropathy and retinopathy. Kelch-like ECH-associated protein 1 (Keap1) is responsible for the cytosolic sequestration of Nrf. Nrf will be released from Keap and translocate into the nucleus where it binds to the antioxidant response element (ARE) sequence and increases the transcription of antioxidant enzymes, such as heme oxygenase-1 (HO-1) [5]. The downregulation of hyperglycemia-associated oxidative stress will aid in the better control of diabetic complications
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