Regulation of Oxidative Stress by Long Non-Coding RNAs in Vascular Complications of Diabetes.
Pei-Ming ChuCheng-Chia YuKun-Ling TsaiPei-Ling HsiehPublished in: Life (Basel, Switzerland) (2022)
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.
Keyphrases
- oxidative stress
- long non coding rna
- type diabetes
- poor prognosis
- risk factors
- dna damage
- diabetic nephropathy
- wound healing
- dna methylation
- ischemia reperfusion injury
- gene expression
- heart failure
- induced apoptosis
- cardiovascular disease
- glycemic control
- atrial fibrillation
- working memory
- network analysis
- signaling pathway