Effect of Hypoxia-Induced MicroRNA-210 Expression on Cardiovascular Disease and the Underlying Mechanism.
Yinuo GuanXianjing SongWei SunYiran WangBing LiuPublished in: Oxidative medicine and cellular longevity (2019)
Cardiovascular diseases have high morbidity and mortality rates worldwide, and their treatment and prevention are challenging. MicroRNAs are a series of noncoding RNAs with highly conserved sequences and regulate gene expression by inhibiting mRNA transcription or degrading targeting proteins. MicroRNA-210 is significantly upregulated during hypoxia and plays a protective role by inhibiting apoptosis and regulating cell proliferation, differentiation, migration, mitochondrial metabolism, and angiogenesis in hypoxic cells. MicroRNA-210 expression is altered in cardiovascular diseases such as atherosclerosis, acute myocardial infarction, preeclampsia, aortic stenosis, and heart failure, and overexpression of microRNA-210 in some of these diseases exerts protective effects on target organs. Furthermore, chronically upregulated miR-210 potentially plays a marked pathogenic role in specific situations. This review primarily focuses on the upstream pathways, downstream targets, clinical progress in cardiovascular disease, and potential applications of microRNA-210.
Keyphrases
- cardiovascular disease
- cell proliferation
- gene expression
- heart failure
- aortic stenosis
- acute myocardial infarction
- left ventricular
- poor prognosis
- oxidative stress
- transcription factor
- type diabetes
- signaling pathway
- endothelial cells
- cardiovascular events
- cell cycle arrest
- cardiovascular risk factors
- long non coding rna
- binding protein
- ejection fraction
- aortic valve
- induced apoptosis
- aortic valve replacement
- early onset
- transcatheter aortic valve implantation
- dna methylation
- cell death
- coronary artery disease
- acute coronary syndrome
- atrial fibrillation
- cardiac resynchronization therapy
- wound healing