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The microRNA in ventricular remodeling: the miR-30 family
- Source :
- Bioscience Reports
- Publication Year :
- 2019
-
Abstract
- Ventricular remodeling (VR) is a complex pathological process of cardiomyocyte apoptosis, cardiac hypertrophy, and myocardial fibrosis, which is often caused by various cardiovascular diseases (CVDs) such as hypertension, acute myocardial infarction, heart failure (HF), etc. It is also an independent risk factor for a variety of CVDs, which will eventually to damage the heart function, promote cardiovascular events, and lead to an increase in mortality. MicroRNAs (miRNAs) can participate in a variety of CVDs through post-transcriptional regulation of target gene proteins. Among them, microRNA-30 (miR-30) is one of the most abundant miRNAs in the heart. In recent years, the study found that the miR-30 family can participate in VR through a variety of mechanisms, including autophagy, apoptosis, oxidative stress, and inflammation. VR is commonly found in ischemic heart disease (IHD), hypertensive heart disease (HHD), diabetic cardiomyopathy (DCM), antineoplastic drug cardiotoxicity (CTX), and other CVDs. Therefore, we will review the relevant mechanisms of the miR-30 in VR induced by various diseases.
- Subjects :
- 0301 basic medicine
medicine.medical_specialty
autophagy
Heart Diseases
Biophysics
Disease
Review Article
030204 cardiovascular system & hematology
Biochemistry
miR-30 family
03 medical and health sciences
0302 clinical medicine
Diabetic cardiomyopathy
Internal medicine
medicine
Animals
Humans
Myocytes, Cardiac
Myocardial infarction
Ventricular remodeling
Molecular Biology
Review Articles
Cardiotoxicity
Ventricular Remodeling
business.industry
apoptosis
Heart
Cell Biology
medicine.disease
Hypertensive heart disease
MicroRNAs
Oxidative Stress
030104 developmental biology
inflammation
Heart failure
Cardiology
Myocardial fibrosis
business
Subjects
Details
- ISSN :
- 15734935
- Volume :
- 39
- Issue :
- 8
- Database :
- OpenAIRE
- Journal :
- Bioscience reports
- Accession number :
- edsair.doi.dedup.....6954a47bda26ef39417ce1d23f645a96