Inhibition of MEG3 ameliorates cardiomyocyte apoptosis and autophagy by regulating the expression of miRNA-129-5p in a mouse model of heart failure

Author:

Mi Shan1,Huang Feng1,Jiao Mingli12,Qian Zhuang3,Han Mingming1,Miao Zheng1,Zhan Heqin1

Affiliation:

1. Department of Pharmacology, College of Pharmacy, Xinxiang Medical University, Xinxiang, Henan, People’s Republic of China

2. Experimental Teaching Center of Public Health and Preventive Medicine, School of Public Health, Xinxiang Medical University, Xinxiang, Henan, People’s Republic of China

3. Institutes of Health Central Plains, Xinxiang Medical University, Xinxiang, Henan, People’s Republic of China.

Funder

Science and technology key projects of Henan Province, China

Publisher

Informa UK Limited

Subject

Biochemistry (medical),Cell Biology,Clinical Biochemistry,Physiology,Biochemistry

Reference46 articles.

1. CDR132L improves systolic and diastolic function in a large animal model of chronic heart failure

2. Rapamycin regulates the balance between cardiomyocyte apoptosis and autophagy in chronic heart failure by inhibiting mTOR signaling;Gao G;Int J Mol Med,2020

3. Inhibition of the Cardiac Fibroblast–Enriched lncRNA Meg3 Prevents Cardiac Fibrosis and Diastolic Dysfunction

4. STAT3-induced upregulation of lncRNA MEG3 regulates the growth of cardiac hypertrophy through miR-361-5p/HDAC9 axis

5. Silencing of long noncoding RNA MEG3 enhances cerebral protection of dexmedetomidine against hypoxic-ischemic brain damage in neonatal mice by binding to miR-129-5p;Zhou XM;J Cell Biochem,2018

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