Research Paper Volume 13, Issue 18 pp 22516—22527
miR-320 accelerates chronic heart failure with cardiac fibrosis through activation of the IL6/STAT3 axis
- 1 Third Division, Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, PR China
- 2 Department of Biochemistry and Molecular Biology, The Hebei Medical University, Shijiazhuang, Hebei 050011, PR China
- 3 Department of Cardiology, The Second Hospital of Hebei Medical University and Hebei Institute of Cardiovascular Research, Shijiazhuang, Hebei 050011, PR China
Received: October 31, 2020 Accepted: August 24, 2021 Published: September 28, 2021https://doi.org/10.18632/aging.203562
How to Cite
Copyright: © 2021 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Cardiac fibrosis could induce abnormal cardiac function and become a novel target for cardiac hypertrophy and chronic heart failure. MiRNA-320 is a crucial miRNA in cardiovascular disease, but it is poorly understood whether it plays a role in cardiac fibrosis pathogenesis. We aimed to identify the specific underlying mechanism of miR-320 in cardiac fibrosis and hypertrophic pathogenesis. In our study, the GEO datasets revealed that STAT3 was significantly highly expressed in cardiomyocyte lines. MiR-320 activation and STAT3 signaling pathways were statistically significantly connected. Furthermore, miR-320 was highly associated with cardiac fibrosis and hypertrophic disease. Interstitial fibrosis was observed in the mice subjected to TAC surgery, markedly enhanced in miR-320 mimics. Mechanistically, we revealed that miR-320 mimics aggravated the pressure overload and induced cardiac hypertrophy and fibrosis via the IL6/STAT3/PTEN axis. MiR-320 mimics accelerated cardiac hypertrophy and cardiac fibrosis via the IL6/STAT3/PTEN axis. These results suggest that targeting miR-320 may represent a potential therapeutic strategy for cardiac hypertrophy and fibrosis.