miR-320 accelerates chronic heart failure with cardiac fibrosis through activation of the IL6/STAT3 axis.

Abstract

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.

• Authors: Fang Li, Shan-Shan Li, Hui Chen, Jian-Zhi Zhao, Jie Hao, Jin-Ming Liu, Xiu-Guang Zu, Wei Cui
• Journal: Aging (Aging (Albany NY)) Vol. 13 Issue 18 Pg. 22516-22527 (09 28 2021) ISSN: 1945-4589 [Electronic] United States
• PMID: 34582362 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Interleukin-6
• MicroRNAs
• Mirn320 microRNA, mouse
• STAT3 Transcription Factor
• STAT3 protein, human

Topics

• Animals
• Cardiomegaly (physiopathology)
• Cells, Cultured
• Datasets as Topic
• Disease Models, Animal
• Fibrosis
• Heart Failure (metabolism)
• Interleukin-6 (metabolism)
• Mice
• MicroRNAs
• Myocytes, Cardiac (metabolism)
• STAT3 Transcription Factor (metabolism)