Is miR-21 A Therapeutic Target in Cardiovascular Disease?

Author:

Holland Antoinette,Enrick Molly,Diaz Arianna,Yin Liya

Abstract

Review Is miR-21 A Therapeutic Target in Cardiovascular Disease? Antoinette Holland, Molly Enrick, Arianna Diaz, and Liya Yin * Department of Integrative Medical Sciences, Northeast Ohio Medical University, Ohio 44272, USA. * Correspondence: lyin@neomed.edu; Tel.: 330-325-6521; Fax: 330-325-5912     Received: 16 November 2022 Accepted: 29 November 2022 Published: 11 January 2023   Abstract: microRNA-21 (miR-21) serves a multitude of functions at the molecular level through its regulation of messenger RNA. Previous research has sparked interest in the role of miR-21 as a potential therapeutic target in cardiovascular diseases. miR-21 expression contributes to the differentiation, proliferation, and maturation of many cell types, such as fibroblasts, endothelial cells, cardiomyocytes, and endothelial progenitor cells. The function of miR-21 depends upon its expression level in the specific cell types and downstream targets, which determine cell fate. Under pathological conditions, the expression level of miR-21 is altered, leading to abnormal gene regulation of downstream signaling and cardiovascular diseases such as hypertension, cardiac hypertrophy and fibrosis, atherosclerosis, and heart failure. Agomirs or antagomirs can be introduced into the respective tissue type to reverse or stop the progression of the disease. Exosomes in the extracellular vesicles, which mediate many cellular events with high biocompatibility, have a high potential of efficiently delivering miR-21 to their targeted cells. The critical role of miR-21 in cardiovascular disease (CVD) is indisputable, but there are controversial reports on the function of miR-21 in the same disease. This discrepancy sparks interest in better understanding the role of miR-21 in different tissues under different stages of various diseases and the mechanism of how miR-21 inhibitors work.

Publisher

Australia Academic Press Pty Ltd

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