Abstract
Cardiovascular diseases are one of the prime reasons for disability and death worldwide. Diseases and conditions, such as hypoxia, pressure overload, infection, and hyperglycemia, might initiate cardiac remodeling and dysfunction by inducing hypertrophy or apoptosis in cardiomyocytes and by promoting proliferation in cardiac fibroblasts. In the vascular system, injuries decrease the endothelial nitric oxide levels and affect the phenotype of vascular smooth muscle cells. Understanding the underlying mechanisms will be helpful for the development of a precise therapeutic approach. Various microRNAs are involved in mediating multiple pathological and physiological processes in the heart. A cardiac enriched microRNA, miR-21, which is essential for cardiac homeostasis, has been demonstrated to act as a cell–cell messenger with diverse functions. This review describes the cell type–specific functions of miR-21 in different cardiovascular diseases and its prospects in clinical therapy.
Highlights
According to the 2013 global burden of disease study (GBD), 17.3 million individuals died due to cardiovascular diseases (CVDs) worldwide
Chen et al (2019) demonstrated that the knockout of exosomal miR-21 in CMs cultured with an oxygen-glucose– deprived media increased the ROS-induced apoptosis in CMs by targeting programmed cell death 4 (PDCD4) and decreased the activation of cardiac fibroblasts (CFs) and angiogenesis mediated by endothelial cells (ECs), demonstrating the interaction between CMs and other cell types in the heart
We demonstrated that the systemic delivery of miR-21 in animals decreased the blood pressure and improved cardiac hypertrophy in the spontaneously hypertensive rat (SHR) by upregulating mitochondrial cytochrome B (CYTB)
Summary
According to the 2013 global burden of disease study (GBD), 17.3 million individuals died due to cardiovascular diseases (CVDs) worldwide. These contradictions might be a result of the abundance and diverse targets of miR-21 in different cell types, which leads to miscellaneous effects on the miR-21 and CVDs cardiac function during different stages and processes of CVDs (Figure 1).
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