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miR-29 family: A potential therapeutic target for cardiovascular disease
Cardiovascular disease (CVD), including heart failure, myocardial fibrosis and myocardial infarction, etc, remains one of the leading causes of mortality worldwide. Evidence shows that miRNA plays an important role in the pathogenesis of CVD. miR-29 family is one of miRNA, and over the past decades,...
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Published in: | Pharmacological research 2021-04, Vol.166, p.105510-105510, Article 105510 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Cardiovascular disease (CVD), including heart failure, myocardial fibrosis and myocardial infarction, etc, remains one of the leading causes of mortality worldwide. Evidence shows that miRNA plays an important role in the pathogenesis of CVD. miR-29 family is one of miRNA, and over the past decades, many studies have demonstrated that miR-29 is involved in maintaining the integrity of arteries and in the regulation of atherosclerosis, especially in the process of myocardial fibrosis. Besides, heart failure, myocardial fibrosis and myocardial infarction are inseparable from the regulatory role of miR-29. Here, we comprehensively review recent studies regarding miR-29 and CVD, illustrate the possibility of miR-29 as a potential marker for prevention, treatment and prognostic observation.
•miR-29 plays an important role in cardiovascular disease, and its regulatory function is almost omni-directional.•The role of miR-29 in myocardial fibrosis is currently a hot topic and he influence of the miR-29 family on fibrocyte activation and extracellular matrix overproduction have been studied in depth.•Both circulating miR-29 and miR-29 in tissues or cells are associated with the occurrence and development of cardiovascular diseases.•The therapeutic effect of miR-29 has been extensively studied, but its role in prevention and prognosis of disease remains to be proved. |
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ISSN: | 1043-6618 1096-1186 |
DOI: | 10.1016/j.phrs.2021.105510 |