Jun Wang1, James F Martin. 1. aDepartment of Molecular Physiology and Biophysics bProgram in Developmental Biology, Baylor College of Medicine, One Baylor Plaza cTexas Heart Institute, Houston, Texas, USA.
Abstract
PURPOSE OF REVIEW: Myocardial injury and disease often result in heart failure, a major cause of death worldwide. To achieve myocardial regeneration and foster development of efficient therapeutics for cardiac injury, it is essential to uncover molecular mechanisms that will promote myocardial regeneration. In this review, we examine the latest progress made in elucidation of the roles of small non-coding RNAs called microRNAs (miRs) in myocardial regeneration. RECENT FINDINGS: Promising progress has been made in studying cardiac regeneration. Several miRs, which include miR-590, miR-199a, miR-17-92 cluster, miR-199a-214 cluster, miR-34a, and miR-15 family, have been recently shown to play an essential role in myocardial regeneration by regulating different processes during cardiac repair, including cell death, proliferation, and metabolism. For example, miR-590 promotes cardiac regeneration through activating cardiomyocyte proliferation, whereas miR-34a inhibits cardiac repair through inducing apoptosis. SUMMARY: These recent findings shed new light on our understanding of myocardial regeneration and suggest potential novel therapeutic targets to treat cardiac disease.
PURPOSE OF REVIEW: Myocardial injury and disease often result in heart failure, a major cause of death worldwide. To achieve myocardial regeneration and foster development of efficient therapeutics for cardiac injury, it is essential to uncover molecular mechanisms that will promote myocardial regeneration. In this review, we examine the latest progress made in elucidation of the roles of small non-coding RNAs called microRNAs (miRs) in myocardial regeneration. RECENT FINDINGS: Promising progress has been made in studying cardiac regeneration. Several miRs, which include miR-590, miR-199a, miR-17-92 cluster, miR-199a-214 cluster, miR-34a, and miR-15 family, have been recently shown to play an essential role in myocardial regeneration by regulating different processes during cardiac repair, including cell death, proliferation, and metabolism. For example, miR-590 promotes cardiac regeneration through activating cardiomyocyte proliferation, whereas miR-34a inhibits cardiac repair through inducing apoptosis. SUMMARY: These recent findings shed new light on our understanding of myocardial regeneration and suggest potential novel therapeutic targets to treat cardiac disease.
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