Anthony M Pettinato1, Feria A Ladha1, J Travis Hinson2,3,4,5. 1. University of Connecticut Health Center, Farmington, CT, 06030, USA. 2. University of Connecticut Health Center, Farmington, CT, 06030, USA. hinson@uchc.edu. 3. The Jackson Laboratory for Genomic Medicine, 10 Discovery Drive, Farmington, CT, 06032, USA. hinson@uchc.edu. 4. Cardiology Center, UConn Health, Farmington, CT, 06030, USA. hinson@uchc.edu. 5. UConn Health, 263 Farmington Ave, Farmington, CT, 06030, USA. hinson@uchc.edu.
Abstract
PURPOSE OF REVIEW: The lack of adult human cardiomyocyte proliferative capacity impairs cardiac regeneration such as after myocardial injury. The sarcomere, a specialized actin cytoskeletal structure that is essential for twitch contraction in cardiomyocytes, has been considered a critical factor limiting adult human cardiomyocyte proliferation through incompletely understood mechanisms. RECENT FINDINGS: This review summarizes known and emerging regulatory mechanisms connecting the human cardiomyocyte sarcomere to cell cycle regulation including structural and signaling mechanisms. Cardiac regeneration could be augmented through targeting the inhibitory effects of the sarcomere on cardiomyocyte proliferation.
PURPOSE OF REVIEW: The lack of adult human cardiomyocyte proliferative capacity impairs cardiac regeneration such as after myocardial injury. The sarcomere, a specialized actin cytoskeletal structure that is essential for twitch contraction in cardiomyocytes, has been considered a critical factor limiting adult human cardiomyocyte proliferation through incompletely understood mechanisms. RECENT FINDINGS: This review summarizes known and emerging regulatory mechanisms connecting the human cardiomyocyte sarcomere to cell cycle regulation including structural and signaling mechanisms. Cardiac regeneration could be augmented through targeting the inhibitory effects of the sarcomere on cardiomyocyte proliferation.
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