Review 10.1172/JCI89786

Redirecting cardiac growth mechanisms for therapeutic regeneration

Ravi Karra1 and Kenneth D. Poss2

1Department of Medicine and

2Department of Cell Biology, Duke University Medical Center, Durham, North Carolina, USA.

Address correspondence to: Ravi Karra, Box 3126, Duke University Medical Center, Durham, North Carolina 27710, USA. Phone: 617.997.8326; E-mail: ravi.karra@duke.edu. Or to: Kenneth D. Poss, Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710, USA. Phone: 919.681.8457; E-mail: kenneth.poss@duke.edu.

Find articles by Karra, R. in: JCI | PubMed | Google Scholar

1Department of Medicine and

2Department of Cell Biology, Duke University Medical Center, Durham, North Carolina, USA.

Address correspondence to: Ravi Karra, Box 3126, Duke University Medical Center, Durham, North Carolina 27710, USA. Phone: 617.997.8326; E-mail: ravi.karra@duke.edu. Or to: Kenneth D. Poss, Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710, USA. Phone: 919.681.8457; E-mail: kenneth.poss@duke.edu.

Find articles by Poss, K. in: JCI | PubMed | Google Scholar

First published February 1, 2017 - More info

Published in Volume 127, Issue 2 (February 1, 2017)
J Clin Invest. 2017;127(2):427–436. doi:10.1172/JCI89786.
Copyright © 2017, American Society for Clinical Investigation

Published February 1, 2017

Heart failure is a major source of morbidity and mortality. Replacing lost myocardium with new tissue is a major goal of regenerative medicine. Unlike adult mammals, zebrafish and neonatal mice are capable of heart regeneration following cardiac injury. In both contexts, the regenerative program echoes molecular and cellular events that occur during cardiac development and morphogenesis, notably muscle creation through division of cardiomyocytes. Based on studies over the past decade, it is now accepted that the adult mammalian heart undergoes a low grade of cardiomyocyte turnover. Recent data suggest that this cardiomyocyte turnover can be augmented in the adult mammalian heart by redeployment of developmental factors. These findings and others suggest that stimulating endogenous regenerative responses can emerge as a therapeutic strategy for human cardiovascular disease.

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