ZFIN ID: ZDB-PUB-170202-3
Redirecting cardiac growth mechanisms for therapeutic regeneration
Karra, R., Poss, K.D.
Date: 2017
Source: The Journal of Clinical Investigation   127: 427-436 (Review)
Registered Authors: Karra, Ravi, Poss, Kenneth D.
Keywords: none
MeSH Terms:
  • Animals
  • Heart Failure*/metabolism
  • Heart Failure*/physiopathology
  • Heart Failure*/therapy
  • Humans
  • Mice
  • Myocardium*/metabolism
  • Myocardium*/pathology
  • Myocytes, Cardiac*/metabolism
  • Myocytes, Cardiac*/pathology
  • Regenerative Medicine*
  • Zebrafish
PubMed: 28145902 Full text @ Journal of Clin. Invest.
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.