PUBLICATION
Redirecting cardiac growth mechanisms for therapeutic regeneration
- Authors
- Karra, R., Poss, K.D.
- ID
- ZDB-PUB-170202-3
- 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.
Citation
Karra, R., Poss, K.D. (2017) Redirecting cardiac growth mechanisms for therapeutic regeneration. The Journal of Clinical Investigation. 127:427-436.
Abstract
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping