期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 127, 期 2, 页码 427-436出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI89786
关键词
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资金
- NIH Mentored Clinical Scientist Award [K08-HL116485]
- Walker P. Inman Endowment
- Edna and Fred L. Mandel, Jr. Foundation
- NIH [R01-HL081674, R01-HL136182, R01-HL131319]
- Fondation Leducq
- American Heart Association
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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