期刊
NATURE REVIEWS MOLECULAR CELL BIOLOGY
卷 14, 期 8, 页码 529-541出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nrm3619
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资金
- National Institutes of Health
- Robert A. Welch Foundation [I-0025]
- Leducq Foundation-Transatlantic Network of Excellence in Cardiovascular Research Program
- American Heart Association-Jon Holden DeHaan Foundation
- Cancer Prevention and Research Institute of Texas (CPRIT)
- SouthWest Affiliate of the American Heart Association
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL093039, R01HL077439, R01HL111665, U01HL100401] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK099653] Funding Source: NIH RePORTER
As the adult mammalian heart has limited potential for regeneration and repair, the loss of cardiomyocytes during injury and disease can result in heart failure and death. The cellular processes and regulatory mechanisms involved in heart growth and development can be exploited to repair the injured adult heart through 'reawakening' pathways that are active during embryogenesis. Heart function has been restored in rodents by reprogramming non-myocytes into cardiomyocytes, by expressing transcription factors (GATA4, HAND2, myocyte-specific enhancer factor 2C (MEF2C) and T-box 5 (TBX5)) and microRNAs (miR-1, miR-133, miR-208 and miR-499) that control cardiomyocyte identity. Stimulating cardiomyocyte dedifferentiation and proliferation by activating mitotic signalling pathways involved in embryonic heart growth represents a complementary approach for heart regeneration and repair. Recent advances in understanding the mechanistic basis of heart development offer exciting opportunities for effective therapies for heart failure.
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