期刊
CURRENT OPINION IN CELL BIOLOGY
卷 61, 期 -, 页码 79-85出版社
CURRENT BIOLOGY LTD
DOI: 10.1016/j.ceb.2019.07.005
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资金
- National Institutes of Health [HL 127717, HL 130804, HL 118761, R56HL142704, K01 DE026561, R03DE025873]
- Department of Defense (CDMRP) [W81XWH-16-PRMRP-IIRA]
- MacDonald Research Fund Award [16RDM001]
- Vivian L. Smith Foundation
- LeDucq Foundation's Transatlantic Networks of Excellence in Cardiovascular Research [14CVD01]
- American Heart Association Scientist Development Grant [14SDG1984000]
Ischemic heart disease is one of the leading causes of mortality. Myocardial infarction causes loss of cardiomyocytes in the injury area accompanied by formation of a fibrotic scar. This initiates a cascade of events including further loss of myocyte, increased fibrosis, and pathological cardiac hypertrophy, eventually leading to the heart failure. Cardiomyocytes in mammals have limited regenerative potential due to post mitotic nature of cardiomyocytes. Recently, multiple studies have provided substantial insights in to the molecular pathways governing this block in adult cardiomyocyte proliferation, and successfully employed that understanding to achieve cardiac regeneration. These strategies include directly reprograming the cardiomyocytes or manipulating the cardiac interstitium to repair the injured heart. In this review, we discuss the recent advances made in the field in the past two years.
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