期刊
AUTOPHAGY
卷 7, 期 9, 页码 1078-1079出版社
LANDES BIOSCIENCE
DOI: 10.4161/auto.7.9.16176
关键词
heart; remodeling; heart failure; histone deacetylase; hypertrophy
类别
资金
- NHLBI NIH HHS [R01 HL090842, HL-075173, HL-090842, R01 HL080144, R01 HL075173, HL-080144] Funding Source: Medline
The heart is a highly plastic organ. In a recent study, we found that autophagy is a required element in load-induced cardiomyocyte growth; when autophagy is suppressed, the heart does not grow. Conversely, afterload stress triggers a transient increase in cardiomyocyte autophagic activity which settles to a new-higher-baseline once the heart has re-achieved steady-state size. Our work went on to decipher the role of histone deacetylases in this biology.
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