医学
粒体自噬
衰老
帕金
心肌细胞
心肌细胞
自噬
细胞凋亡
程序性细胞死亡
心肌
内科学
细胞生物学
疾病
遗传学
生物
帕金森病
作者
Yifan Huang,Jing Zhang,Jian Yang
标识
DOI:10.1016/j.ijcard.2021.11.067
摘要
Recently, we have read an experimental research titled “Muscle-specific programmed cell death 5 deletion attenuates cardiac aging” reported by Naz and his colleagues [ [1] Naz A. Zhang S. An L. et al. Muscle-specific programmed cell death 5 deletion attenuates cardiac aging[J]. Int. J. Cardiol. 2021; 345: 98-104 Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar ]. They investigated the role of Pdcd5 in cell senescence and found that Muscle-specific Pdcd5 deficiency alleviates age-related myocardial apoptosis and mitochondrial dysfunction by improving Parkin-mediated mitophagy via p53. However, the potential mechanisms regulating the accumulation of Pdcd5 in aging myocardium need further exploration.
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