粒体自噬
帕金
医学
线粒体
自噬
线粒体生物发生
细胞生物学
心肌梗塞
心肌保护
内科学
内分泌学
生物
细胞凋亡
生物化学
疾病
帕金森病
作者
Lizhuo Ai,Juliana de Freitas Germano,Chengqun Huang,Marianne Aniag,Savannah Sawaged,Jon Sin,Reetu Thakur,Deepika Rai,Christopher Rainville,David E. Sterner,Yang Song,Honit Piplani,Suresh Kumar,Tauseef R. Butt,Robert M. Mentzer,Aleksandr Stotland,Roberta A. Gottlieb,Jennifer E. Van Eyk
标识
DOI:10.1093/eurheartj/ehae782
摘要
Almost 30% of survivors of myocardial infarction (MI) develop heart failure (HF), in part due to damage caused by the accumulation of dysfunctional mitochondria. Organelle quality control through Parkin-mediated mitochondrial autophagy (mitophagy) is known to play a role in mediating protection against HF damage post-ischaemic injury and remodelling of the subsequent deteriorated myocardium.
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