粒体自噬
生物
坏死性下垂
线粒体融合
线粒体
细胞生物学
线粒体生物发生
上睑下垂
线粒体分裂
程序性细胞死亡
肾
DNAJA3公司
自噬
线粒体DNA
细胞凋亡
内分泌学
遗传学
基因
作者
Tomohito Doke,Katalin Suszták
标识
DOI:10.1016/j.tcb.2022.03.012
摘要
More than 800 million people suffer from kidney disease. Genetic studies and follow-up animal models and cell biological experiments indicate the key role of proximal tubule metabolism. Kidneys have one of the highest mitochondrial densities. Mitochondrial biogenesis, mitochondrial fusion and fission, and mitochondrial recycling, such as mitophagy are critical for proper mitochondrial function. Mitochondrial dysfunction can lead to an energetic crisis, orchestrate different types of cell death (apoptosis, necroptosis, pyroptosis, and ferroptosis), and influence cellular calcium levels and redox status. Collectively, mitochondrial defects in renal tubules contribute to epithelial atrophy, inflammation, or cell death, orchestrating kidney disease development.
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