The multifaceted role of kidney tubule mitochondrial dysfunction in kidney disease development

被引：90

作者：

Doke, Tomohito ^{[1
,2
]}

Susztak, Katalin ^{[1
,2
]}

机构：

[1] Univ Penn, Dept Med, Renal Electrolyte & Hypertens Div, Philadelphia, PA 19104 USA

[2] Univ Penn, Perelman Sch Med, Dept Genet, Philadelphia, PA 19104 USA

来源：

TRENDS IN CELL BIOLOGY | 2022年 / 32卷 / 10期

关键词：

FATTY-ACID OXIDATION; PPAR-ALPHA AGONIST; INTERSTITIAL FIBROSIS; RENAL-FUNCTION; CELL-DEATH; INJURY; NECROPTOSIS; RECOVERY; INFLAMMATION; CONTRIBUTES;

D O I：

10.1016/j.tcb.2022.03.012

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

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 mito-chondrial recycling, such as mitophagy are critical for proper mitochondrial func-tion. 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, mitochon-drial defects in renal tubules contribute to epithelial atrophy, inflammation, or cell death, orchestrating kidney disease development.

引用

页码：841 / 853

页数：13

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