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Tomohito Doke, Katalin Susztak
Department of Medicine, Renal Electrolyte and Hypertension Division, University of Pennsylvania, Philadelphia, PA, USA; Department of Genetics, University of Pennsylvania, Perelman School of Medicine, Philadelphia, PA 19104, USA.
Trends Cell Biol. 2022 Oct;32(10):841-853. doi: 10.1016/j.tcb.2022.03.012. Epub 2022 Apr 25.
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.
超过 8 亿人患有肾脏疾病。遗传研究以及后续的动物模型和细胞生物学实验表明，近端肾小管代谢起着关键作用。肾脏的线粒体密度是所有器官中最高的之一。线粒体生物发生、线粒体融合和裂变，以及线粒体回收，如线粒体自噬，对于正常的线粒体功能至关重要。线粒体功能障碍可导致能量危机，调控不同类型的细胞死亡（细胞凋亡、坏死性凋亡、细胞焦亡和铁死亡），并影响细胞内钙水平和氧化还原状态。总之，肾小管中的线粒体缺陷导致上皮萎缩、炎症或细胞死亡，从而影响肾脏疾病的发展。
