粒体自噬
线粒体
医学
线粒体生物发生
生物能学
线粒体融合
肾
细胞生物学
疾病
线粒体DNA
自噬
生物
病理
内科学
生物化学
细胞凋亡
基因
作者
Jingyi Sheng,Xian Li,Juan Lei,Weihua Gan,Jiayu Song
标识
DOI:10.1007/s40620-023-01582-3
摘要
Acute kidney disease (AKD) involves multiple pathogenic mechanisms, including maladaptive repair of renal cells that are rich in mitochondria. Maintenance of mitochondrial homeostasis and quality control is crucial for normal kidney function. Mitochondrial quality control serves to maintain mitochondrial function under various conditions, including mitochondrial bioenergetics, mitochondrial biogenesis, mitochondrial dynamics (fusion and fission) and mitophagy. To date, increasing evidence indicates that mitochondrial quality control is disrupted when acute kidney disease develops. This review describes the mechanisms of mitochondria quality control in acute kidney disease, aiming to provide clues to help design new clinical treatments.
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