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线粒体与肾纤维化。

Mitochondria and Renal Fibrosis.

机构信息

Department of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing, China.

出版信息

Adv Exp Med Biol. 2019;1165:501-524. doi: 10.1007/978-981-13-8871-2_25.

DOI:10.1007/978-981-13-8871-2_25
PMID:31399982
Abstract

Mitochondria are important organelles in eukaryotic cells and perform a variety of biosynthetic and metabolic functions. Many human diseases are closely related to mitochondrial dysfunction. Kidney is an organ with high-energy requirements, which is distributed with a large number of mitochondria. Mitochondrial dysfunction plays a crucial role in the pathogenesis of kidney disease, and studies have shown that mitochondrial dysfunction is involved in the physiological process of renal fibrosis. This review introduced the biogenesis and pathophysiology of mitochondria, illustrated the involvement of mitochondrial dysfunction in renal fibrosis based on various kinds of cells, and finally summarized the latest mitochondria-targeted therapies.

摘要

线粒体是真核细胞中的重要细胞器,执行多种生物合成和代谢功能。许多人类疾病与线粒体功能障碍密切相关。肾脏是一个能量需求较高的器官,分布着大量的线粒体。线粒体功能障碍在肾脏疾病的发病机制中起着关键作用,研究表明线粒体功能障碍参与了肾纤维化的生理过程。本综述介绍了线粒体的生物发生和病理生理学,根据各种细胞阐明了线粒体功能障碍在肾纤维化中的作用,并总结了最新的线粒体靶向治疗。

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Mitochondria and Renal Fibrosis.线粒体与肾纤维化。
Adv Exp Med Biol. 2019;1165:501-524. doi: 10.1007/978-981-13-8871-2_25.
2
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Focus on podocytes: diabetic kidney disease and renal fibrosis - a global bibliometric analysis (2000-2024).
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DKK3 promotes renal fibrosis by increasing MFF-mediated mitochondrial dysfunction in Wnt/β-catenin pathway-dependent manner.DKK3 通过增加 MFF 介导的线粒体功能障碍促进肾脏纤维化,该过程依赖于 Wnt/β-catenin 通路。
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