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线粒体功能障碍与肾结石病

Mitochondrial Dysfunction and Kidney Stone Disease.

作者信息

Chaiyarit Sakdithep, Thongboonkerd Visith

机构信息

Medical Proteomics Unit, Office for Research and Development, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.

出版信息

Front Physiol. 2020 Oct 20;11:566506. doi: 10.3389/fphys.2020.566506. eCollection 2020.

Abstract

Mitochondrion is a pivotal intracellular organelle that plays crucial roles in regulation of energy production, oxidative stress, calcium homeostasis, and apoptosis. Kidney stone disease (nephrolithiasis/urolithiasis), particularly calcium oxalate (CaOx; the most common type), has been shown to be associated with oxidative stress and tissue inflammation/injury. Recent evidence has demonstrated the involvement of mitochondrial dysfunction in CaOx crystal retention and aggregation as well as Randall's plaque formation, all of which are the essential mechanisms for kidney stone formation. This review highlights the important roles of mitochondria in renal cell functions and provides the data obtained from previous investigations of mitochondria related to kidney stone disease. In addition, mechanisms for the involvement of mitochondrial dysfunction in the pathophysiology of kidney stone disease are summarized. Finally, future perspectives on the novel approach to prevent kidney stone formation by mitochondrial preservation are discussed.

摘要

线粒体是一种关键的细胞内细胞器,在能量产生、氧化应激、钙稳态和细胞凋亡的调节中发挥着至关重要的作用。肾结石病(肾石症/尿路结石症),尤其是草酸钙结石(CaOx;最常见的类型),已被证明与氧化应激和组织炎症/损伤有关。最近的证据表明,线粒体功能障碍参与了草酸钙晶体的滞留和聚集以及兰德尔斑的形成,所有这些都是肾结石形成的基本机制。这篇综述强调了线粒体在肾细胞功能中的重要作用,并提供了先前关于与肾结石病相关的线粒体研究的数据。此外,还总结了线粒体功能障碍参与肾结石病病理生理学的机制。最后,讨论了通过线粒体保护预防肾结石形成新方法的未来前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa8a/7606861/dd4a40608eeb/fphys-11-566506-g001.jpg

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