Katz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Peggy and Harold Katz Family Drug Discovery Center, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Cells. 2022 Nov 16;11(22):3635. doi: 10.3390/cells11223635.
Diabetes is the leading cause of chronic kidney disease worldwide. Despite the burden, the factors contributing to the development and progression of diabetic kidney disease (DKD) remain to be fully elucidated. In recent years, increasing evidence suggests that mitochondrial dysfunction is a pathological mediator in DKD as the kidney is a highly metabolic organ rich in mitochondria. Furthermore, low grade chronic inflammation also contributes to the progression of DKD, and several inflammatory biomarkers have been reported as prognostic markers to risk-stratify patients for disease progression and all-cause mortality. Interestingly, the term "sterile inflammation" appears to be used in the context of DKD describing the development of intracellular inflammation in the absence of bacterial or viral pathogens. Therefore, a link between mitochondrial dysfunction and inflammation in DKD exists and is a hot topic in both basic research and clinical investigations. This review summarizes how mitochondria contribute to sterile inflammation in renal cells in DKD.
糖尿病是全球慢性肾脏病的主要病因。尽管负担沉重,但导致糖尿病肾病(DKD)发生和进展的因素仍未完全阐明。近年来,越来越多的证据表明,线粒体功能障碍是 DKD 的病理介质,因为肾脏是富含线粒体的高度代谢器官。此外,低度慢性炎症也会促进 DKD 的进展,并且已经报道了几种炎症生物标志物作为预后标志物,以对疾病进展和全因死亡率进行风险分层。有趣的是,“无菌炎症”一词似乎在 DKD 中用于描述在没有细菌或病毒病原体的情况下细胞内炎症的发展。因此,DKD 中线粒体功能障碍与炎症之间存在联系,这是基础研究和临床研究中的一个热门话题。这篇综述总结了线粒体如何导致 DKD 中肾细胞的无菌炎症。