Mitochondria in Diabetic Kidney Disease.
Mitochondria in Diabetic Kidney Disease.
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DOI：
10.3390/cells10112945
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发表时间：
2021-10-29
期刊：
影响因子：
6
通讯作者：
Rosca M
中科院分区：
文献类型：
--
作者：
Ahmad AA;Draves SO;Rosca M
糖尿病肾病（DKD）是美国终末期肾病（ESRD）的主要原因。 DKD 的发病机制是多因素的，涉及多种信号通路的激活，并产生多种结果，包括基底膜增厚、足细胞丢失、系膜扩张、肾小管萎缩以及间质炎症和纤维化。肾小球-肾小管平衡和肾小管-肾小球反馈支持肾小球滤过和肾小管重吸收的增加，后者严重依赖 ATP 并增加能量需求。有证据表明，肾细胞线粒体生物能的改变会导致这些病理变化，并导致 DKD 进展为 ESRD。本综述将重点关注肾小球和肾小管细胞生物能学的改变及其在 DKD 发展中的作用之间的对话。将讨论能量底物选择、电子传递链、ATP 生成、氧化应激、氧化还原状态、蛋白质翻译后修饰、线粒体动力学和质量控制的变化。了解生物能量学在糖尿病 DKD 进展中的作用可能会提供新的治疗方法来延缓其进展为 ESRD。
Diabetic kidney disease (DKD) is the leading cause of end stage renal disease (ESRD) in the USA. The pathogenesis of DKD is multifactorial and involves activation of multiple signaling pathways with merging outcomes including thickening of the basement membrane, podocyte loss, mesangial expansion, tubular atrophy, and interstitial inflammation and fibrosis. The glomerulo-tubular balance and tubule-glomerular feedback support an increased glomerular filtration and tubular reabsorption, with the latter relying heavily on ATP and increasing the energy demand. There is evidence that alterations in mitochondrial bioenergetics in kidney cells lead to these pathologic changes and contribute to the progression of DKD towards ESRD. This review will focus on the dialogue between alterations in bioenergetics in glomerular and tubular cells and its role in the development of DKD. Alterations in energy substrate selection, electron transport chain, ATP generation, oxidative stress, redox status, protein posttranslational modifications, mitochondrial dynamics, and quality control will be discussed. Understanding the role of bioenergetics in the progression of diabetic DKD may provide novel therapeutic approaches to delay its progression to ESRD.
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