足细胞
生物能学
肾小球基底膜
线粒体
纤维化
糖尿病肾病
医学
肾小球硬化
炎症
自噬
氧化应激
肾
终末期肾病
发病机制
疾病
内科学
内分泌学
细胞生物学
化学
生物
肾小球肾炎
蛋白尿
生物化学
细胞凋亡
作者
Amna Ayesha Ahmad,Shayna Odeal Draves,M. Rosca
出处
期刊:Cells
[MDPI AG]
日期:2021-10-29
卷期号:10 (11): 2945-2945
被引量:54
标识
DOI:10.3390/cells10112945
摘要
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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