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Mitochondrial energetics in the kidney
Nature Reviews Nephrology ( IF 41.5 ) Pub Date : 2017-08-14 00:00:00 , DOI: 10.1038/nrneph.2017.107
Pallavi Bhargava , Rick G. Schnellmann

The kidney requires a large number of mitochondria to remove waste from the blood and regulate fluid and electrolyte balance. Mitochondria provide the energy to drive these important functions and can adapt to different metabolic conditions through a number of signalling pathways (for example, mechanistic target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK) pathways) that activate the transcriptional co-activator peroxisome proliferator-activated receptor-γ co-activator 1α (PGC1α), and by balancing mitochondrial dynamics and energetics to maintain mitochondrial homeostasis. Mitochondrial dysfunction leads to a decrease in ATP production, alterations in cellular functions and structure, and the loss of renal function. Persistent mitochondrial dysfunction has a role in the early stages and progression of renal diseases, such as acute kidney injury (AKI) and diabetic nephropathy, as it disrupts mitochondrial homeostasis and thus normal kidney function. Improving mitochondrial homeostasis and function has the potential to restore renal function, and administering compounds that stimulate mitochondrial biogenesis can restore mitochondrial and renal function in mouse models of AKI and diabetes mellitus. Furthermore, inhibiting the fission protein dynamin 1-like protein (DRP1) might ameliorate ischaemic renal injury by blocking mitochondrial fission.

中文翻译:

肾脏的线粒体能量

肾脏需要大量的线粒体才能从血液中清除废物,并调节体液和电解质的平衡。线粒体提供了驱动这些重要功能的能量,并且可以通过多种信号通路(例如雷帕霉素(mTOR)的机械靶标和AMP激活的蛋白激酶(AMPK)通路)适应不同的代谢条件,从而激活转录共激活因子。活化剂过氧化物酶体增殖物激活受体γ共激活剂1 α(PGC1 α),并通过平衡线粒体动力学和能量学来维持线粒体的体内平衡。线粒体功能障碍导致ATP产生减少,细胞功能和结构改变以及肾功能丧失。持续性线粒体功能障碍在肾脏疾病(例如急性肾损伤(AKI)和糖尿病性肾病)的早期和进展中起作用,因为它会破坏线粒体体内稳态,从而破坏正常的肾功能。改善线粒体稳态和功能具有恢复肾脏功能的潜力,在AKI和糖尿病小鼠模型中,给予刺激线粒体生物发生的化合物可恢复线粒体和肾脏功能。此外,
更新日期:2017-09-06
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