Huang Ruizhen, Zhang Chiyu, Xiang Zhengjie, Lin Tao, Ling Jian, Hu Honglin
Department of Urology, The Second Affiliated Hospital of Nanchang University, China.
FEBS J. 2024 Dec;291(24):5365-5378. doi: 10.1111/febs.17130. Epub 2024 Apr 3.
Acute kidney injury (AKI) induced by renal ischemia-reperfusion injury (IRI) has a high morbidity and mortality, representing a worldwide problem. The kidney is an essential organ of metabolism that has high blood perfusion and is the second most mitochondria-rich organ after the heart because of the high ATP demands of its essential functions of nutrient reabsorption, acid-base and electrolyte balance, and hemodynamics. Thus, these energy-intensive cells are particularly vulnerable to mitochondrial dysfunction. As the bulk of glomerular ultrafiltrate reabsorption by proximal tubules occurs via active transport, the mitochondria of proximal tubules must be equipped for detecting and responding to fluctuations in energy availability to guarantee efficient basal metabolism. Any insults to mitochondrial quality control mechanisms may lead to biological disruption, blocking the clearance of damaged mitochondria and resulting in morphological change and tissue dysfunction. Extensive research has shown that mitochondria have pivotal roles in acute kidney disease, so in this article, we discuss the role of mitochondria, their dynamics and mitophagy in renal ischemia-reperfusion injury.
肾缺血再灌注损伤（IRI）所致的急性肾损伤（AKI）发病率和死亡率高，是一个全球性问题。肾脏是重要的代谢器官，血液灌注丰富，由于其营养重吸收、酸碱和电解质平衡以及血流动力学等基本功能对ATP需求高，是仅次于心脏的第二大富含线粒体的器官。因此，这些能量消耗大的细胞特别容易发生线粒体功能障碍。由于近端小管对肾小球超滤液的重吸收大部分通过主动转运进行，近端小管的线粒体必须具备检测和响应能量供应波动的能力，以保证高效的基础代谢。线粒体质量控制机制受到的任何损害都可能导致生物紊乱，阻碍受损线粒体的清除，进而导致形态改变和组织功能障碍。大量研究表明，线粒体在急性肾疾病中起关键作用，因此在本文中，我们将探讨线粒体、其动力学及线粒体自噬在肾缺血再灌注损伤中的作用。
