Department of Emergency and Critical Care Medicine, The Second Hospital of Jilin University, Changchun, China.
International Renal Research Institute of Vicenza, Vicenza, Italy.
J Am Soc Nephrol. 2019 Jul;30(7):1151-1161. doi: 10.1681/ASN.2018111126. Epub 2019 May 10.
AKI is a common clinical condition associated with the risk of developing CKD and ESKD. Sepsis is the leading cause of AKI in the intensive care unit (ICU) and accounts for nearly half of all AKI events. Patients with AKI who require dialysis have an unacceptably high mortality rate of 60%-80%. During sepsis, endothelial activation, increased microvascular permeability, changes in regional blood flow distribution with resulting areas of hypoperfusion, and hypoxemia can lead to AKI. No effective drugs to prevent or treat human sepsis-induced AKI are currently available. Recent research has identified dysfunction in energy metabolism as a critical contributor to the pathogenesis of AKI. Mitochondria, the center of energy metabolism, are increasingly recognized to be involved in the pathophysiology of sepsis-induced AKI and mitochondria could serve as a potential therapeutic target. In this review, we summarize the potential role of mitochondria in sepsis-induced AKI and identify future therapeutic approaches that target mitochondrial function in an effort to treat sepsis-induced AKI.
急性肾损伤（AKI）是一种常见的临床病症，与慢性肾脏病（CKD）和终末期肾病（ESKD）的发生风险相关。脓毒症是重症监护病房（ICU）中 AKI 的主要病因，几乎占所有 AKI 事件的一半。需要透析的 AKI 患者死亡率高得令人无法接受，为 60%-80%。在脓毒症中，内皮细胞激活、微血管通透性增加、区域性血流分布改变导致灌注不足区域以及低氧血症，这些都可能导致 AKI。目前尚无有效的药物可预防或治疗人类脓毒症引起的 AKI。最近的研究表明，能量代谢功能障碍是 AKI 发病机制的关键因素之一。线粒体是能量代谢的中心，其在脓毒症诱导的 AKI 的病理生理学中作用日益受到重视，并且线粒体可能成为一个有潜力的治疗靶点。在这篇综述中，我们总结了线粒体在脓毒症诱导的 AKI 中的潜在作用，并确定了未来针对线粒体功能的治疗方法，以期治疗脓毒症诱导的 AKI。
