Li Chao, Wang Wei, Xie Shuai-Shuai, Ma Wen-Xian, Fan Qian-Wen, Chen Ying, He Yuan, Wang Jia-Nan, Yang Qin, Li Hai-di, Jin Juan, Liu Ming-Ming, Meng Xiao-Ming, Wen Jia-Gen
Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, The Key Laboratory of Anti-Inflammatory of Immune Medicines (Ministry of Education), Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, China.
Anhui Province Key Laboratory of Genitourinary Diseases, Department of Urology and Institute of Urology, The First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, China.
Front Med (Lausanne). 2021 Dec 2;8:796724. doi: 10.3389/fmed.2021.796724. eCollection 2021.
Sepsis is a systemic inflammatory response syndrome caused by infection, following with acute injury to multiple organs. Sepsis-induced acute kidney injury (AKI) is currently recognized as one of the most severe complications related to sepsis. The pathophysiology of sepsis-AKI involves multiple cell types, including macrophages, vascular endothelial cells (ECs) and renal tubular epithelial cells (TECs), etc. More significantly, programmed cell death including apoptosis, necroptosis and pyroptosis could be triggered by sepsis in these types of cells, which enhances AKI progress. Moreover, the cross-talk and connections between these cells and cell death are critical for better understanding the pathophysiological basis of sepsis-AKI. Mitochondria dysfunction and oxidative stress are traditionally considered as the leading triggers of programmed cell death. Recent findings also highlight that autophagy, mitochondria quality control and epigenetic modification, which interact with programmed cell death, participate in the damage process in sepsis-AKI. The insightful understanding of the programmed cell death in sepsis-AKI could facilitate the development of effective treatment, as well as preventive methods.
脓毒症是一种由感染引起的全身炎症反应综合征，随后会导致多器官急性损伤。脓毒症诱导的急性肾损伤（AKI）目前被认为是与脓毒症相关的最严重并发症之一。脓毒症相关性急性肾损伤的病理生理学涉及多种细胞类型，包括巨噬细胞、血管内皮细胞（ECs）和肾小管上皮细胞（TECs）等。更重要的是，脓毒症可在这些类型的细胞中引发程序性细胞死亡，包括凋亡、坏死性凋亡和焦亡，这会加速急性肾损伤的进展。此外，这些细胞与细胞死亡之间的相互作用和联系对于更好地理解脓毒症相关性急性肾损伤的病理生理基础至关重要。线粒体功能障碍和氧化应激传统上被认为是程序性细胞死亡的主要触发因素。最近的研究结果还强调，自噬、线粒体质量控制和表观遗传修饰与程序性细胞死亡相互作用，参与了脓毒症相关性急性肾损伤的损伤过程。对脓毒症相关性急性肾损伤中程序性细胞死亡的深入理解有助于开发有效的治疗方法以及预防措施。
