The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI

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 cel...

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Autores principales:	Chao Li, Wei Wang, Shuai-shuai Xie, Wen-xian Ma, Qian-wen Fan, Ying Chen, Yuan He, Jia-nan Wang, Qin Yang, Hai-di Li, Juan Jin, Ming-ming Liu, Xiao-ming Meng, Jia-gen Wen
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	sepsis acute kidney injury apoptosis pyroptosis necroptosis Medicine (General) R5-920
Acceso en línea:	https://doaj.org/article/99a83f8bd8744877b927ede07bfa6625
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spelling	oai:doaj.org-article:99a83f8bd8744877b927ede07bfa66252021-12-02T09:06:07ZThe Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI2296-858X10.3389/fmed.2021.796724https://doaj.org/article/99a83f8bd8744877b927ede07bfa66252021-12-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fmed.2021.796724/fullhttps://doaj.org/toc/2296-858XSepsis 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.Chao LiWei WangShuai-shuai XieWen-xian MaQian-wen FanYing ChenYuan HeJia-nan WangQin YangHai-di LiJuan JinMing-ming LiuXiao-ming MengJia-gen WenFrontiers Media S.A.articlesepsisacute kidney injuryapoptosispyroptosisnecroptosisMedicine (General)R5-920ENFrontiers in Medicine, Vol 8 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	sepsis acute kidney injury apoptosis pyroptosis necroptosis Medicine (General) R5-920
spellingShingle	sepsis acute kidney injury apoptosis pyroptosis necroptosis Medicine (General) R5-920 Chao Li Wei Wang Shuai-shuai Xie Wen-xian Ma Qian-wen Fan Ying Chen Yuan He Jia-nan Wang Qin Yang Hai-di Li Juan Jin Ming-ming Liu Xiao-ming Meng Jia-gen Wen The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI
description	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.
format	article
author	Chao Li Wei Wang Shuai-shuai Xie Wen-xian Ma Qian-wen Fan Ying Chen Yuan He Jia-nan Wang Qin Yang Hai-di Li Juan Jin Ming-ming Liu Xiao-ming Meng Jia-gen Wen
author_facet	Chao Li Wei Wang Shuai-shuai Xie Wen-xian Ma Qian-wen Fan Ying Chen Yuan He Jia-nan Wang Qin Yang Hai-di Li Juan Jin Ming-ming Liu Xiao-ming Meng Jia-gen Wen
author_sort	Chao Li
title	The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI
title_short	The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI
title_full	The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI
title_fullStr	The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI
title_full_unstemmed	The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI
title_sort	programmed cell death of macrophages, endothelial cells, and tubular epithelial cells in sepsis-aki
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/99a83f8bd8744877b927ede07bfa6625
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The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI

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