Renal tubular epithelial cells response to injury in acute kidney injury

被引:0
|
作者
Li, Zuo-Lin [1 ]
Li, Xin-Yan [1 ]
Zhou, Yan [1 ]
Wang, Bin [1 ]
Lv, Lin-Li [1 ]
Liu, Bi-Cheng [1 ]
机构
[1] Southeast Univ, Sch Med, Zhongda Hosp, Inst Nephrol, Nanjing, Jiangsu, Peoples R China
来源
EBIOMEDICINE | 2024年 / 107卷
基金
中国国家自然科学基金;
关键词
Acute kidney injury; Renal tubular epithelial cells; Adaptive repair; Phenotypic transformation; PERICYTE-MYOFIBROBLAST TRANSITION; MESENCHYMAL TRANSITION; GROWTH-FACTOR; STEM-CELLS; INTERSTITIAL FIBROBLASTS; INFLAMMASOME ACTIVATION; MOLECULAR-MECHANISMS; NLRP3; INFLAMMASOME; PROXIMAL TUBULE; SONIC HEDGEHOG;
D O I
10.1016/j.ebiom.2024.105294
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Acute kidney injury (AKI) is a clinical syndrome characterized by a rapid and significant fi cant decrease in renal function that can arise from various etiologies, and is associated with high morbidity and mortality. The renal tubular epithelial cells (TECs) represent the central cell type affected by AKI, and their notable regenerative capacity is critical for the recovery of renal function in afflicted fl icted patients. The adaptive repair process initiated by surviving TECs following mild AKI facilitates full renal recovery. Conversely, when injury is severe or persistent, it allows the TECs to undergo pathological responses, abnormal adaptive repair and phenotypic transformation, which will lead to the development of renal fi brosis. Given the implications of TECs fate after injury in renal outcomes, a deeper understanding of these mechanisms is necessary to identify promising therapeutic targets and biomarkers of the repair process in the human kidney. Copyright (c) 2024 The Author(s). Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). eBioMedicine 2024;107: Published https://doi.org/10. 1016/j.ebiom.2024. 105294
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页数:18
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