Knockdown of ELF4 aggravates renal injury in ischemia/reperfusion mice through promotion of pyroptosis, inflammation, oxidative stress, and endoplasmic reticulum stress

BMC Molecular and Cell Biology

Research

Wenming Wang¹  Shunying Wang¹  Li Li² 

[1]Department of Cadre Health Section, Jinan City People’s Hospital, 271199, Jinan, Shandong, People’s Republic of China

[2]Department of Nephrology, Jinan City People’s Hospital, No. 001, Changshao North Road, 271199, Laiwu District, Jinan, Shandong, People’s Republic of China

关键词: Acute kidney injury;    ELF4;    Inflammation;    Pyroptosis;    Oxidative stress;   

DOI  :  10.1186/s12860-023-00485-2

 received in 2023-01-17, accepted in 2023-07-13,  发布年份 2023

来源: Springer

【 摘 要 】

BackgroundRenal ischemia/reperfusion (I/R) injury is a major cause of acute kidney injury (AKI). Dysfunction of E74-like ETS transcription factor 4 (ELF4) leads to inflammation. This research intended to look into the function and mechanisms of ELF4 in I/R and oxygen–glucose deprivation/reperfusion (OGD/R) model.ResultsIn I/R and OGD/R model, ELF4 expression was downregulated. ELF4 knockout aggravated I/R-induced kidney injury, oxidative stress (OS), endoplasmic reticulum stress (ERS), apoptosis, inflammation, and pyroptosis in mice. In HK-2 cells treated with OGD/R, suppression of ELF4 expression inhibited cell proliferation and promoted cell apoptosis, OS, ERS, inflammation, and pyroptosis. Moreover, ELF4 overexpression led to the opposite results.ConclusionELF4 deficiency aggravated I/R induced AKI, which was involved in apoptosis, OS, ERS, inflammation, and pyroptosis. Targeting ELF4 may be a promising new therapeutic strategy for preventing inflammation after IR-AKI.

【 授权许可】

CC BY   
© The Author(s) 2023

【 图 表 】

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