敲低ELF4通过促进焦下垂、炎症、氧化应激和内质网应激加重缺血/再灌注小鼠的肾损伤。

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS
Li Li, Shunying Wang, Wenming Wang
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引用次数: 0

摘要

背景:肾缺血/再灌注(I/R)损伤是急性肾损伤(AKI)的主要原因之一。E74样ETS转录因子4(ELF4)的功能障碍导致炎症。本研究旨在探讨ELF4在I/R和氧-葡萄糖剥夺/再灌注(OGD/R)模型中的作用和机制。结果:在I/R和OGD/R模型中,ELF4表达下调。ELF4敲除加重了I/R诱导的小鼠肾损伤、氧化应激(OS)、内质网应激(ERS)、细胞凋亡、炎症和pyroptosis。在用OGD/R处理的HK-2细胞中,ELF4表达的抑制抑制细胞增殖并促进细胞凋亡、OS、ERS、炎症和pyroptosis。此外,ELF4过表达导致了相反的结果。结论:ELF4缺乏加重I/R诱导的AKI,参与细胞凋亡、OS、ERS、炎症和pyroptosis。靶向ELF4可能是预防IR-AKI后炎症的一种有前景的新治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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

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

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

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

Background: Renal 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.

Results: In 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.

Conclusion: ELF4 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.

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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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