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Research Article | Open Access | Just Accepted

Elaidic acid-induced inhibition of mitophagy activated renal tubular cell necroptosis via ROS/RIPK3/MLKL pathway

Shuang GuanaZelin YuaShengzhuo ZhangaXiujuan BuaXuming Dengb()Jing Lua()

a College of Food science and Engineering, Jilin University, Changchun, Jilin 130062, China

b State Key Laboratory for Zoonotic Diseases, Key Laboratory for Zoonosis Research, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun 130012, China

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Abstract

Elaidic acid (EA) is a typical trans fatty acid (TFA) that emerges during the processing of various fatty foods. In this study, we found that EA induced renal injury with necroptosis. Pretreatment with a ROS inhibitor and a RIPK3 inhibitor alleviated EA-induced necroptosis. The data indicated that EA induced renal necroptosis through ROS/RIPK3/MLKL pathway. In mechanistic studies, we explored how EA induced ROS production. We found EA caused mitochondrial damage by testing MMP, MFN1, VDAC, and FIS1. Further, we also found EA suppressed mitophagy by testing the levels of LC3, p62, PINK1, Parkin, colocalization of LC3 and Mito-Tracker Red. Mitophagy is a process of selective degradation of damaged mitochondria. A large number of damaged mitochondria couldn’t be cleared by mitophagy in time, which increased ROS levels in renal cells. Pretreatment with a mitophagy activator decreased EA-induced ROS levels and mitochondrial damage. Taken together, our data identified that EA induced renal necroptosis by destroying mitochondria and inhibiting mitophagy, thereby activating the ROS/RIPK3/MLKL pathway.

Food Science and Human Wellness
Cite this article:
Guan S, Yu Z, Zhang S, et al. Elaidic acid-induced inhibition of mitophagy activated renal tubular cell necroptosis via ROS/RIPK3/MLKL pathway. Food Science and Human Wellness, 2024, https://doi.org/10.26599/FSHW.2024.9250357
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