@article{Guan2026, 
author = {Shuang Guan and Zelin Yu and Shengzhuo Zhang and Xiujuan Bu and Xuming Deng and Jing Lu},
title = {Elaidic acid-induced inhibition of mitophagy activated renal tubular cell necroptosis via ROS/RIPK3/MLKL pathway},
year = {2026},
journal = {Food Science and Human Wellness},
volume = {15},
number = {2},
pages = {9250357},
keywords = {Elaidic acid, Renal, Necroptosis, Mitophagy, Reactive oxygen species},
url = {https://www.sciopen.com/article/10.26599/FSHW.2024.9250357},
doi = {10.26599/FSHW.2024.9250357},
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 reactive oxygen species (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. Results indicated that EA caused mitochondrial damage by testing MMP, MFN1, VDAC, and FIS1. Further, 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.}
}