α-Tocopherol rescues lipid-induced impairment of autophagy via mTOR/ULK1 signaling in macrophages

findings suggest that α-TOC reduces lipid accumulation and inhibits foam cell formation in macrophages by enhancing autophagic activity in association with reduced mTOR phosphorylation and increased ULK1 Ser555 phosphorylation. This study provides mechanistic insights into the potential anti-atherosclerotic effects of α-TOC at the cellular level, offering a theoretical basis for its further investigation as a therapeutic candidate for atherosclerosis.

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Publication Details

Journal
Korean Journal of Physiology and Pharmacology
Published
2026-09-16
DOI
https://doi.org/10.4196/kjpp.25.375
Primary Topic
Autophagy in Disease and Therapy
Type
article
Field-Weighted Citation Impact
0.00

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article

α-Tocopherol rescues lipid-induced impairment of autophagy via mTOR/ULK1 signaling in macrophages

S Wu, Limei Wu, Jiaxing Zhao, Xuehui Liu et al.
Korean Journal of Physiology and Pharmacology
Autophagy in Disease and Therapy
article

α-Tocopherol rescues lipid-induced impairment of autophagy via mTOR/ULK1 signaling in macrophages

S Wu, Limei Wu, Jiaxing Zhao, Xuehui Liu, Zenghui Liu, Qijun Chen, Huayu Yin, Lu Kuang, Dabin Liu
article en

Abstract

findings suggest that α-TOC reduces lipid accumulation and inhibits foam cell formation in macrophages by enhancing autophagic activity in association with reduced mTOR phosphorylation and increased ULK1 Ser555 phosphorylation. This study provides mechanistic insights into the potential anti-atherosclerotic effects of α-TOC at the cellular level, offering a theoretical basis for its further investigation as a therapeutic candidate for atherosclerosis.

Korean Journal of Physiology and Pharmacology
Mudanjiang Medical University (CN), Twelfth Guangzhou City People's Hospital (CN), Guangzhou Medical University (CN)
Guangzhou Municipal Science and Technology Project, Basic and Applied Basic Research Foundation of Guangdong Province
Openalex Percentile: Top 10%
Autophagy in Disease and Therapy
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