OLFML3 Promotes IRG1 Mitochondrial Localization and Modulates Mitochondrial Function in Macrophages

作者：Qijun Yu, Hong Mei, Qian Gu, Ran Zeng, Yanan Li, Junjie Zhang, Chenxu Gao, Hai Fang, Jieming Qu, Jia Liu · 发表于：International Journal of Biological Sciences · 年份：2025 · DOI：10.7150/ijbs.103859 · 被引用次数：12 · 研究领域：Cancer, Hypoxia, and Metabolism、Eicosanoids and Hypertension Pharmacology、Immune cells in cancer

-aconitate to itaconate, a myeloid-borne mitochondrial metabolite with immunomodulatory activities. Further investigation showed that OLFML3 could prevent LPS-induced mitochondrial dysfunction in macrophages by maintaining the homeostasis of mitochondrial membrane potential (MMP), mitochondrial reactive oxygen species (mtROS) and itaconate-related metabolites. In-depth protein-protein interaction studies showed that OLFML3 could promote IRG1 mitochondrial localization via a mitochondrial transport protein, apoptosis inducing factor mitochondria associated 1 (AIFM1). In summary, our study showed that OLFML3 could facilitate IRG1 mitochondrial localization and prevent LPS-induced mitochondrial dysfunction in macrophages.