Authors: Ning Liu, Yinghua Jiang, Yuwen Xiu, Giovane G. Tortelote, Winna Xia, Yingjie Wang, Yadan Li, Samuel Shi, Jinrui Han, Charles Vidoudez, Aim Niamnud, Mitchell D. Kilgore, Di Zhou, Mengxuan Shi, Stephen A. Graziose, Jia Fan, Prasad V. G. Katakam, Aaron S. Dumont, Xiaoying Wang
Published: 2025-03-12
DOI: 10.1126/scitranslmed.adn2635
Source: Full article
Traumatic brain injury (TBI) rapidly triggers proinflammatory activation of microglia, contributing to secondary brain damage post-TBI. Although the governing role of energy metabolism in shaping the inflammatory phenotype and function of immune cells has been increasingly recognized, the specific alterations in microglial bioenergetics post-TBI remain poorly understood. Itaconate, a metabolite produced by the enzyme aconitate decarboxylase 1 [IRG1; encoded by immune responsive gene 1 (