Kaixuan Huang, Jie Li, Zeng He, Yang Li, Xingye Liu, Yuhe Wan, Xiaolin Yang, Dong-Min Sang, Shujing Li, Zhongke Wang, Shiyong Liu
tlooto Summary
GPR32 is a key regulator of inflammation resolution and the roles of GPR32 in cortical lesions of patients with FCDIIb and TSC are explored to explore the roles of GPR32 in cortical lesions of patients with FCDIIb.
Abstract
Focal cortical dysplasia IIb (FCDIIb) and tuberous sclerosis complex (TSC) show persistent neuroinflammation that promotes epileptogenesis and epilepsy progression, suggesting that endogenous resolution of inflammation is inadequate to relieve neuronal network hyperexcitability. G‐protein‐coupled receptor 32 (GPR32) is a key regulator of inflammation resolution and we aimed to explore the roles of GPR32 in cortical lesions of patients with FCDIIb and TSC.
Citation format
HUANG, Kaixuan, et al. G protein‐coupled receptor 32 contributes to inflammation resolution and neuronal excitability dysfunction in patients with focal cortical dysplasia iib and tuberous sclerosis complex. NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, 2026, 52(1): e70062.