Lack of FGF21 promotes NASH-HCC transition <i>via</i> hepatocyte-TLR4-IL-17A signaling
Qianqian Zheng, Robert C.G. Martin, Xiaoju Shi, Harshul Pandit, Youxi Yu, Xingkai Liu, Wei Guo, Min Tan, Ou Bai, Xin Meng, Yan Li
Abstract
This study revealed a novel anti-inflammatory mechanism of FGF21 via inhibiting the hepatocyte-TLR4-IL-17A signaling in NASH-HCC models. The negative feedback loop on the hepatocyte-TLR4-IL-17A axis could be a potential anti-carcinogenetic mechanism for FGF21 to prevent NASH-HCC transition.
Topics & Concepts
HepatocyteTLR4Cancer researchFGF21Cell biologySignal transductionChemistryMedicineBiologyInternal medicineFibroblast growth factorBiochemistryIn vitroReceptorFibroblast Growth Factor ResearchEpigenetics and DNA MethylationKruppel-like factors research