GCSF deficiency attenuates nonalcoholic fatty liver disease through regulating GCSFR-SOCS3-JAK-STAT3 pathway and immune cells infiltration
Yuwei Zhang, Xuefeng Zhou, Peihao Liu, Xueyang Chen, Jie Zhang, Hong Zhang, Sha Li, Yishu Chen, Xin Song, Jinghua Wang, Hang Zeng, Xiaofen Zhang, Chenxi Tang, Chaohui Yu, Youming Li, Chengfu Xu
Abstract
We found GCSF was involved in lipid metabolism and NAFLD development. GCSF administration increased serum triglyceride levels in patients. GCSF deficiency alleviated HFD-induced insulin resistance and hepatic steatosis in mice. GCSF could directly act on hepatocytes through GCSFR-SOCS3-JAK-STAT3 pathway, and regulate the infiltration of immune cells into the liver to indirectly modulate NAFLD. Our finding indicates that GCSF may provide new strategies for the treatment of NAFLD.
Topics & Concepts
Nonalcoholic fatty liver diseaseSOCS3Immune systemMedicineSTAT3statInfiltration (HVAC)Fatty liverInternal medicineImmunologyDiseaseSignal transductionBiologyBiochemistryPhysicsThermodynamicsLiver Disease Diagnosis and TreatmentEndoplasmic Reticulum Stress and DiseaseDiabetes and associated disorders