GCSF deficiency attenuates nonalcoholic fatty liver disease through regulating GCSFR-SOCS3-JAK-STAT3 pathway and immune cells infiltration

作者：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 · 发表于：American Journal of Physiology-Gastrointestinal and Liver Physiology · 年份：2021 · DOI：10.1152/ajpgi.00342.2020 · 被引用次数：28 · 研究领域：Liver Disease Diagnosis and Treatment、Endoplasmic Reticulum Stress and Disease、Diabetes and associated disorders

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.