摘要Hepatic fibrosis is a consequence of chronic liver disease,which can lead to cirrhosis and liver failure.There is no Food and Drugs Administration approved therapy for liver fibrosis to date;hence,identifying effective therapeutic targets is an urgent need.Hepatic macrophages play a critical role in both initiation and progression of fibrosis.While resident liver macrophages,Kupffer cells are considered more anti-inflammatory,recent view has demonstrated that monocyte-derived macrophages(MoMs)are more pro-inflammatory and pro-fibrogenic[1].Moreover,MoMs exhibit more plasticity and undergo M1/M2"polarization"The research by Zhang et al.[2]identified GPR65 signaling as a novel mechanism responsible for hepatic macrophage M1 polarization during liver injury and fibrosis.Notably,the role of this receptor in modulating inflammatory responses by various cells in other tissues has been previously reported[3].However,the role of GPR65 in liver inflammation and fibrosis has not been examined until now.