Hepatic stellate cells(HSCs),a distinct category of non-parenchymal cells in the liver,are critical for liver homeostasis.In healthy livers,HSCs remain non-proliferative and quiescent.However,under conditions of acute...Hepatic stellate cells(HSCs),a distinct category of non-parenchymal cells in the liver,are critical for liver homeostasis.In healthy livers,HSCs remain non-proliferative and quiescent.However,under conditions of acute or chronic liver damage,HSCs are activated and participate in the progression and regulation of liver diseases such as liver fibrosis,cirrhosis,and liver cancer.Fatty liver diseases(FLD),including nonalcoholic(NAFLD)and alcoholrelated(ALD),are common chronic inflammatory conditions of the liver.These diseases,often resulting from multiple metabolic disorders,can progress through a sequence of inflammation,fibrosis,and ultimately,cancer.In this review,we focused on the activation and regulatory mechanism of HSCs in the context of FLD.We summarized the molecular pathways of activated HSCs(aHSCs)in mediating FLD and their role in promoting liver tumor development from the perspectives of cell proliferation,invasion,metastasis,angiogenesis,immunosuppression,and chemo-resistance.We aimed to offer an in-depth discussion on the reciprocal regulatory interactions between FLD and HSC activation,providing new insights for researchers in this field.展开更多
基金supported by grants from the Ministry of Science and Technology of the People’s Republic of China(grant number:2020YFA0803300)the National Natural Science Foundation of China(grant numbers:32270783,32100949,32300642)Figures were prepared using Figdraw。
文摘Hepatic stellate cells(HSCs),a distinct category of non-parenchymal cells in the liver,are critical for liver homeostasis.In healthy livers,HSCs remain non-proliferative and quiescent.However,under conditions of acute or chronic liver damage,HSCs are activated and participate in the progression and regulation of liver diseases such as liver fibrosis,cirrhosis,and liver cancer.Fatty liver diseases(FLD),including nonalcoholic(NAFLD)and alcoholrelated(ALD),are common chronic inflammatory conditions of the liver.These diseases,often resulting from multiple metabolic disorders,can progress through a sequence of inflammation,fibrosis,and ultimately,cancer.In this review,we focused on the activation and regulatory mechanism of HSCs in the context of FLD.We summarized the molecular pathways of activated HSCs(aHSCs)in mediating FLD and their role in promoting liver tumor development from the perspectives of cell proliferation,invasion,metastasis,angiogenesis,immunosuppression,and chemo-resistance.We aimed to offer an in-depth discussion on the reciprocal regulatory interactions between FLD and HSC activation,providing new insights for researchers in this field.
