《Table 3 Novel therapeutic agents for non-alcoholic fatty liver disease/non-alcoholic steatohepatiti

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《"Current status, problems, and perspectives of non-alcoholic fatty liver disease research"》

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How do organs and cells crosstalk in NAFLD/NASH?Crosstalk among normal/steatotic hepatocytes，immune cells，HSCs and the organ network is anintriguing theme in the context of NAFLD/NASH pathogenesis.Especially，contribution of gut-liver axis and microbiota to NASH development is drawing much attention（Table 4）[94-96].Although the merits of direct manipulation of the intestinal microbiota with antibiotics，prebiotics，or probiotics are debatable for human NAFLD/NASH due to the sheer diversity of microbiota，modulation of the gut-liver axis to target microbiota-derived metabolites is considered an attractive option.For instance，microbiota-derived deoxycholate evoked senescence-associated secretory phenotypes in HSCs and facilitated HCC development in hepatocarcinogen-primed genetically obese or high fat diet-fed mice[97].Microbiota-derived taurocholate stimulated ceramide synthesis in enterocytes through FXR in mice，after which circulating ceramide promotes hepatic steatosis[28].However，the applicability of these mechanisms to humans remains unclear.Recently，it was reported that microbiotaderived short-chain fatty acids lowered resting regulatory T-cells and associated with systemic T-cell activation in humans[96].As such，discovering the pathogenic molecules that mediate organ/cell crosstalk and contribute to NAFLD/NASHdevelopment in humans will provide much needed insights into disease management[31，98].