[1] Aron-Wisnewsky J, Vigliotti C, Witjes J, et al. Gut microbiota and human NAFLD: disentangling microbial signatures from metabolic disorders. Nat Rev Gastroenterol Hepatol, 2020, 17(5): 279-297. [2] Eslam M, Sanyal A J, George J, et al. MAFLD: a consensus-driven proposed nomenclature for metabolic associated fatty liver disease. Gastroenterology, 2020, 158(7): 1999-2014,e1. [3] 柳雅立, 张晶. 儿童和青少年代谢相关脂肪性肝病研究进展. 实用肝脏病杂志, 2024, 27(4): 488-492. [4] Friedman S L, Neuschwander-Tetri B A, Rinella M, et al. Mechanisms of NAFLD development and therapeutic strategies. Nat Med, 2018, 24(7): 908-922. [5] 王梦雨, 杨蕊旭, 范建高. 重视代谢相关脂肪性肝病的特征与预后临床研究. 实用肝脏病杂志, 2021, 24(3): 308-311. [6] Sharpton S R, Schnabl B, Knight R, et al. Current concepts, opportunities, and challenges of gut microbiome-based personalized medicine in nonalcoholic fatty liver disease. Cell Metab, 2021, 33(1): 21-32. [7] Boursier J, Mueller O, Barret M, et al. The severity of nonalcoholic fatty liver disease is associated with gut dysbiosis and shift in the metabolic function of the gut microbiota. Hepatology, 2016, 63(3): 764-775. [8] Alferink L J M, Radjabzadeh D, Erler N S, et al. Microbiomics, metabolomics, predicted metagenomics, and hepatic steatosis in a population-based study of 1,355 adults. Hepatology, 2021, 73(3): 968-982. [9] Louis P, Flint H J. Formation of propionate and butyrate by the human colonic microbiota. Environ Microbiol, 2017, 19(1): 29-41. [10] Qin J, Li Y, Cai Z, et al. A metagenome-wide association study of gut microbiota in type 2 diabetes. Nature, 2012, 490(7418): 55-60. [11] Miao L, Targher G, Byrne C D, et al. Current status and future trends of the global burden of MASLD. Trends Endocrinol Metab, 2024, 35(8): 697-707. [12] Canfora E E, Meex R C R, Venema K, et al. Gut microbial metabolites in obesity, NAFLD and T2DM. Nat Rev Endocrinol, 2019, 15(5): 261-273. [13] Schwimmer J B, Johnson J S, Angeles J E, et al. Microbiome signatures associated with steatohepatitis and moderate to severe fibrosis in children with nonalcoholic fatty liver disease. Gastroenterology, 2019, 157(4): 1109-1122. [14] Flessa C M, Nasiri-Ansari N, Kyrou I, et al. Genetic and diet-induced animal models for non-alcoholic fatty liver disease (NAFLD) research. Int J Mol Sci, 2022, 23(24): 15791. [15] Suriano F, Vieira-Silva S, Falony G, et al. Novel insights into the genetically obese (ob/ob) and diabetic (db/db) mice: two sides of the same coin. Microbiome, 2021, 9: 147. [16] Scorletti E, Carr R M. A new perspective on NAFLD: focusing on lipid droplets. J Hepatol, 2022, 76(4): 934-945. [17] Sun D Q, Liu W Y, Wu S J, et al. Increased levels of low-density lipoprotein cholesterol within the normal range as a risk factor for nonalcoholic fatty liver disease. Oncotarget, 2016, 7(5): 5728-5737. [18] Xiao Y, Yang Y, Xiong H, et al. The implications of FASN in immune cell biology and related diseases. Cell Death Dis, 2024, 15(1): 88. [19] Sun J, Esplugues E, Bort A, et al. Fatty acid binding protein 5 suppression attenuates obesity-induced hepatocellular carcinoma by promoting ferroptosis and intratumoral immune rewiring. Nat Metab, 2024, 6(4): 741-763. [20] Kumar V, Xin X, Ma J, et al. Therapeutic targets, novel drugs, and delivery systems for diabetes associated NAFLD and liver fibrosis. Adv Drug Deliv Rev, 2021, 176: 113888. [21] Ahmed H, Umar M I, Imran S, et al. TGF-β1 signaling can worsen NAFLD with liver fibrosis backdrop. Exp Mol Pathol, 2022, 124: 104733. [22] Song Y, Wei J, Li R, et al. Tyrosine kinase receptor B attenuates liver fibrosis by inhibiting TGF-β/SMAD signaling. Hepatology, 2023, 78(5): 1433. |