[1] Cotter TG, Rinella M. Nonalcoholic fatty liver disease 2020: the state of the disease. Gastroenterology, 2020, 158(7):1851-1864. [2] Loomba R, Friedman SL, Shulman GI. Mechanisms and disease consequences of nonalcoholic fatty liver disease. Cell, 2021, 184(10):2537-2564. [3] Hu H, Lin A, Kong M, et al. Intestinal microbiome and NAFLD: molecular insights and therapeutic perspectives. J Gastroenterol, 2020, 55(2):142-158. [4] Mukherji A, Dachraoui M, Baumert TF. Perturbation of the circadian clock and pathogenesis of NAFLD. Metabolism, 2020, 111S:154337. [5] Wei F, Li J, Chen C, et al. Higher serum uric acid level predicts non-alcoholic fatty liver disease: a 4-year prospective cohort study. Front Endocrinol (Lausanne), 2020, 11:179. [6] Sharaf EDU, Salem MM, Abdulazim DO. Uric acid in the pathogenesis of metabolic, renal, and cardiovascular diseases: a review. J Adv Res, 2017, 8(5):537-548. [7] Chen YL, Li H, Li S, et al. Prevalence of and risk factors for metabolic associated fatty liver disease in an urban population in China: a cross-sectional comparative study. BMC Gastroenterol, 2021, 21(1):212. [8] Ma Z, Zhang J, Kang X, et al. Hyperuricemia precedes non-alcoholic fatty liver disease with abdominal obesity moderating this unidirectional relationship: three longitudinal analyses. Atherosclerosis, 2020, 311:44-51. [9] Liu D, Yun Y, Yang D, et al. What is the biological function of uric acid? An antioxidant for neural protection or a biomarker for cell death. Dis Markers, 2019, 2019:4081962. [10] Yanai H, Adachi H, Hakoshima M, et al. Molecular biological and clinical understanding of the pathophysiology and treatments of hyperuricemia and its association with metabolic syndrome, cardiovascular diseases and chronic kidney disease. Int J Mol Sci, 2021, 22(17):9221. [11] Zheng X, Gong L, Luo R, et al. Serum uric acid and non-alcoholic fatty liver disease in non-obesity Chinese adults. Lipids Health Dis, 2017, 16(1): 202. [12] Cho HC. Prevalence and factors associated with nonalcoholic fatty liver disease in a nonobese Korean population. Gut Liver, 2016, 10(1):117-125. [13] Pafili K, Roden M. Nonalcoholic fatty liver disease (NAFLD) from pathogenesis to treatment concepts in humans. Mol Metab, 2021, 50:101122. [14] Chakrabarty RP, Chandel NS. Mitochondria as signaling organelles control mammalian stem cell fate. Cell Stem Cell, 2021, 28(3):394-408. [15] Sakurai Y, Kubota N, Yamauchi T, et al. Role of insulin resistance in MAFLD. Int J Mol Sci, 2021, 22(8):4156. [16] Hossain IA, Faruque MO, Akter S, et al. Elevated levels of serum uric acid and insulin resistance are associated with nonalcoholic fatty liver disease among prediabetic subjects. Trop Gastroenterol, 2016, 37(2): 101-111. [17] Zhu Y, Hu Y, Huang T, et al. High uric acid directly inhibits insulin signalling and induces insulin resistance. Biochem Biophys Res Commun, 2014, 447(4):707-714. [18] Wan X, Xu C, Lin Y, et al. Uric acid regulates hepatic steatosis and insulin resistance through the NLRP3 inflammasome-dependent mechanism. J Hepatol, 2016, 64(4):925-932. [19] Nishikawa T, Nagata N, Shimakami T, et al. Xanthine oxidase inhibition attenuates insulin resistance and diet-induced steatohepatitis in mice. Sci Rep, 2020, 10(1):815. [20] Song D, Zhao X, Wang F, et al. A brief review of urate transporter 1 (URAT1) inhibitors for the treatment of hyperuricemia and gout: current therapeutic options and potential applications. Eur J Pharmacol, 2021, 907:174291. [21] Tanaka Y, Nagoshi T, Takahashi H, et al. URAT1-selective inhibition ameliorates insulin resistance by attenuating diet-induced hepatic steatosis and brown adipose tissue whitening in mice. Mol Metab, 2022, 55:101411. [22] Moncan M, Mnich K, Blomme A, et al. Regulation of lipid metabolism by the unfolded protein response. J Cell Mol Med, 2021, 25(3):1359-1370. [23] Choi YJ, Shin HS, Choi HS, et al. Uric acid induces fat accumulation via generation of endoplasmic reticulum stress and SREBP-1c activation in hepatocytes. Lab Invest, 2014, 94(10):1114-1125. [24] Ferré P, Phan F, Foufelle F. SREBP-1c and lipogenesis in the liver: an update1. Biochem J, 2021, 478(20):3723-3739. [25] Yu W, Cheng JD. Uric acid and cardiovascular disease: an update from molecular mechanism to clinical perspective. Front Pharmacol, 2020, 11:582680. [26] Sun X, Jiao H, Zhao J, et al. Unexpected effect of urate on hydrogen peroxide-induced oxidative damage in embryonic chicken cardiac cells. Free Radic Res, 2017, 51(7-8):693-707. [27] Solano-Urrusquieta A, Morales-González JA, Castro-Narro GE, et al. NRF-2 and nonalcoholic fatty liver disease. Ann Hepatol, 2020, 19(5):458-465. [28] Chen Z, Tian R, She Z, et al. Role of oxidative stress in the pathogenesis of nonalcoholic fatty liver disease. Free Radic Biol Med, 2020, 152:116-141. [29] Zhou Y, You H, Zhang A, et al. Lipoxin A4 attenuates uric acid-activated, NADPH oxidase-dependent oxidative stress by interfering with translocation of p47phox in human umbilical vein endothelial cells. Exp Ther Med, 2020, 20(2):1682-1692. [30] Xie D, Zhao H, Lu J, et al. High uric acid induces liver fat accumulation via ROS/JNK/AP-1 signaling. Am J Physiol Endocrinol Metab, 2021, 320(6):E1032-E1043. [31] Yue J, López JM. Understanding MAPK signaling pathways in apoptosis. Int J Mol Sci, 2020, 21(7):2346. [32] Kawachi Y, Fujishima Y, Nishizawa H, et al. Increased plasma XOR activity induced by NAFLD/NASH and its possible involvement in vascular neointimal proliferation. JCI Insight, 2021, 6(17):e144762. [33] Toledo-Ibelles P, Gutiérrez-Vidal R, Calixto-Tlacomulco S, et al. Hepatic accumulation of hypoxanthine: a link between hyperuricemia and nonalcoholic fatty liver disease. Arch Med Res, 2021, 52(7):692-702. [34] Lanaspa MA, Sanchez-Lozada LG, Choi YJ, et al. Uric acid induces hepatic steatosis by generation of mitochondrial oxidative stress: potential role in fructose-dependent and-independent fatty liver. J Biol Chem, 2012, 287(48):40732-40744. [35] Castro L, Tórtora V, Mansilla S, et al. Aconitases: non-redox iron-sulfur proteins sensitive to reactive species. Acc Chem Res, 2019, 52(9):2609-2619. [36] Sharma BR, Kanneganti TD. NLRP3 inflammasome in cancer and metabolic diseases. Nat Immunol, 2021, 22(5):550-559. [37] Zheng M, Kanneganti TD. The regulation of the ZBP1-NLRP3 inflammasome and its implications in pyroptosis, apoptosis, and necroptosis (PANoptosis). Immunol Rev, 2020, 297(1):26-38. [38] Shaker ME. The contribution of sterile inflammation to the fatty liver disease and the potential therapies. Biomed Pharmacother, 2022, 148:112789. [39] Huang Y, Xu W, Zhou R. NLRP3 inflammasome activation and cell death. Cell Mol Immunol, 2021, 18(9):2114-2127. [40] Wan X, Xu C, Lin Y, et al. Uric acid regulates hepatic steatosis and insulin resistance through the NLRP3 inflammasome-dependent mechanism. J Hepatol, 2016, 64(4):925-932. [41] Xu C, Wan X, Xu L, et al. Xanthine oxidase in non-alcoholic fatty liver disease and hyperuricemia: one stone hits two birds. J Hepatol, 2015, 62(6):1412-1419. [42] Lv Y, Gao X, Luo Y, et al. Apigenin ameliorates HFD-induced NAFLD through regulation of the XO/NLRP3 pathways. J Nutr Biochem, 2019, 71:110-121. [43] Su Q, Kumar V, Sud N, et al. MicroRNAs in the pathogenesis and treatment of progressive liver injury in NAFLD and liver fibrosis. Adv Drug Deliv Rev, 2018, 129:54-63. [44] Chen S, Chen D, Yang H, et al. Uric acid induced hepatocytes lipid accumulation through regulation of miR-149-5p/FGF21 axis. BMC Gastroenterol, 2020, 20(1):39. [45] Niimi N, Yako H, Takaku S, et al. Aldose reductase and the polyol pathway in schwann cells: old and new problems. Int J Mol Sci, 2021, 22(3):1031. [46] Cen L, Xing F, Xu L, et al. Potential role of gene regulator nfat5 in the pathogenesis of diabetes mellitus. J Diabetes Res, 2020, 2020:6927429. [47] Sanchez-Lozada LG, Andres-Hernando A, Garcia-Arroyo FE, et al. Uric acid activates aldose reductase and the polyol pathway for endogenous fructose and fat production causing development of fatty liver in rats. J Biol Chem, 2019, 294(11):4272-4281. [48] Lanaspa MA, Ishimoto T, Li N, et al. Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome. Nat Commun, 2013, 4:2434. |