2017
DOI: 10.1002/hep.28709
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Bile acids and nonalcoholic fatty liver disease

Abstract: Nonalcoholic fatty liver disease (NAFLD) is a burgeoning health problem worldwide and an important risk factor for both hepatic and cardiometabolic mortality. The rapidly increasing prevalence of this disease and of its aggressive form nonalcoholic steatohepatitis (NASH) will require novel therapeutic approaches to prevent disease progression to advanced fibrosis or cirrhosis and cancer. In recent years, bile acids have emerged as relevant signaling molecules that act at both hepatic and extrahepatic tissues t… Show more

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Cited by 483 publications
(475 citation statements)
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References 102 publications
(163 reference statements)
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“…Hepatosteatosis (nonalcoholic fatty liver, NAFL) is a classic complication of obesity. Both endocrine FGFs and BAs are involved in regulating hepatic lipid metabolism (47,48). Previous murine studies have demonstrated that genetic ablation or adenoviral knockdown of Fgf21 promotes hepatic fat accumulation (27,49).…”
Section: Tgr5mentioning
confidence: 99%
“…Hepatosteatosis (nonalcoholic fatty liver, NAFL) is a classic complication of obesity. Both endocrine FGFs and BAs are involved in regulating hepatic lipid metabolism (47,48). Previous murine studies have demonstrated that genetic ablation or adenoviral knockdown of Fgf21 promotes hepatic fat accumulation (27,49).…”
Section: Tgr5mentioning
confidence: 99%
“…The cholesterol 7a hydroxylase 1 (CYP7A1) and cholesterol 27a hydroxylase 1 (CYP27A1) proteins are both involved in the catabolism of cholesterol to bile acids [11] . The CYP7A1 mRNA was almost not altered (Supplementary Figure S2F).…”
Section: Wwwnaturecom/aps Liu MX Et Almentioning
confidence: 99%
“…Abundant FC in the liver causes liver injury that induces inflammation and fibrogenesis [7] , mediated by the increased production of reactive oxygen species (ROS) resulting in mitochondrial dysfunction, and by triggering the unfolded protein response (UPR) in the endoplasmic reticulum (ER), which causes ER stress and apoptosis [8] . Cholesterol accumulation may be attributed to increased de novo synthesis [9] , increased uptake from lipoproteins [10] , decreased conversion to bile acids [11] or decreased cholesterol excretion in the bile [3] . However, the molecular mechanism triggering these abnormalities and the relative contribution of these pathways to cholesterol accumulation in NAFLD remain to be elucidated.…”
Section: Introductionmentioning
confidence: 99%
“…FXR -ядерный рецептор, чьим эндогенным лигандом являются желчные кислоты, прежде всего -хенодезокси-холевая кислота [8]. Связываясь с желчными кислотами в цитоплазме, FXR транспортируется в ядро, где активи-рует экспрессию множества генов.…”
Section: биология фарнезоидного рецептораunclassified