Autophagy is a lysosomal degradation pathway in which the cell self-digests its own components to provide nutrients in harsh environmental conditions. It also represents an opportunity to rid the cell of superfluous and damaged organelles, misfolded proteins or invaded microorganisms. Liver autophagy contributes to basic hepatic functions such as lipid, glycogen and protein turnover. Deregulated hepatic autophagy has been linked to many liver diseases including alpha-1-antitrypsin deficiency, alcoholic and non-alcoholic fatty liver diseases, hepatitis B and C infections, liver fibrosis as well as liver cancer. Recently, bile acids and the bile acid receptor FXR have been implicated in the regulation of hepatic autophagy, which implies a role of autophagy also for cholestatic liver diseases. This review summarizes the current evidence of bile acid mediated effects on autophagy and how this affects cholestatic liver diseases. Although detailed studies are lacking, we suggest a concept that the activity of autophagy in cholestasis depends on the disease stage, where autophagy may be induced at early stages (“cholestophagy”) but may be impaired in prolonged cholestatic states (“cholestopagy”).

自噬是一种溶酶体降解途径，细胞在其中自我消化其自身成分以在恶劣的环境条件下提供营养。它还代表了一个机会，可以清除细胞中多余和受损的细胞器、错误折叠的蛋白质或入侵的微生物。肝脏自噬有助于基本的肝功能，例如脂质、糖原和蛋白质周转。肝脏自噬失调与许多肝脏疾病有关，包括 α-1-抗胰蛋白酶缺乏症、酒精性和非酒精性脂肪肝疾病、乙型和丙型肝炎感染、肝纤维化以及肝癌。最近，胆汁酸和胆汁酸受体 FXR 与肝脏自噬的调节有关，这意味着自噬对胆汁淤积性肝病也有作用。本综述总结了目前胆汁酸介导的自噬作用的证据，以及它如何影响胆汁淤积性肝病。虽然缺乏详细的研究，但我们提出了一个概念，即自噬在胆汁淤积中的活性取决于疾病阶段，其中自噬可能在早期阶段被诱导（“胆汁淤积”），但在长时间的胆汁淤积状态下可能受损（“胆汁淤积”）。