FXR在胆囊结石形成中的作用机制与研究进展
The Mechanisms and Research Progress on the Farnesoid X Receptor (FXR) in Gallstone Formation
DOI: 10.12677/acm.2026.162452, PDF,   
作者: 胡 彪, 王兴志, 曹 松, 苏鹏伟, 杨子贤, 徐鹏远*:昆明医科大学第二附属医院胃肠外科二病区,云南 昆明
关键词: 法尼醇X受体胆汁酸胆囊结石胆固醇结石Farnesoid X Receptor Bile Acid Gallstone Cholesterol Gallstone
摘要: 本文主要以FXR (法尼醇X受体)为核心,当前研究明确了其在胆囊结石形成中的核心枢纽作用。FXR功能失调通过多维度机制致病:在肝脏,它导致胆汁酸合成反馈抑制失效与肝胆转运紊乱,直接引起胆固醇过饱和胆汁;在胆囊,其活性降低削弱收缩动力并诱发炎症纤维化,为胆固醇结晶滞留生长创造条件;在肠道,FXR-FGF15/19信号通路中断及伴随的屏障损伤与菌群紊乱,通过肠–肝轴放大肝脏代谢失衡。针对FXR的激动剂(如奥贝胆酸)及微生物组干预策略已展现出防治潜力。未来研究应致力于开发高效低毒的组织特异性FXR调节剂,并深入探索肠道菌群–胆汁酸–FXR轴在胆石症中的精细调控网络,以推动针对病因的精准防治新策略。
Abstract: Taking FXR (Farnesoid X Receptor) as the core, current research has clarified its pivotal role as a central hub in the formation of gallstones. FXR dysfunction promotes pathogenesis through multi-dimensional mechanisms: in the liver, it leads to failed feedback inhibition of bile acid synthesis and disrupted hepatobiliary transport, directly causing cholesterol-supersaturated bile; in the gallbladder, reduced FXR activity impairs contractile motility and induces inflammation and fibrosis, creating conditions for cholesterol crystal retention and growth; in the intestine, disruption of the FXR-FGF15/19 signaling pathway, coupled with impaired barrier function and gut microbiota dysbiosis, amplifies hepatic metabolic imbalances via the gut-liver axis. Therapeutic strategies targeting FXR, such as agonists (e.g., Obeticholic Acid) and microbiome interventions, have shown preventive potential. Future research should focus on developing highly effective and low-toxicity tissue-specific FXR modulators and delve deeper into the intricate regulatory network of the gut microbiota-bile acid-FXR axis in cholelithiasis to advance precise, etiology-targeted prevention and treatment strategies.
文章引用:胡彪, 王兴志, 曹松, 苏鹏伟, 杨子贤, 徐鹏远. FXR在胆囊结石形成中的作用机制与研究进展[J]. 临床医学进展, 2026, 16(2): 783-793. https://doi.org/10.12677/acm.2026.162452

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