肠道菌群通过影响胆汁酸代谢参与胆石症形成的研究进展
Research Progress on the Role of Gut Microbiota in Gallstone Formation through Bile Acid Metabolism

胆石症是一种常见的消化系统疾病，其主要特征是胆囊内形成结石。现有研究表明，胆囊结石(GSD)的发生发展涉及多重病理生理机制。流行病学调查显示，膳食结构异常、体质量指数超标等外源性因素与遗传易感性等内源性因素共同参与了疾病进程。从病理生理学角度分析，胆汁成分改变(如胆固醇过饱和状态)、胆囊动力学异常(包括收缩功能障碍和排空受阻)以及胆汁酸代谢紊乱等内在机制，构成了GSD形成的关键环节。这些因素相互作用，共同促进了胆固醇结晶的成核、生长和聚集。其流行病学特征在不同地区和人群中存在显著差异，影响其发病率的因素包括性别、年龄、种族和生活方式等。本文通过研究查阅国内外文献，综述了胆汁酸在肠道菌群对胆石症作用机制中的最新研究进展，包括肠道菌群对胆汁酸代谢的调控、胆汁酸代谢紊乱与胆石症的关系，本研究致力于深入探讨GSD的病理生理机制，通过系统分析其分子调控网络，识别关键作用靶点，进而开发创新性治疗策略。研究结果将为GSD的早期预防、临床治疗及预后改善提供理论依据和实践指导，推动该领域研究向纵深发展。
Gallstone disease (GSD) is a common digestive system disorder characterized by the formation of stones within the gallbladder. Current research indicates that the development of gallbladder stones involves multiple pathophysiological mechanisms. Epidemiological investigations reveal that both exogenous factors, such as abnormal dietary patterns and excessive body mass index, and endogenous factors, including genetic susceptibility, contribute to the disease process. From a pathophysiological perspective, intrinsic mechanisms such as alterations in bile composition (e.g., cholesterol supersaturation), gallbladder motility disorders (including impaired contractile function and obstructed emptying), and bile acid metabolism dysregulation constitute key components in the formation of GSD. These factors interact synergistically, collectively promoting the nucleation, growth, and aggregation of cholesterol crystals. Its epidemiological characteristics exhibit significant variations across different regions and populations, with factors influencing its incidence including gender, age, ethnicity, and lifestyle. This article reviews the latest research progress on the role of bile acids in the mechanism of gallstone disease mediated by gut microbiota by studying and referencing both domestic and international literature. This includes the regulation of bile acid metabolism by gut microbiota and the relationship between bile acid metabolism disorders and gallstone disease. This study aims to delve into the pathophysiological mechanisms of GSD, identify key targets through systematic analysis of its molecular regulatory network, and subsequently develop innovative therapeutic strategies. The research findings will provide a theoretical basis and practical guidance for the early prevention, clinical treatment, and prognosis improvement of GSD, driving the field's research towards greater depth and advancement.