MHD患者AVF狭窄的胆汁酸谱代谢组学研究进展

Research Progress on the Bile Acid Metabolome in Arteriovenous Fistula Stenosis among Maintenance Hemodialysis Patients

摘要: 目的：探讨胆汁酸代谢紊乱在维持性血液透析(MHD)患者自体动静脉内瘘(AVF)狭窄中的作用机制及研究进展。方法：广泛查阅并归纳相关文献。结果：AVF狭窄的发生涉及内皮损伤、炎症反应、氧化应激、血管钙化及新生内膜增生等多个病理生理过程。MHD患者因肾功能衰竭及透析治疗，胆汁酸代谢谱发生显著改变，特定的胆汁酸及其信号通路(如FXR、TGR5等)可通过调控全身炎症、血管钙化和直接影响血管内皮细胞功能参与AVF狭窄。结论：胆汁酸代谢紊乱是连接慢性肾脏病全身状态与AVF局部血管病变的重要代谢桥梁，其深入研究为理解AVF狭窄的机制提供了新的研究方向。未来研究需进一步明确关键致病性胆汁酸作用靶点及信号通路，以期发现潜在的生物标志物和治疗新靶点。

Abstract: Objective: To explore the mechanism and research progress of bile acid metabolism disorder in the stenosis of autologous arteriovenous fistula (AVF) in maintenance hemodialysis (MHD) patients. Methods: Conduct extensive research and summarize relevant literature. Results: The occurrence of AVF stenosis involves multiple pathophysiological processes such as endothelial injury, inflammatory response, oxidative stress, vascular calcification, and neointimal hyperplasia. Due to renal failure and dialysis treatment, the bile acid metabolism profile of MHD patients undergoes significant changes. Specific bile acids and their signaling pathways (such as FXR, TGR5, etc.) can participate in AVF stenosis by regulating systemic inflammation, vascular calcification, and directly affecting the function of vascular endothelial cells. Conclusion: Bile acid metabolism disorder is an important metabolic bridge connecting the systemic state of chronic kidney disease and local vascular lesions of AVF. In-depth research provides a new research direction for understanding the mechanism of AVF stenosis. Future studies need to further clarify the key pathogenic bile acid action targets and signaling pathways in order to discover potential biomarkers and new therapeutic targets.