胆囊收缩机制研究进展

Research Progress on the Mechanisms of Gallbladder Contraction

摘要: 胆囊收缩是对胆汁适时排入十二指肠加以调控的核心环节，此过程依靠精密且复杂的神经–体液网络来实现，同时也是维持消化道稳态的重要基础。虽说分子生物学及功能影像技术方面取得一定进展，这推动了针对相关机制展开的研究朝着更深入的方向去发展，然而，如何整合多维调控网络、解析病理生理细节、统一疾病诊断标准，依旧面临着不小的挑战。本文系统梳理了胆囊收缩所具备的生理基础及其调控网络的情况，着重对胆囊收缩素(CCK)所占据的核心地位、自主神经和肠神经系统之间的交互路径、平滑肌细胞内部的信号转导级联等进行剖析，并且还就收缩功能出现的障碍在相关疾病领域中的最新进展情况展开探讨。经过分析发现，通过靶向激活CCK-A受体信号通路使Cajal间质细胞网络的完整性得以恢复，或许能够成为在改善胆囊动力方面极为关键的治疗突破口，进而为临床精准干预策略的制定提供分子层面的理论依据。

Abstract: Gallbladder contraction constitutes the central mechanism regulating the timely delivery of bile into the duodenum. This process is mediated by a highly coordinated and intricate neurohumoral network and represents a fundamental prerequisite for maintaining gastrointestinal homeostasis. Although advances in molecular biology and functional imaging techniques have facilitated deeper investigation into the underlying mechanisms, substantial challenges remain in integrating multidimensional regulatory networks, elucidating detailed pathophysiological processes, and achieving standardized diagnostic criteria across related disorders. This review systematically summarizes the physiological basis of gallbladder contraction and its regulatory networks, with particular emphasis on the pivotal role of cholecystokinin (CCK), the interactive pathways between the autonomic nervous system and the enteric nervous system, and the intracellular signal transduction cascades within smooth muscle cells. In addition, recent advances concerning gallbladder contractile dysfunction in disease contexts are discussed. Emerging evidence suggests that targeted activation of the CCK-A receptor signaling pathway to restore the integrity of the interstitial cells of Cajal network may represent a critical therapeutic breakthrough for improving gallbladder motility, thereby providing a molecular-level theoretical foundation for the development of precision clinical intervention strategies.