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胆汁淤积在肝脏损害的病理过程中起重要作用,并可能导致原发性硬化和肝功能衰竭,淤胆胆汁酸可诱导肝细胞凋亡和坏死,但它可以通过利胆胆汁酸的药理作用得以缓解,这些作用的实施需要肝细胞内钙库中Ca2+释放的改变和Ca2+内流。而钙池操纵的钙通道系存在于细胞膜表面的一种新发现的钙通道,它是非兴奋性细胞Ca2+内流的主要通道,然而Ca2+内流通道性质的影响因素仍未明了,本文综述了胆汁酸调控SOC的机制及对基质相互作用分子(STIM1)的影响。
Cholestasis plays an important role in the pathological process of liver damage and may lead to primary sclerosis and liver failure. Cholestatic bile acids can induce hepatocyte apoptosis and necrosis, but it can be obtained through the pharmacological action of bile acid Mitigation, the implementation of these effects requires changes in Ca2 + release and Ca2 + influx in the hepatocyte calcium pool. However, Ca2 + - operated Ca2 + channel is a newly discovered Ca2 + channel on the surface of the cell membrane, which is the main channel of Ca2 + influx in non - excitable cells. However, the factors influencing the Ca2 + influx channel are still unclear. The Mechanism of Acid Regulation of SOC and Its Effect on Substance Interacting Molecule (STIM1).