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作 者:赵贵全 赵贵勇 王艳梅[3] 王文博 王映珍[1] ZHAO Guiquan;ZHAO Guiyong;WANG Yanmei;WANG Wenbo;WANG Yingzhen(Emergency Center,Lanzhou University Second Hosipital,Lanzhou 730000,China;People’s Hospital of Gaolan County,Lanzhou City,Lanzhou 730200,China;Department of Endocrinology,Lanzhou University Second Hosipital,Lanzhou 730000,China)
机构地区:[1]兰州大学第二医院急救中心,兰州730000 [2]兰州市皋兰县人民医院,兰州730200 [3]兰州大学第二医院内分泌科,兰州730000
出 处:《中国细胞生物学学报》2024年第3期576-583,共8页Chinese Journal of Cell Biology
基 金:甘肃省自然科学基金(批准号:21JR7RA396);甘肃省兰州市人才创新创业项目(批准号:2020-RC-96)资助的课题。
摘 要:Ca^(2+)信号在胰腺正常生理过程中扮演着重要的角色,具有调控胰岛素和消化酶分泌的作用,而当涉及到急性胰腺炎(AP)时,细胞内异常Ca^(2+)信号是其发生的重要中心事件。在多种病因作用下胰腺组织内不同类型的细胞通过多种途径介导胞内Ca^(2+)信号异常和Ca^(2+)超载,导致胰腺细胞死亡和炎症反应,最终加速AP的发生和发展。近年来,一系列针对不同Ca^(2+)信号触发机制的抑制剂在AP的防治中取得了显著效果,其中部分药物已经进入临床试验阶段,这为AP的治疗提供了新思路。该文对Ca^(2+)信号及其抑制剂在AP中的研究进展进行综述。Calcium(Ca^(2+))signaling plays a crucial role in normal pancreatic physiology,regulating the secretion of insulin and digestive enzymes.However,in the AP(acute pancreatitis),abnormal intracellular Ca^(2+)sig-naling is a central event in its pathogenesis.Under the influence of various triggers,different cell types within pan-creatic tissue mediate aberrant intracellular Ca^(2+)signaling and Ca^(2+)overload through multiple pathways,leading to cell death and inflammatory responses in pancreatic cells,ultimately accelerating the onset and progression of acute pancreatitis.In recent years,a series of inhibitors targeting various Ca^(2+)signaling trigger mechanisms have shown significant promise in the prevention and treatment of AP,with some drugs advancing to clinical trial stages,offer-ing novel approaches to AP therapy.This article provides a review of the research progress on Ca^(2+)signaling and its inhibitors in AP.
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