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作 者:孙志鹏 董树素 马川程 王琛莹 陈飞 王海英 SUN Zhi-peng;DONG Shu-su;MA Chuan-cheng;WANG Chen-ying;CHEN Fei;WANG Hai-ying(Clinical Medical College,Jining Medical University,Jining 272067,Shandong Province,China;Second Clinical Medical College,Jining Medical University,Jining 272067,Shandong Province,China;Basic Medical College,Jining Medical University,Jining 272067,Shandong Province,China;Department of Physiology,Jining Medical University,Jining 272067,Shandong Province,China)
机构地区:[1]济宁医学院临床医学院,山东济宁272067 [2]济宁医学院第二临床医学院,山东济宁272067 [3]济宁医学院基础医学院,山东济宁272067 [4]济宁医学院生理学教研室,山东济宁272067
出 处:《中国临床药理学杂志》2024年第13期1972-1976,共5页The Chinese Journal of Clinical Pharmacology
基 金:国家自然科学基金青年基金资助项目(81703490);山东省医药卫生科技发展计划基金资助项目(202002061311);济宁医学院教师科研扶持基金资助项目(JYFC2019KJ013);济宁医学院大学生创新训练计划基金资助项目(cx2021140)。
摘 要:Wnt信号通路包括经典通路和非经典通路,Wnt5a-Frizzled-2通路参与非经典通路中的Wnt/Ca^(2+)信号通路,该通路由Wnt相关蛋白Wnt5a与其配体Frizzled-2结合后被激活,可调控细胞中的部分关键位点影响细胞的信号转导,且与细胞的生长进程密切相关。在某些血供丰富的组织,如心脏和脑组织等发生缺血再灌注时,均存在Wnt5a-Fizzled-2通路的激活。Wnt5a-Frizzled-2通路激活后引起细胞内钙超载,最终促进细胞凋亡。本文综述Wnt5a-Frizzled-2信号通路在缺血再灌注损伤类疾病中的异常激活和引起的钙超载导致细胞凋亡,以期为缺血再灌注损伤的生理机制研究提供参考。The Wnt signaling pathway includes both classical and non classical pathways,Wnt5a-Frizzled-2 pathway participates in the Wnt/Ca^(2+)signaling pathway in the non-classical pathway,which is activated by the Wnt-related protein Wnt5a and its ligand Frizzled-2.It can regulate some key sites in cells to affect cell signal transduction,and is closely related to cell growth process.Activation of Wnt5a-Fizzled-2 pathway occurs in some tissues with abundant blood supply,such as heart and brain tissues,during ischemia-reperfusion.Activation of the Wnt5a-Frizzled-2 pathway causes these intracellular calcium overload,ultimately promoting apoptosis.This article reviews the abnormal activation of Wnt5a-Frizzled-2 signaling pathway in ischemia-reperfusion injury diseases and the induced calcium overload leading to apoptosis,in order to provide reference for the study of physiological mechanisms of ischemia-reperfusion injury.
关 键 词:Wnt5a-跨膜蛋白受体2通路 细胞凋亡 细胞自噬 缺血再灌注损伤
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