瞬时受体电位香草酸受体1在缺血再灌注损伤中潜在作用的研究进展
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1.安徽医科大学第一临床学院 麻醉系, 安徽 合肥 230032;2.安徽医科大学第三附属医院 麻醉科, 安徽 合肥 230061;3.安徽医科大学第一附属医院 麻醉科, 安徽 合肥 230022

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通讯作者:

陆姚,E-mail:luyao-mz@163.com

中图分类号:

R54

基金项目:

国家自然科学基金(No:81770295);国家级大学生创新创业训练计划项目(No:201810366018)


Research progress on potential involvement of TRPV1 channels in ischemia-reperfusion injury
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Affiliation:

1.Department of Anesthesiology, The First Clinical College, Anhui Medical University, Hefei, Anhui 230032, China;2.Department of Anesthesiology, The Third Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230061, China;3.Department of Anesthesiology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, China

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    摘要:

    瞬时受体电位香草酸受体1(TRPV1)通道是一种非选择性的阳离子通道,在缺血再灌注损伤中起关键作用。TRPV1主要在支配着心脏和血管神经纤维的感觉神经元上表达,TRPV1的激活能够减轻包括心脏、肺、肾和脑在内的多种器官的缺血再灌注诱导的损伤。多项研究表明,TRPV1通道的激活刺激降钙素基因相关肽和P物质的释放,这在心脏保护中具有重要的作用;此外,TRPV1通道的激活能减少自由基和炎症细胞因子的释放,抑制中性粒细胞浸润,并增强抗炎细胞因子的产生以减少缺血再灌注损伤。该文就TRPV1通道及其信号级联在缺血再灌注损伤中的作用进行综述。

    Abstract:

    The transient receptor potential vanilloid 1 (TRPV1) channel is a non selective cation channel that plays a vital role in ischemia-reperfusion injury. TRPV1 predominantly expressed in sensory neurons with the nerve fibers innervating the heart and blood vessels. Activation of TRPV1 channels attenuates ischemia-reperfusion induced injury in various organs including heart, lungs, kidneys and brain. Multiple studies have demonstrated that the activation of TRPV1 channels on peripheral blood vessels stimulates the release of calcitonin gene-related peptides and substance P to produce cardioprotection. In addition, TRPV1 channels activation reduces the production of free radicals and inflammatory cytokines, inhibits neutrophil infiltration, and enhances the production of anti-inflammatory cytokines to reduce ischemia-reperfusion-induced tissue injury. This article reviews the potential involvement of TRPV1 channels and signal cascades in ischemia-reperfusion injury.

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王其锋,胡珍,高慧,吴利宁,陆姚.瞬时受体电位香草酸受体1在缺血再灌注损伤中潜在作用的研究进展[J].中国现代医学杂志,2022,(7):47-51

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  • 收稿日期:2021-09-10
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  • 在线发布日期: 2023-10-30
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