TRPV1通道在小鼠组织纤维化中的作用研究进展  

Progress in study of the function of transient receptor potential vanillin subfamily 1 channel in tissue fibrosis of mouse models

作　　者：师雨琛 李小强 SHI Yuchen;LI Xiaoqiang(Department of Chinese Materia Medica and Natural Medicines,School of Pharmacy,Air Force Medical University,Xi’an 710032,China;College of Basic Medicine,Air Force Medical University,Xi’an 710032,China)

机构地区：[1]空军军医大学药学系中药与天然药物学教研室,西安710032 [2]空军军医大学基础医学院,西安710032

出　　处：《中国实验动物学报》2025年第2期259-266,共8页Acta Laboratorium Animalis Scientia Sinica

基　　金：国家自然科学基金(82270357);空军军医大学“青苗”基金(2024QMJJ013)。

摘　　要：纤维化的主要病理特征为纤维结缔组织增多、实质细胞减少,如持续进展可致器官结构破坏和功能减退。近年来研究发现,非选择性阳离子通道-瞬时感受器电位香草酸亚型1(transient receptor potential vanilloid subfamily 1,TRPV1)通道与纤维化密切相关。该通道被激活后可使胞内阳离子浓度升高,引起相应的生理和病理变化,特别是在调控组织纤维化过程中发挥关键作用。为了深入研究TRPV1通道参与组织纤维化的发生机制,动物模型已成为了该类研究的重要工具。本文将综述TRPV1通道在小鼠心脏、肾、胰腺等脏器纤维化中的作用,对TRPV1通道参与调控纤维化的相关信号通路进行总结,以期为纤维化发病机制研究和药物研发提供新的思路。Fibrosis is a pathological process characterized by an increase in connective tissue and a decrease in parenchymal cells within organ tissues.During its progression,fibrosis can lead to structural damage and functional decline of the affected organ.In recent years,it has found that non⁃selective cation channel transient receptor potential vanilloid subfamily 1(TRPV1)channel is closely related to fibrosis.When this channel is activated,it can increase the intracellular cation concentration and cause corresponding physiological and pathological changes,playing a particularly crucial role in regulating tissue fibrosis.Animal models have become important tools in studies into the mechanism by which the TRPV1 channel induces organ fibrosis.This article reviews the role of TRPV1 channels in the fibrosis of organs such as the heart,kidney,and pancreas in mice.The relevant signaling pathways in which TRPV1 channels participate to regulate fibrosis are summarized to provide new ideas for studying the pathogenesis of fibrosis and the development of targeted drugs.

关 键 词：纤维化 瞬时感受器电位香草酸亚型1通道 小鼠模型 信号通路 药物靶点 

分 类 号：Q95-33[生物学—动物学]