肺损伤中的血管重塑的机制  

The mechanism of vascular remodeling in lung injury

作　　者：达瓦曲珍 卓馨 江舟[1,3] 成姝婷[1,3] Dawaquzhen;Zhuo Xin;Jiang Zhou;Cheng Shu-ting(West China School of Basic Medical Sciences&Forensic Medicine,Sichuan University,Chengdu 610041,China;West China Second Hospital,Sichuan University,Chengdu 610041,China;NHC Key Laboratory of Chronobiology(Sichuan University),Chengdu 610041,China)

机构地区：[1]四川大学华西基础医学与法医学院,四川成都610041 [2]四川大学华西第二医院,四川成都610041 [3]国家卫生健康委员会时间生物学重点实验室(四川大学),四川成都610041

出　　处：《四川生理科学杂志》2024年第7期1646-1649,共4页

基　　金：西藏自治区科技计划项目(编号:CGZH2023000335);中央高校基本科研业务专项资金资助(编号:SCU2023D022)。

摘　　要：肺损伤过程中的血管重塑是一个极其复杂的生物学过程,涉及了细胞的增殖、凋亡、迁移以及细胞外基质(Extracellular matrix,ECM)的重组,在维持和修复肺组织结构中起着至关重要的作用。血管平滑肌细胞(Vascular smooth muscle cells,VSMCs)和内皮细胞(Endothelial cells,ECs)是这一过程的主要参与者,它们通过相互作用及响应一系列生物活性分子的调节,如血管紧张素Ⅱ(Angiotensin Ⅱ,Ang Ⅱ)、血管内皮生长因子(Vascular endothelial growth factor,VEGF)、转化生长因子-β(Transforming growth factor-β,TGF-β)等,共同推动血管重塑的进行。这些分子不仅影响VSMCs和ECs的增殖与迁移,还涉及到血管收缩和扩张的精细调控以及信号转导途径的激活,如通过丝裂原活化蛋白激酶(Mitogen-activated protein kinase,MAPK)、Ras同源基因家族成员A(Ras homolog gene family,Rho A)、蛋白激酶C(Protein kinase C,PKC)等途径调控细胞功能。此外,缺氧环境下的细胞应激响应,如增强的活性氧(Reactive oxygen species,ROS)生成和钙信号通路的激活,也在血管重塑中扮演着关键角色。了解这些复杂的相互作用及其背后的分子机制对于开发针对肺损伤及相关血管病变的治疗策略具有重要意义。本综述旨在探讨VSMCs和ECs在血管重塑中的作用,生物活性分子如何影响这一过程,以及这些生物学过程如何相互作用和被调节,期望为未来的研究和临床治疗提供新的思路和策略。Vascular remodeling during lung injury is an extremely complex biological process that involves cell proliferation,apoptosis,migration,and reorganization of the extracellular matrix(ECM).Vascular smooth muscle cells(VSMCs)and endothelial cells(ECs)play a vital role in the maintenance and repair of lung tissue structure.Through interactions and responses to various bioactive molecules like angiotensin Ⅱ(Ang Ⅱ),vascular endothelial growth factor(VEGF),and transforming growth factor-beta(TGF-β),they facilitate vascular remodeling.These molecules not only affect the proliferation and migration of VSMCs and ECs but also involve the fine regulation of vascular constriction,dilation,and activation of signaling pathways.These pathways include mitogen-activated protein kinase(MAPK),Rho A,and protein kinase C(PKC),which regulate cellular functions.Furthermore,the activation of calcium signaling pathways and increased generation of reactive oxygen species(ROS)due to cellular stress responses in hypoxic conditions are also essential factors in vascular remodeling.Understanding these complex interactions and the underlying molecular mechanisms is of great significance for developing therapeutic strategies for lung injury and related vascular disorders.This review aims to explore the roles of VSMCs and ECs in vascular remodeling,how bioactive molecules influence this process,and how these biological processes interact and are regulated,in order to provide new insights and strategies for future research and clinical treatment.

关 键 词：血管重塑 肺损伤 平滑肌细胞 内皮细胞 信号转导途径 

分 类 号：R563[医药卫生—呼吸系统]