Department of Hand and Foot Surgery, The Second Hospital, Cheeloo College of Medicine, Shandong University, No.247, Beiyuan Street, Jinan, Shandong Province, 250031, China.
Department of Hand and Foot Surgery, The First Hospital of Jilin University, No.71, Xinmin Street, Changchun, Jilin Province, 130021, China.
Trends Cardiovasc Med. 2022 Feb;32(2):61-70. doi: 10.1016/j.tcm.2020.12.010. Epub 2021 Jan 3.
Currently, endothelium-dependent vasodilatation involves three main mechanisms: production of nitric oxide (NO) by endothelial nitric oxide synthase (eNOS), synthesis of prostanoids by cyclooxygenase, and/or opening of calcium-sensitive potassium channels. Researchers have proposed multiple mechanosensors that may be involved in flow-mediated vasodilation (FMD), including G protein-coupled receptors (GPCRs), ion channels, and intercellular junction proteins, among others. However, GPCRs are considered the major mechanosensors that play a pivotal role in shear stress signal transduction. Among mechanosensitive GPCRs, G protein-coupled receptor 68, histamine H1 receptors, sphingosine-1-phosphate receptor 1, and bradykinin B2 receptors have been identified as endothelial sensors of flow shear stress regulating flow-mediated vasodilation. Thus, this review aims to expound on the mechanism whereby flow shear stress promotes vasodilation through the proposed mechanosensitive GPCRs in ECs.
目前，内皮依赖性血管舒张涉及三种主要机制：内皮型一氧化氮合酶（eNOS）产生一氧化氮（NO）、环氧化酶合成前列腺素，和/或钙敏钾通道开放。研究人员提出了多种可能参与血流介导的血管舒张（FMD）的机械感受器，包括 G 蛋白偶联受体（GPCRs）、离子通道和细胞间连接蛋白等。然而，GPCR 被认为是主要的机械感受器，在剪切力信号转导中发挥关键作用。在机械敏感 GPCR 中，G 蛋白偶联受体 68、组胺 H1 受体、鞘氨醇 1-磷酸受体 1 和缓激肽 B2 受体已被确定为调节血流介导的血管舒张的内皮细胞血流剪切力感受器。因此，本综述旨在阐述通过 ECs 中拟议的机械敏感 GPCR，血流剪切力如何促进血管舒张的机制。
