The transient receptor potential vanilloid type 4 (TRPV4) channel, a Ca²⁺-permeable nonselective cation channel, is widely distributed in the circulatory system, particularly in vascular endothelial cells (ECs) and smooth muscle cells (SMCs). The TRPV4 channel is activated by various endogenous and exogenous stimuli, including shear stress, low intravascular pressure, and arachidonic acid. TRPV4 has a role in mediating vascular tone and arterial blood pressure. The activation of the TRPV4 channel induces Ca²⁺ influx, thereby resulting in endothelium-dependent hyperpolarization and SMC relaxation through SK_Ca and IK_Ca activation on ECs or through BK_Ca activation on SMCs. Ca²⁺ binds to calmodulin, which leads to the production of nitric oxide, causing vasodilation. Furthermore, the TRPV4 channel plays an important role in angiogenesis and arteriogenesis and is critical for tumor angiogenesis and growth, since it promotes or inhibits the development of various types of cancer. The TRPV4 channel is involved in the active growth of collateral arteries induced by flow shear stress, which makes it a promising therapeutic target in the occlusion or stenosis of the main arteries. In this review, we explore the role and the potential mechanism of action of the TRPV4 channel in the regulation of vascular tone and in the induction of neovascularization to provide a reference for future research.

中文翻译：

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TRPV4 通道在血管扩张和新生血管形成中的作用

瞬态受体电位香草素 4 型 (TRPV4) 通道是一种可渗透 Ca ²⁺的非选择性阳离子通道，广泛分布于循环系统，特别是血管内皮细胞 (EC) 和平滑肌细胞 (SMC)。TRPV4 通道被各种内源性和外源性刺激激活，包括剪切应力、低血管内压力和花生四烯酸。TRPV4 在调节血管张力和动脉血压中起作用。TRPV4 通道的激活诱导 Ca ^{2+流入，从而通过 EC 上的 SK} _Ca和 IK _Ca激活或通过 SMC 上的 BK _Ca激活导致内皮依赖性超极化和 SMC 松弛。钙²⁺与钙调蛋白结合，导致一氧化氮的产生，引起血管舒张。此外，TRPV4 通道在血管生成和动脉生成中起重要作用，对肿瘤血管生成和生长至关重要，因为它促进或抑制各种癌症的发展。TRPV4通道参与由流动剪切应力诱导的侧支动脉的活跃生长，这使其成为主要动脉闭塞或狭窄的有希望的治疗靶点。在这篇综述中，我们探讨了TRPV4通道在调节血管张力和诱导新生血管形成中的作用及其潜在作用机制，为今后的研究提供参考。