Therapeutic angiogenesis represents an emerging strategy to treat ischemic diseases by stimulating blood vessel growth to rescue local blood perfusion. Therefore, injured microvasculature may be repaired by stimulating resident endothelial cells or circulating endothelial colony forming cells (ECFCs) or by autologous cell-based therapy. Endothelial Ca²⁺ signals represent a crucial player in angiogenesis and vasculogenesis; indeed, several angiogenic stimuli induce neovessel formation through an increase in intracellular Ca²⁺ concentration. Several members of the Transient Receptor Potential (TRP) channel superfamily are expressed and mediate Ca²⁺-dependent functions in vascular endothelial cells and in ECFCs, the only known truly endothelial precursor. TRP Vanilloid 1 (TRPV1), a polymodal cation channel, is emerging as an important player in endothelial cell migration, proliferation, and tubulogenesis, through the integration of several chemical stimuli. Herein, we first summarize TRPV1 structure and gating mechanisms. Next, we illustrate the physiological roles of TRPV1 in vascular endothelium, focusing our attention on how endothelial TRPV1 promotes angiogenesis. In particular, we describe a recent strategy to stimulate TRPV1-mediated pro-angiogenic activity in ECFCs, in the presence of a photosensitive conjugated polymer. Taken together, these observations suggest that TRPV1 represents a useful target in the treatment of ischemic diseases.

中文翻译：

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内皮TRPV1作为促进治疗性血管生成的新兴分子靶标。

通过刺激血管生长以抢救局部血液灌注，治疗性血管生成代表了一种治疗缺血性疾病的新兴策略。因此，可以通过刺激驻留的内皮细胞或循环的内皮集落形成细胞（ECFC）或通过基于自体细胞的疗法来修复受损的微血管。内皮细胞Ca ²⁺信号代表血管生成和血管生成中的关键角色。实际上，几种血管生成性刺激通过细胞内Ca ²⁺浓度的增加诱导新生血管形成。瞬时受体电位（TRP）通道超家族的几个成员被表达并介导Ca ²⁺血管内皮细胞和ECFCs（唯一已知的真正的内皮前体）中的依赖依赖性功能。TRP Vanilloid 1（TRPV1）是一种多峰阳离子通道，通过整合多种化学刺激物，已成为内皮细胞迁移，增殖和微管生成的重要参与者。在这里，我们首先总结TRPV1的结构和门控机制。接下来，我们说明了TRPV1在血管内皮中的生理作用，并将我们的注意力集中在内皮TRPV1如何促进血管生成上。特别是，我们描述了在光敏共轭聚合物存在下刺激ECFC中TRPV1介导的促血管生成活性的最新策略。综上所述，这些观察结果表明TRPV1代表了治疗缺血性疾病的有用靶标。