Yuan Shuai, Kevil Christopher G
Departments of Pathology, Molecular and Cellular Physiology, and Cell Biology and Anatomy, LSU Health Shreveport, Shreveport, Louisiana, USA.
Microcirculation. 2016 Feb;23(2):134-45. doi: 10.1111/micc.12248.
Blockage or restriction of blood flow through conduit arteries results in tissue ischemia downstream of the disturbed area. Local tissues can adapt to this challenge by stimulating vascular remodeling through angiogenesis and arteriogenesis thereby restoring blood perfusion and removal of wastes. Multiple molecular mechanisms of vascular remodeling during ischemia have been identified and extensively studied. However, therapeutic benefits from these findings and insights are limited due to the complexity of various signaling networks and a lack of understanding central metabolic regulators governing these responses. The gasotransmitters NO and H2 S have emerged as master regulators that influence multiple molecular targets necessary for ischemic vascular remodeling. In this review, we discuss how NO and H2 S are individually regulated under ischemia, what their roles are in angiogenesis and arteriogenesis, and how their interaction controls ischemic vascular remodeling.
流经输送动脉的血流受阻或受限会导致受干扰区域下游的组织缺血。局部组织可以通过血管生成和动脉生成刺激血管重塑来适应这一挑战,从而恢复血液灌注并清除废物。缺血期间血管重塑的多种分子机制已被识别并广泛研究。然而,由于各种信号网络的复杂性以及对控制这些反应的核心代谢调节因子缺乏了解,这些发现和见解的治疗益处有限。气体信号分子一氧化氮(NO)和硫化氢(H2S)已成为影响缺血性血管重塑所需多个分子靶点的主要调节因子。在本综述中,我们讨论了NO和H2S在缺血状态下如何分别受到调节,它们在血管生成和动脉生成中的作用是什么,以及它们的相互作用如何控制缺血性血管重塑。