Suppr超能文献

血管生成中的氧化还原信号传导

Redox signaling in vascular angiogenesis.

作者信息

Maulik Nilanjana, Das Dipak K

机构信息

Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, CT 06030-1110, USA.

出版信息

Free Radic Biol Med. 2002 Oct 15;33(8):1047-60. doi: 10.1016/s0891-5849(02)01005-5.

Abstract

Angiogenesis is thought to be regulated by several growth factors (EGF, TGF-alpha, beta-FGF, VEGF). Induction of these angiogenic factors is triggered by various stresses. For instance, tissue hypoxia exerts its pro-angiogenic action through various angiogenic factors, the most notable being vascular endothelial growth factor, which has been mainly associated with initiating the process of angiogenesis through the recruitment and proliferation of endothelial cells. Recently, reactive oxygen species (ROS) have been found to stimulate angiogenic response in the ischemic reperfused hearts. Short exposure to hypoxia/reoxygenation, either directly or indirectly, produces ROS that induce oxidative stress which is associated with angiogenesis or neovascularization. ROS can cause tissue injury in one hand and promote tissue repair in another hand by promoting angiogenesis. It thus appears that after causing injury to the cells, ROS promptly initiate the tissue repair process by triggering angiogenic response.

摘要

血管生成被认为受多种生长因子(表皮生长因子、转化生长因子-α、碱性成纤维细胞生长因子、血管内皮生长因子)调节。这些血管生成因子的诱导由多种应激触发。例如,组织缺氧通过多种血管生成因子发挥其促血管生成作用,其中最显著的是血管内皮生长因子,它主要通过内皮细胞的募集和增殖参与启动血管生成过程。最近,发现活性氧(ROS)可刺激缺血再灌注心脏中的血管生成反应。短期直接或间接暴露于缺氧/复氧会产生ROS,进而诱导与血管生成或新生血管形成相关的氧化应激。ROS一方面可导致组织损伤,另一方面可通过促进血管生成来促进组织修复。因此,在对细胞造成损伤后,ROS似乎通过触发血管生成反应迅速启动组织修复过程。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验