血管生成
活性氧
NADPH氧化酶
新生血管
氧化应激
内科学
内分泌学
化学
生物
细胞生物学
癌症研究
医学
作者
Silvana Balzan,Laura Sabatino,Valter Lubrano
出处
期刊:PubMed
日期:2017-01-01
卷期号:110 (1-2): 13-23
被引量:1
标识
DOI:10.19272/201711402002
摘要
Angiogenesis is a physiological process required for embryonic vascular development and involved in the pathophysiological progress of diseases such as atherosclerosis. In fact, hypoxia, ischemia and oxidative stress are common events in atherosclerotic plaque that stimulate angiogenesis, leading to the formation of a neovascularization in the intima of atherosclerotic lesions. The presence of these capillaries favours the progression of the plaque instability. Several studies indicate oxidized low-density lipoprotein (ox-LDL) and its endothelial receptor lectin-like oxidized low-density lipoprotein (LOX-1) as the major responsible for the occurrence and progression of atherosclerosis through apoptosis. At the same time, some authors showed that moderate concentrations of ox-LDL stimulate angiogenesis via LOX-1 activation of NADPH oxidase, MAPKs-NF-KB pathways and the generation of low levels of reactive oxygen species (ROS). Thyroid hormones have well documented effects on angiogenesis through genomic and non-genomic action and increased levels of ROS have been reported in hyperthyroidism. Moreover, by in vitro studies triiodothyronine (T3) and L-thyroxine (T4) significantly increased the intracellular ROS production based on the oxidation of 2',7'-dichloro dihydrofluorescein to a fluorescent 2',7'-dichlorofluoresein. Previous findings showed that ROS directly increase LOX-1 production in microvascular endothelial cells. New in vitro studies demonstrated the capability of T3 at supra-physiological doses to upregulate the LOX-1 expression in human microvascular endothelial cells. Thus, we can speculate the existence of a crosstalk between LOX-1-ROS and high levels of T3, suggesting that high levels of T3, as in hyperthyroidism, could cause a worsening of plaque vulnerability inducing angiogenesis.
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