HYPERTENSION AND THE PATHOGENESIS OF ATHEROSCLEROSIS - OXIDATIVE STRESS AND THE MEDIATION OF ARTERIAL INFLAMMATORY RESPONSE - A NEW PERSPECTIVE
HYPERTENSION AND THE PATHOGENESIS OF ATHEROSCLEROSIS - OXIDATIVE STRESS AND THE MEDIATION OF ARTERIAL INFLAMMATORY RESPONSE - A NEW PERSPECTIVE
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DOI：
10.1161/01.hyp.25.2.155
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发表时间：
1995-02-01
期刊：
影响因子：
8.3
通讯作者：
ALEXANDER, RW
中科院分区：
文献类型：
--
作者：
ALEXANDER, RW
高血压是动脉粥样硬化发展的危险因素，尽管其机制尚未得到很好的阐明。随着动脉粥样硬化发病机制和高血压效应的细胞和分子机制越来越明确，这两个过程显然具有某些共同的机制。内皮细胞可能是这两种疾病影响的中心焦点。越来越多的证据表明动脉粥样硬化从根本上应被视为一种炎症性疾病。致动脉粥样硬化的刺激，如高脂血症，似乎通过引起单核白细胞募集机制的表达来激活炎症反应。其中之一的基因，血管细胞粘附分子-1，至少部分地由氧化应激调节的转录因子控制，其改变内皮细胞的氧化还原状态。动脉壁氧化还原状态的改变也可能有助于血管平滑肌细胞的生长。以某种平行的方式，存在由氧化应激调节的转录因子，其改变内皮细胞的氧化还原状态。动脉壁氧化还原状态的改变也可能有助于血管平滑肌细胞的生长。在某种程度上平行的方式，有证据表明，高血压也可能对动脉壁施加氧化应激。本文综述了导致高血压易患和加速动脉粥样硬化的假设的证据，至少部分是因为血压升高和其他促动脉粥样硬化刺激之间的协同作用，以诱导动脉壁的氧化应激。
Hypertension is a risk factor for the development of atherosclerosis, although the mechanisms have not been well elucidated. As the cellular and molecular mechanisms of the pathogenesis of atherosclerosis and the effects of hypertension are being more clearly defined, it becomes apparent that the two processes have certain common mechanisms. The endothelium is a likely central focus for the effect of both diseases. There is increasing evidence that atherosclerosis should be viewed fundamentally as an inflammatory disease. Atherogenic stimuli such as hyperlipidemia appear to activate the inflammatory response by causing expression of mononuclear leukocyte recruiting mechanisms. The gene for one of these, the vascular cell adhesion molecule-1, is controlled at least in part by transcriptional factors regulated by oxidative stress, which modifies the redox state of the endothelial cell. Alterations in the redox state of the arterial wall also may contribute to vascular smooth muscle cell growth. In a somewhat parallel fashion, there is by transcriptional factors regulated by oxidative stress, which modifies the redox state of the endothelial cell. Alterations in the redox state of the arterial wall also may contribute to vascular smooth muscle cell growth. In a somewhat parallel fashion, there is evidence that hypertension may also exert oxidative stress on the arterial wall. This article reviews evidence that leads to the postulate that hypertension predisposes to and accelerates atherosclerosis at least in part because of synergy between elevated blood pressure and other antherogenic stimuli to induce oxidative stress on the arterial wall.