Inflammation, blood pressure, and stroke: An opportunity to target primary prevention?
Inflammation, blood pressure, and stroke: An opportunity to target primary prevention?
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DOI：
10.1007/s11906-005-0054-8
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发表时间：
2005-02-01
影响因子：
5.6
通讯作者：
Papa, F
中科院分区：
文献类型：
--
作者：
Di Napoli, M;Papa, F
近年来的研究表明，全身炎症和神经炎症是脑血管病的重要特征。炎症机制也是高血压病理生理学的重要参与者。炎症标志物已被证明在不同形式的脑血管疾病中上调，并与血管风险相关。核因子-κ B/核因子-κ B系统被认为是主要的细胞内炎症通路，介导大多数血管炎症反应。越来越多的证据表明，高血压通过血管活性肽血管紧张素和内皮素-1，通过炎症机制促进和加速动脉粥样硬化过程。血管紧张素II的促炎特性已得到证实。识别有用的炎症标志物、干扰这些机制的新治疗靶点以及评估抗炎治疗的疗效将使我们对抗脑血管疾病和高血压并发症的能力取得进展。这些靶点是否可用于开发风险预测策略或治疗人类中风的疗法还远未明确。
Promising findings suggests that the systemic inflammation and neuroinflammation are central features in cerebrovascular disease. Inflammatory mechanisms are also important participants in the pathophysiology of hypertension. Markers of inflammation have been shown to be upregulated in different forms of cerebrovascular disease, and to correlate with vascular risk. The inhibitor nuclear factor-kappa B/nuclear factor-kappa B systems is considered a major intracellular inflammatory pathway, mediating most of the vascular inflammatory responses. Increasing evidence indicates that hypertension, through the vasoactive peptides angiotensin and endothelin-1, promotes and accelerates the atherosclerotic process via inflammatory mechanisms. Proinflammatory properties of angiotensin II have been demonstrated. The identification of useful markers of inflammation, of new therapeutic targets to interfere with these mechanisms, and the evaluation of the efficacy of anti-inflammatory treatments will allow progress in our ability to combat cerbrovascular disease and the complications of hypertension. Whether these targets will be useful in the development of risk prediction strategies or therapies for the treatment of stroke in humans is far from clear.