The extracellular signal-regulated kinase (ERK) pathway: a potential therapeutic target in hypertension.

The extracellular signal-regulated kinase (ERK) pathway: a potential therapeutic target in hypertension.
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DOI:
10.2147/jep.s28907
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发表时间:
2012
影响因子:
--
通讯作者:
Roberts RE
Roberts RE
中科院分区:
其他
文献类型:
--
作者:
Roberts RE

文献摘要

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高血压是心肌梗死、中风、肾衰竭、心力衰竭和外周血管疾病的危险因素。高血压的一个特征是对收缩剂的高反应性,并且抑制血管收缩形成高血压的一些治疗的基础。高血压还与血管平滑肌细胞的生长和增殖增加有关,这可导致血管平滑肌层增厚和管腔直径减小。靶向增强的收缩反应和增加的血管平滑肌细胞生长可能是高血压的重要药理学治疗。细胞外信号调节激酶(ERK)是丝裂原活化蛋白激酶家族的成员,其参与血管收缩和血管平滑肌细胞生长,因此使其成为治疗高血压的有吸引力的治疗靶点。ERK活性在高血压动物模型的血管平滑肌细胞中升高,抑制ERK活化可降低血管平滑肌细胞生长和血管收缩。本文综述了靶向ERK活性治疗高血压的可能性。
Hypertension is a risk factor for myocardial infarction, stroke, renal failure, heart failure, and peripheral vascular disease. One feature of hypertension is a hyperresponsiveness to contractile agents, and inhibition of vasoconstriction forms the basis of some of the treatments for hypertension. Hypertension is also associated with an increase in the growth and proliferation of vascular smooth muscle cells, which can lead to a thickening of the smooth muscle layer of the blood vessels and a reduction in lumen diameter. Targeting both the enhanced contractile responses, and the increased vascular smooth muscle cell growth could potentially be important pharmacological treatment of hypertension. Extracellular signal-regulated kinase (ERK) is a member of the mitogen-activated protein kinase family that is involved in both vasoconstriction and vascular smooth muscle cell growth and this, therefore, makes it attractive therapeutic target for treatment of hypertension. ERK activity is raised in vascular smooth muscle cells from animal models of hypertension, and inhibition of ERK activation reduces both vascular smooth muscle cell growth and vasoconstriction. This review discusses the potential for targeting ERK activity in the treatment of hypertension.