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The Extracellular Signal-regulated Kinase (ERK) Pathway: a Potential Therapeutic Target in Hypertension

Overview
Journal J Exp Pharmacol
Publisher Dove Medical Press
Date 2016 May 18
PMID 27186119
Citations 18
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Abstract

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.

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References
1.
Cruzado M, Risler N, Miatello R, Yao G, Schiffrin E, Touyz R . Vascular smooth muscle cell NAD(P)H oxidase activity during the development of hypertension: Effect of angiotensin II and role of insulinlike growth factor-1 receptor transactivation. Am J Hypertens. 2005; 18(1):81-7. DOI: 10.1016/j.amjhyper.2004.09.001. View

2.
Lee S, Wang W, Finlay G, Fanburg B . Serotonin stimulates mitogen-activated protein kinase activity through the formation of superoxide anion. Am J Physiol. 1999; 277(2):L282-91. DOI: 10.1152/ajplung.1999.277.2.L282. View

3.
Kida T, Chuma H, Murata T, Yamawaki H, Matsumoto S, Hori M . Chronic treatment with PDGF-BB and endothelin-1 synergistically induces vascular hyperplasia and loss of contractility in organ-cultured rat tail artery. Atherosclerosis. 2010; 214(2):288-94. DOI: 10.1016/j.atherosclerosis.2010.11.001. View

4.
Eguchi S, Dempsey P, Frank G, Motley E, Inagami T . Activation of MAPKs by angiotensin II in vascular smooth muscle cells. Metalloprotease-dependent EGF receptor activation is required for activation of ERK and p38 MAPK but not for JNK. J Biol Chem. 2000; 276(11):7957-62. DOI: 10.1074/jbc.M008570200. View

5.
Childs T, WATSON M, Sanghera J, Campbell D, Pelech S, Mak A . Phosphorylation of smooth muscle caldesmon by mitogen-activated protein (MAP) kinase and expression of MAP kinase in differentiated smooth muscle cells. J Biol Chem. 1992; 267(32):22853-9. View