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MEK1-ERK2 signaling pathway protects myocardium from ischemic injury in vivo.

Authors: Daniel J Lips|||Orlando F Bueno|||Benjamin J Wilkins|||Nicole H Purcell|||Robert A Kaiser|||John N Lorenz|||Laure Voisin|||Marc K Saba-El-Leil|||Sylvain Meloche|||Jacques Pouysségur|||Gilles Pagès|||Leon J De Windt|||Pieter A Doevendans|||Jeffery D Molkentin

Journal: Circulation

Publication Type: Journal Article

Date: 2004

DOI: 10.1161/01.CIR.0000127126.73759.23

ID: 15096454

Affiliations:

Affiliations

    Department of Cardiology, Maastricht University, and Heart Lung Center Utrecht, Maastricht and Utrecht, Netherlands.|||||||||||||||||||||||||||||||||||||||

Abstract

Myocardial infarction causes a rapid and largely irreversible loss of cardiac myocytes that can lead to sudden death, ventricular dilation, and heart failure. Members of the mitogen-activated protein kinase (MAPK) signaling cascade have been implicated as important effectors of cardiac myocyte cell death in response to diverse stimuli, including ischemia-reperfusion injury. Specifically, activation of the extracellular signal-regulated kinases 1/2 (ERK1/2) has been associated with cardioprotection, likely through antagonism of apoptotic regulatory pathways.


Chemical List

    Mitogen-Activated Protein Kinase 1|||Mitogen-Activated Protein Kinase 3|||Mitogen-Activated Protein Kinases|||MAP Kinase Kinase 1|||Map2k1 protein, mouse|||Mitogen-Activated Protein Kinase Kinases