MEK1-induced physiological hypertrophy inhibits chronic post-myocardial infarction remodeling in mice
Author:
Publisher
Wiley
Subject
Cell Biology,Molecular Biology,Biochemistry
Link
http://onlinelibrary.wiley.com/wol1/doi/10.1002/jcb.24299/fullpdf
Reference32 articles.
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3. Divergent effects of tissue inhibitor of metalloproteinase-1, −2, or −3 overexpression on rat vascular smooth muscle cell invasion, proliferation, and death in vitro: TIMP-3 promotes apoptosis;Baker;J Clin Invest,1998
4. Regional myocardial ischemia-induced activation of MAPKs is associated with subcellularredistribution of caveolin and cholesterol;Ballard-Croft;Am J Physiol Heart Circ Physiol,2006
5. The MEK1-ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice;Bueno;EMBO J,2000
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3. Shift toward greater pathologic post-myocardial infarction remodeling with loss of the adaptive hypertrophic signaling of alpha1 adrenergic receptors in mice;PLOS ONE;2017-12-07
4. Atrial ERK1/2 activation in the embryo leads to incomplete Septal closure: a novel mouse model of atrial Septal defect;Journal of Biomedical Science;2017-11-24
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