Activation of the p38 MAP kinase pathway is required for foam cell formation from macrophages exposed to oxidized LDL
M. Zhao et al. Activation of the p38 MAP kinase pathway is required for foam cell formation from macrophages exposed to oxidized LDL Acta Pathol. Microbiol. Scand. 110 2002 458-468
OxLDL upregulates CXCR2 expression in monocytes via scavenger receptors and activation of p38 mitogen-activated protein kinase
Z.B. Lei et al. OxLDL upregulates CXCR2 expression in monocytes via scavenger receptors and activation of p38 mitogen-activated protein kinase Cardiovasc. Res. 53 2002 524-532
Z. Wang et al. Reactive oxygen species-sensitive p38 MAPK controls thrombin-induced migration of vascular smooth muscle cells J. Mol. Cell. Cardiol. 36 2004 49-56
An inhibitor of p38 mitogen-activated protein kinase protects neonatal cardiac myocytes from ischemia
K. MacKay D. Mochly-Rosen An inhibitor of p38 mitogen-activated protein kinase protects neonatal cardiac myocytes from ischemia J. Biol. Chem. 274 1999 6272-6279
Targeted inhibition of p38 mitogen-activated protein kinase antagonizes cardiac injury and cell death following ischemia-reperfusion in vivo
R.A. Kaiser et al. Targeted inhibition of p38 mitogen-activated protein kinase antagonizes cardiac injury and cell death following ischemia-reperfusion in vivo J. Biol. Chem. 279 2004 15524-15530
p38 MAPK inhibition reduces myocardial reperfusion injury via inhibition of endothelial adhesion molecule expression and blockade of PMN accumulation
F. Gao et al. p38 MAPK inhibition reduces myocardial reperfusion injury via inhibition of endothelial adhesion molecule expression and blockade of PMN accumulation Cardiovasc. Res. 53 2002 414-422
Inhibition of p38 mitogen-activated protein kinase decreases cardiomyocyte apoptosis and improves cardiac function after myocardial ischemia and reperfusion
X.L. Ma et al. Inhibition of p38 mitogen-activated protein kinase decreases cardiomyocyte apoptosis and improves cardiac function after myocardial ischemia and reperfusion Circulation 99 1999 1685-1691
Effects of adding p38 mitogen-activated protein-kinase inhibitor to celsior solution in canine heart transplantation from non-heart-beating donors
N. Koike et al. Effects of adding p38 mitogen-activated protein-kinase inhibitor to celsior solution in canine heart transplantation from non-heart-beating donors Transplantation 77 2004 286-292
Activation of c-Jun N-terminal kinases and p38-mitogen-activated protein kinases in human heart failure secondary to ischaemic heart disease
S.A. Cook et al. Activation of c-Jun N-terminal kinases and p38-mitogen-activated protein kinases in human heart failure secondary to ischaemic heart disease J. Mol. Cell. Cardiol. 31 1999 1429-1434
p38 Mitogen-activated protein kinase inhibition improves cardiac function and attenuates left ventricular remodeling following myocardial infarction in the rat
See F. et al. 2004 p38 Mitogen-activated protein kinase inhibition improves cardiac function and attenuates left ventricular remodeling following myocardial infarction in the rat J. Am. Coll. Cardiol. 44 1679-1689
Vascular endothelial dysfunction and superoxide anion production in heart failure are p38 MAP kinase-dependent
J. Widder et al. Vascular endothelial dysfunction and superoxide anion production in heart failure are p38 MAP kinase-dependent Cardiovasc. Res. 63 2004 161-167
Hypertensive end-organ damage and premature mortality are p38 mitogen-activated protein kinase-dependent in a rat model of cardiac hypertrophy and dysfunction
T.M. Behr et al. Hypertensive end-organ damage and premature mortality are p38 mitogen-activated protein kinase-dependent in a rat model of cardiac hypertrophy and dysfunction Circulation 104 2001 1292-1298
p38 MAPK inhibitors ameliorate target organ damage in hypertension: Part 1. p38 MAPK-dependent endothelial dysfunction and hypertension
H. Ju et al. p38 MAPK inhibitors ameliorate target organ damage in hypertension: Part 1. p38 MAPK-dependent endothelial dysfunction and hypertension J. Pharmacol. Exp. Ther. 307 2003 932-938
Interactions between p38 mitogen-activated protein kinase and caspase-3 in cerebral endothelial cell death after hypoxia-reoxygenation
S.R. Lee E.H. Lo Interactions between p38 mitogen-activated protein kinase and caspase-3 in cerebral endothelial cell death after hypoxia-reoxygenation Stroke 34 2003 2704-2709
The MKK6-p38 MAPK pathway prolongs the cardiac contractile calcium transient, downregulates SERCA2, and activates NF-AT
C. Andrews et al. The MKK6-p38 MAPK pathway prolongs the cardiac contractile calcium transient, downregulates SERCA2, and activates NF-AT Cardiovasc. Res. 59 2003 46-56
Targeted inhibition of p38 MAPK promotes hypertrophic cardiomyopathy through upregulation of calcineurin-NFAT signaling
J. Braz et al. Targeted inhibition of p38 MAPK promotes hypertrophic cardiomyopathy through upregulation of calcineurin-NFAT signaling J. Clin. Invest. 111 2003 1475-1486
Decreased p38 MAPK activity in end-stage failing human myocardium: p38 MAPK [alpha] is the predominant isoform expressed in human heart
L.E. Lemke et al. Decreased p38 MAPK activity in end-stage failing human myocardium: P38 MAPK [alpha] is the predominant isoform expressed in human heart J. Mol. Cell. Cardiol. 33 2001 1527-1540