Potential of p38-MAPK inhibitors in the treatment of ischaemic heart disease.
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MMI-0100 inhibits cardiac fibrosis in myocardial infarction by direct actions on cardiomyocytes and fibroblasts via MK2 inhibition.Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale.MAPKAPK-2 modulates p38-MAPK localization and small heat shock protein phosphorylation but does not mediate the injury associated with p38-MAPK activation during myocardial ischemia.Mitogen-activated protein kinases in male reproductive functionThe potential of p38 MAPK inhibitors to modulate periodontal infections.The contribution of reactive oxygen species and p38 mitogen-activated protein kinase to myofilament oxidation and progression of heart failure in rabbits.The p38 mitogen-activated protein kinase pathway--a potential target for intervention in infarction, hypertrophy, and heart failure.Crosstalk between mitogen-activated protein kinases and mitochondria in cardiac diseases: therapeutic perspectivesA novel cardioprotective p38-MAPK/mTOR pathway.MAPK usage in periodontal disease progression.Update on the Pathophysiological Role of Intracellular Signaling Pathways in Atherosclerotic Plaques and Ischemic MyocardiumNeuroendocrine and cardiac metabolic dysfunction and NLRP3 inflammasome activation in adipose tissue and pancreas following chronic spinal cord injury in the mouse.Comparative mRNA and MicroRNA Profiling during Acute Myocardial Infarction Induced by Coronary Occlusion and Ablation Radio-Frequency Currents.Developing small molecules to inhibit kinases unkind to the heart: p38 MAPK as a case in point.Targeting fibrosis for the treatment of heart failure: a role for transforming growth factor-β.Therapeutic regulation of cardiac fibroblast function: targeting stress-activated protein kinase pathways.Role of p38 inhibition in cardiac ischemia/reperfusion injury.Therapeutic potential of p38 MAP kinase inhibition in the management of cardiovascular disease.Mitogen-activated protein kinases pathways mediate the sunitinib-induced hypertrophy in rat cardiomyocyte H9c2 cells.Balance between IL-3 and type Iinterferons and their interrelationship with FasL dictates lifespan and effector functions of human basophils.The activation of p38 alpha, and not p38 beta, mitogen-activated protein kinase is required for ischemic preconditioning.Modulatory effect of interleukin-1α on expression of structural matrix proteins, MMPs and TIMPs in human cardiac myofibroblasts: role of p38 MAP kinase.LATITUDE-TIMI: is there still hope for anti-inflammatory therapy in acute myocardial infaction?A chemical genetic approach reveals that p38alpha MAPK activation by diphosphorylation aggravates myocardial infarction and is prevented by the direct binding of SB203580.The role of fatty acids and caveolin-1 in tumor necrosis factor alpha-induced endothelial cell activation.p38 MAPK alpha mediates cytokine-induced IL-6 and MMP-3 expression in human cardiac fibroblasts.The role of RIP2 in p38 MAPK activation in the stressed heart.Apoptosis-induced inhibition of CD1d-mediated antigen presentation: different roles for caspases and signal transduction pathways.Inhibition of p38 MAPK activation protects cardiac mitochondria from ischemia/reperfusion injury.TAB1-induced auto-activation of p38α mitogen-activated protein kinase is crucially dependent on Threonine 185.Toll-like receptor 5 deficiency exacerbates cardiac injury and inflammation induced by myocardial ischaemia-reperfusion in the mouse.Melatonin modulates endoplasmic reticulum stress and Akt/GSK3-beta signaling pathway in a rat model of renal warm ischemia reperfusion.SB203580, a p38 mitogen-activated protein kinase inhibitor, suppresses the development of endometriosis by down-regulating proinflammatory cytokines and proteolytic factors in a mouse model.MicroRNA-378 suppresses myocardial fibrosis through a paracrine mechanism at the early stage of cardiac hypertrophy following mechanical stress.Studies on mitogen-activated protein kinase signaling pathway in the alveolar macrophages of chronic bronchitis rats.Hypoxic stabilization of mRNA is HIF-independent but requires mtROS
P2860
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P2860
Potential of p38-MAPK inhibitors in the treatment of ischaemic heart disease.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
Potential of p38-MAPK inhibitors in the treatment of ischaemic heart disease.
@en
type
label
Potential of p38-MAPK inhibitors in the treatment of ischaemic heart disease.
@en
prefLabel
Potential of p38-MAPK inhibitors in the treatment of ischaemic heart disease.
@en
P2093
P1476
Potential of p38-MAPK inhibitors in the treatment of ischaemic heart disease.
@en
P2093
James E Clark
Michael S Marber
Negin Sarafraz
P304
P356
10.1016/J.PHARMTHERA.2007.06.013
P577
2007-07-24T00:00:00Z