Glycogen synthase kinase-3α limits ischemic injury, cardiac rupture, post-myocardial infarction remodeling and death.
about
The GSK-3 family as therapeutic target for myocardial diseasesHeart mitochondrial proteome study elucidates changes in cardiac energy metabolism and antioxidant PRDX3 in human dilated cardiomyopathyA New Therapeutic Modality for Acute Myocardial Infarction: Nanoparticle-Mediated Delivery of Pitavastatin Induces Cardioprotection from Ischemia-Reperfusion Injury via Activation of PI3K/Akt Pathway and Anti-Inflammation in a Rat ModelProtein Kinase Signaling at the Crossroads of Myocyte Life and Death in Ischemic Heart Disease.Wild-type p53-induced Phosphatase 1 Deficiency Exacerbates Myocardial Infarction-induced Ischemic Injury.Cardiomyocyte-specific deletion of Gsk3α mitigates post-myocardial infarction remodeling, contractile dysfunction, and heart failure.The intersection of genetic and chemical genomic screens identifies GSK-3α as a target in human acute myeloid leukemia.Preventive effect of yuzu and hesperidin on left ventricular remodeling and dysfunction in rat permanent left anterior descending coronary artery occlusion model.ATP synthase subunit alpha and LV mass in ischaemic human hearts.Differential effects of Akt1 signaling on short- versus long-term consequences of myocardial infarction and reperfusion injuryToll-interacting protein contributes to mortality following myocardial infarction through promoting inflammation and apoptosisDisruption of circadian rhythmicity and suprachiasmatic action potential frequency in a mouse model with constitutive activation of glycogen synthase kinase 3.Attenuation of ER stress prevents post-infarction-induced cardiac rupture and remodeling by modulating both cardiac apoptosis and fibrosis.A pathway and network review on beta-adrenoceptor signaling and beta blockers in cardiac remodeling.Glycogen synthase kinase-3 (GSK3): regulation, actions, and diseasesWnt Signaling in Cardiac Disease.Signaling Pathways in Cardiac Myocyte Apoptosis.GSK-3α is a central regulator of age-related pathologies in mice.Vinexin-β exacerbates cardiac dysfunction post-myocardial infarction via mediating apoptotic and inflammatory responses.Response by Zhou et al to Letter Regarding Article, "Loss of Adult Cardiac Myocyte GSK-3 Leads to Mitotic Catastrophe Resulting in Fatal Dilated Cardiomyopathy".The allosteric glycogen synthase kinase-3 inhibitor NP12 limits myocardial remodeling and promotes angiogenesis in an acute myocardial infarction model.Cardiomyocyte-specific deletion of GSK-3β leads to cardiac dysfunction in a diet induced obesity model.Global Approaches to Understanding Protein Kinase Functions
P2860
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P2860
Glycogen synthase kinase-3α limits ischemic injury, cardiac rupture, post-myocardial infarction remodeling and death.
description
2011 nî lūn-bûn
@nan
2011 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի նոյեմբերին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Glycogen synthase kinase-3α li ...... farction remodeling and death.
@ast
Glycogen synthase kinase-3α li ...... farction remodeling and death.
@en
type
label
Glycogen synthase kinase-3α li ...... farction remodeling and death.
@ast
Glycogen synthase kinase-3α li ...... farction remodeling and death.
@en
prefLabel
Glycogen synthase kinase-3α li ...... farction remodeling and death.
@ast
Glycogen synthase kinase-3α li ...... farction remodeling and death.
@en
P2093
P2860
P50
P1433
P1476
Glycogen synthase kinase-3α li ...... farction remodeling and death.
@en
P2093
Jibin Zhou
Morgan Decaul
Raihana Zaka
Ronald J Vagnozzi
P2860
P356
10.1161/CIRCULATIONAHA.111.050666
P407
P577
2011-11-15T00:00:00Z