Bax deficiency reduces infarct size and improves long-term function after myocardial infarction.
about
Acute humanin therapy attenuates myocardial ischemia and reperfusion injury in miceBAX unleashed: the biochemical transformation of an inactive cytosolic monomer into a toxic mitochondrial poreBuilding blocks of the apoptotic pore: how Bax and Bak are activated and oligomerize during apoptosisHeme oxygenase-1 induction improves cardiac function following myocardial ischemia by reducing oxidative stressDysregulated IER3 Expression is Associated with Enhanced Apoptosis in Titin-Based Dilated CardiomyopathyApoptosis in cardiovascular diseases: mechanism and clinical implications.Identification of temporal and region-specific myocardial gene expression patterns in response to infarction in swine.Cardiomyocyte death: mechanisms and translational implicationsAttenuation of cardiac dysfunction and remodeling of myocardial infarction by microRNA-130a are mediated by suppression of PTEN and activation of PI3K dependent signaling.Mitochondrial membrane permeabilization and cell death during myocardial infarction: roles of calcium and reactive oxygen species.Decreased expression level of apoptosis-related genes and/or proteins in skeletal muscles, but not in hearts, of growth hormone receptor knockout miceThe rationale for cardiomyocyte resuscitation in myocardial salvage.The non-anticoagulant heparin-like K5 polysaccharide derivative K5-N,OSepi attenuates myocardial ischaemia/reperfusion injuryMechanisms of cell death in heart disease.bcl-2/Adenovirus E1B 19-kd interacting protein 3 (BNIP3) regulates hypoxia-induced neural precursor cell death.P2Y2 receptor agonist with enhanced stability protects the heart from ischemic damage in vitro and in vivoXinfuli improves cardiac function, histopathological changes and attenuate cardiomyocyte apoptosis in rats with doxorubicin-induced cardiotoxicity.Pathophysiology of Myocardial Infarction.Ischemia/Reperfusion.Simulated microgravity increases myocardial susceptibility to ischemia-reperfusion injury via a deficiency of AMP-activated protein kinase.Co-expression of POU4F2/Brn-3b with p53 may be important for controlling expression of pro-apoptotic genes in cardiomyocytes following ischaemic/hypoxic insultsCell death, dysglycemia and myocardial infarction.Apoptosis in Human Acute Myocardial Infarction: The Rationale for Clinical Trials of Apoptosis Inhibition in Acute Myocardial Infarction
P2860
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P2860
Bax deficiency reduces infarct size and improves long-term function after myocardial infarction.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年学术文章
@wuu
2007年学术文章
@zh-cn
2007年学术文章
@zh-hans
2007年学术文章
@zh-my
2007年学术文章
@zh-sg
2007年學術文章
@yue
2007年學術文章
@zh
2007年學術文章
@zh-hant
name
Bax deficiency reduces infarct ...... n after myocardial infarction.
@en
Bax deficiency reduces infarct ...... n after myocardial infarction.
@nl
type
label
Bax deficiency reduces infarct ...... n after myocardial infarction.
@en
Bax deficiency reduces infarct ...... n after myocardial infarction.
@nl
prefLabel
Bax deficiency reduces infarct ...... n after myocardial infarction.
@en
Bax deficiency reduces infarct ...... n after myocardial infarction.
@nl
P2093
P2860
P356
P1476
Bax deficiency reduces infarct ...... n after myocardial infarction.
@en
P2093
Cheporko Y
Hochhauser E
Yasovich N
P2860
P2888
P356
10.1385/CBB:47:1:11
P577
2007-01-01T00:00:00Z
P6179
1029950709