β-AR blockers suppresses ER stress in cardiac hypertrophy and heart failure. - Wikidata - awgldk - TriplyDB

β-AR blockers suppresses ER stress in cardiac hypertrophy and heart failure.

β-AR blockers suppresses ER stress in cardiac hypertrophy and heart failure.

http://www.wikidata.org/entity/Q34071906

about

Toll-like receptor 9 protects non-immune cells from stress by modulating mitochondrial ATP synthesis through the inhibition of SERCA2 Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases DPP4 deficiency preserved cardiac function in abdominal aortic banding rats Protective Role for LPA3 in Cardiac Hypertrophy Induced by Myocardial Infarction but Not by Isoproterenol.Klotho suppresses cardiomyocyte apoptosis in mice with stress-induced cardiac injury via downregulation of endoplasmic reticulum stress.MicroRNA regulation of unfolded protein response transcription factor XBP1 in the progression of cardiac hypertrophy and heart failure in vivo.New concepts of endoplasmic reticulum function in the heart: programmed to conserve.An involvement of oxidative stress in endoplasmic reticulum stress and its associated diseases.CYP2J2 overexpression increases EETs and protects against angiotensin II-induced abdominal aortic aneurysm in mice.Chronic inhibition of cGMP-specific phosphodiesterase 5 suppresses endoplasmic reticulum stress in heart failure.CYP2J2-derived epoxyeicosatrienoic acids suppress endoplasmic reticulum stress in heart failure.Endoplasmic reticulum and the unfolded protein response: dynamics and metabolic integration White Adipose Tissue Browning: A Double-edged Sword.Endoplasmic reticulum stress in the heart: insights into mechanisms and drug targets.A non-canonical pathway regulates ER stress signaling and blocks ER stress-induced apoptosis and heart failure.CYP epoxygenase 2J2 prevents cardiac fibrosis by suppression of transmission of pro-inflammation from cardiomyocytes to macrophages.Depressed calcium-handling proteins due to endoplasmic reticulum stress and apoptosis in the diabetic heart are attenuated by argirein.Chronic inhibition of cyclic guanosine monophosphate-specific phosphodiesterase 5 prevented cardiac fibrosis through inhibition of transforming growth factor β-induced Smad signaling.Exogenous hydrogen sulfide prevents cardiomyocyte apoptosis from cardiac hypertrophy induced by isoproterenol.Exploration of pharmacological interventions to prevent isoproterenol-induced myocardial infarction in experimental models.The endoplasmic reticulum stress-autophagy pathway is involved in apelin-13-induced cardiomyocyte hypertrophy in vitro.2-Methoxyestradiol protects against pressure overload-induced left ventricular hypertrophy.Activation of the unfolded protein response downregulates cardiac ion channels in human induced pluripotent stem cell-derived cardiomyocytes.Reversal of cardiac dysfunction and subcellular alterations by metoprolol in heart failure due to myocardial infarction.

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β-AR blockers suppresses ER stress in cardiac hypertrophy and heart failure.

http://www.wikidata.org/entity/Q34071906

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

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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

β-AR blockers suppresses ER stress in cardiac hypertrophy and heart failure.

@ast

β-AR blockers suppresses ER stress in cardiac hypertrophy and heart failure.

@en

β-AR blockers suppresses ER stress in cardiac hypertrophy and heart failure.

@nl

type

label

β-AR blockers suppresses ER stress in cardiac hypertrophy and heart failure.

@ast

β-AR blockers suppresses ER stress in cardiac hypertrophy and heart failure.

@en

β-AR blockers suppresses ER stress in cardiac hypertrophy and heart failure.

@nl

prefLabel

β-AR blockers suppresses ER stress in cardiac hypertrophy and heart failure.

@ast

β-AR blockers suppresses ER stress in cardiac hypertrophy and heart failure.

@en

β-AR blockers suppresses ER stress in cardiac hypertrophy and heart failure.

@nl

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JOURNAL.PONE.0027294

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β-AR blockers suppresses ER stress in cardiac hypertrophy and heart failure.

@en

P2093

Changqing Zhou

http://www.w3.org/2001/XMLSchema#string

Dao Wen Wang

http://www.w3.org/2001/XMLSchema#string

Jiagao Lv

http://www.w3.org/2001/XMLSchema#string

Li Ni

http://www.w3.org/2001/XMLSchema#string

Quanlu Duan

http://www.w3.org/2001/XMLSchema#string

Xiangning Fu

http://www.w3.org/2001/XMLSchema#string

Yong Xia

http://www.w3.org/2001/XMLSchema#string

P2860

Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1

PKA phosphorylation dissociates FKBP12.6 from the calcium release channel (ryanodine receptor): defective regulation in failing hearts

Role of Ca2+/calmodulin-dependent protein kinase (CaMK) in excitation-contraction coupling in the heart

Endoplasmic reticulum stress induces calcium-dependent permeability transition, mitochondrial outer membrane permeabilization and apoptosis

Prolonged endoplasmic reticulum stress in hypertrophic and failing heart after aortic constriction: possible contribution of endoplasmic reticulum stress to cardiac myocyte apoptosis

Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF)

CHOP is implicated in programmed cell death in response to impaired function of the endoplasmic reticulum

ER stress contributes to ischemia-induced cardiomyocyte apoptosis

Regulator of G protein signaling 2 mediates cardiac compensation to pressure overload and antihypertrophic effects of PDE5 inhibition in mice

The mammalian unfolded protein response

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