Cardiomyocyte NF-κB p65 promotes adverse remodelling, apoptosis, and endoplasmic reticulum stress in heart failure. - Wikidata - awgldk - TriplyDB

Cardiomyocyte NF-κB p65 promotes adverse remodelling, apoptosis, and endoplasmic reticulum stress in heart failure.

Cardiomyocyte NF-κB p65 promotes adverse remodelling, apoptosis, and endoplasmic reticulum stress in heart failure.

http://www.wikidata.org/entity/Q39662869

about

Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases Endoplasmic reticulum stress stimulates p53 expression through NF-κB activation Diacerein improves left ventricular remodeling and cardiac function by reducing the inflammatory response after myocardial infarction MicroRNA-122 regulates caspase-8 and promotes the apoptosis of mouse cardiomyocytes.Tauroursodeoxycholic acid (TUDCA) attenuates pressure overload-induced cardiac remodeling by reducing endoplasmic reticulum stress.MicroRNA-15a inhibition protects against hypoxia/reoxygenation-induced apoptosis of cardiomyocytes by targeting mothers against decapentaplegic homolog 7.Nuclear factor κB inhibition reduces lung vascular lumen obliteration in severe pulmonary hypertension in rats.Bovine model of doxorubicin-induced cardiomyopathy Conditional knockout of prolyl hydroxylase domain protein 2 attenuates high fat-diet-induced cardiac dysfunction in mice.Recombinant adeno-associated virus serotype 9 with p65 ribozyme protects H9c2 cells from oxidative stress through inhibiting NF-κB signaling pathway.Cardiomyocyte p65 nuclear factor-κB is necessary for compensatory adaptation to pressure overload Potential role of nuclear factor κB in diabetic cardiomyopathy.Exercise preconditioning attenuates pressure overload-induced pathological cardiac hypertrophy Targeted inhibition of calpain reduces myocardial hypertrophy and fibrosis in mouse models of type 1 diabetes Signal regulatory protein-α protects against cardiac hypertrophy via the disruption of toll-like receptor 4 signaling Up-regulated TLR4 in cardiomyocytes exacerbates heart failure after long-term myocardial infarction.Interaction between NFκB and NFAT coordinates cardiac hypertrophy and pathological remodeling.Increased expression of 78 kD glucose-regulated protein promotes cardiomyocyte apoptosis in a rat model of liver cirrhosis.HDAC inhibition attenuates cardiac hypertrophy by acetylation and deacetylation of target genes.Retinoic acid protects cardiomyocytes from high glucose-induced apoptosis through inhibition of NF-κB signaling pathway A novel rat model of heart failure induced by high methionine diet showing evidence of association between hyperhomocysteinemia and activation of NF-kappaB.Abrogation of CC chemokine receptor 9 ameliorates ventricular remodeling in mice after myocardial infarction.Cardiomyocyte-specific p65 NF-κB deletion protects the injured heart by preservation of calcium handling.The NO/ONOO-cycle as the central cause of heart failure.Redox signaling in cardiovascular health and disease.Is the lack of adiponectin associated with increased ER/SR stress and inflammation in the heart?Cardiomyocyte Ogt is essential for postnatal viability.Activation of toll-like receptors and inflammasome complexes in the diabetic cardiomyopathy-associated inflammation.Interferon regulatory factor 7 functions as a novel negative regulator of pathological cardiac hypertrophy Alternatively spliced tissue factor and full-length tissue factor protect cardiomyocytes against TNF-α-induced apoptosis.RelA/p65 inhibition prevents tendon adhesion by modulating inflammation, cell proliferation, and apoptosis.The innate immune response in reperfused myocardium.Do multiple nuclear factor kappa B activation mechanisms explain its varied effects in the heart?Post-myocardial infarct inflammation and the potential role of cell therapy.Genetic polymorphisms associated with heart failure: A literature review.NF-κB activation is cell type-specific in the heart.Signaling Pathways in Cardiac Myocyte Apoptosis.Delayed, oral pharmacological inhibition of calpains attenuates adverse post-infarction remodelling.The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis.MiR-146a/b: a family with shared seeds and different roots.

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P2860

Cardiomyocyte NF-κB p65 promotes adverse remodelling, apoptosis, and endoplasmic reticulum stress in heart failure.

http://www.wikidata.org/entity/Q39662869

description

2010 nî lūn-bûn

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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2010年论文

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2010年论文

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name

Cardiomyocyte NF-κB p65 promot ...... culum stress in heart failure.

@en

Cardiomyocyte NF-κB p65 promot ...... culum stress in heart failure.

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type

label

Cardiomyocyte NF-κB p65 promot ...... culum stress in heart failure.

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Cardiomyocyte NF-κB p65 promot ...... culum stress in heart failure.

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prefLabel

Cardiomyocyte NF-κB p65 promot ...... culum stress in heart failure.

@en

Cardiomyocyte NF-κB p65 promot ...... culum stress in heart failure.

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Cardiovascular Research

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Cardiomyocyte NF-κB p65 promot ...... culum stress in heart failure.

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P2093

Buddhadeb Dawn

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Justin R Kingery

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Shang Z Guo

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Sumanth D Prabhu

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Tariq Hamid

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Xilin Xiang

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P2860

The phosphorylation status of nuclear NF-kappa B determines its association with CBP/p300 or HDAC-1

Endoplasmic reticulum stress: cell life and death decisions.

Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method

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

Activation of NF-kappa B is required for hypertrophic growth of primary rat neonatal ventricular cardiomyocytes

beta-adrenergic blockade in developing heart failure: effects on myocardial inflammatory cytokines, nitric oxide, and remodeling

Signaling to NF-kappaB

Shaping the nuclear action of NF-kappaB

Mediators of endoplasmic reticulum stress-induced apoptosis

Mechanisms of acrolein-induced myocardial dysfunction: implications for environmental and endogenous aldehyde exposure.

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1

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89

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20797985

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endoplasmic reticulum

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3002872

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