Targeted disruption of p53 attenuates doxorubicin-induced cardiac toxicity in mice. - Wikidata - wikimedia - TriplyDB

Targeted disruption of p53 attenuates doxorubicin-induced cardiac toxicity in mice.

Targeted disruption of p53 attenuates doxorubicin-induced cardiac toxicity in mice.

http://www.wikidata.org/entity/Q46597560

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Mitochondria and mitophagy: the yin and yang of cell death control p53 Regulates oxidative stress-mediated retrograde signaling: a novel mechanism for chemotherapy-induced cardiac injury Berberine inhibits doxorubicin-triggered cardiomyocyte apoptosis via attenuating mitochondrial dysfunction and increasing Bcl-2 expression Schisandrin B prevents doxorubicin induced cardiac dysfunction by modulation of DNA damage, oxidative stress and inflammation through inhibition of MAPK/p53 signaling Nucleolar stress is an early response to myocardial damage involving nucleolar proteins nucleostemin and nucleophosmin p53 and TIGAR regulate cardiac myocyte energy homeostasis under hypoxic stress.Doxorubicin impairs the insulin-like growth factor-1 system and causes insulin-like growth factor-1 resistance in cardiomyocytes.Cardiomyocyte death in doxorubicin-induced cardiotoxicity WNT1-inducible signaling pathway protein-1 activates diverse cell survival pathways and blocks doxorubicin-induced cardiomyocyte death Cardiomyocyte specific ablation of p53 is not sufficient to block doxorubicin induced cardiac fibrosis and associated cytoskeletal changes Influence of p53 in the transition of myotrophin-induced cardiac hypertrophy to heart failure P53 inhibition exacerbates late-stage anthracycline cardiotoxicity.Lysine methyltransferase Smyd2 suppresses p53-dependent cardiomyocyte apoptosis.Focal adhesion kinase antagonizes doxorubicin cardiotoxicity via p21(Cip1.).Mechanism of anthracycline-mediated down-regulation of GATA4 in the heart Activation of the aryl hydrocarbon receptor by doxorubicin mediates cytoprotective effects in the heart Endothelial p53 deletion improves angiogenesis and prevents cardiac fibrosis and heart failure induced by pressure overload in mice.Modulation of anthracycline-induced cardiotoxicity by aerobic exercise in breast cancer: current evidence and underlying mechanisms.Apoptosis in Anthracycline Cardiomyopathy MicroRNA-208a Silencing Attenuates Doxorubicin Induced Myocyte Apoptosis and Cardiac Dysfunction.Inhibition of AMP-activated protein kinase α (AMPKα) by doxorubicin accentuates genotoxic stress and cell death in mouse embryonic fibroblasts and cardiomyocytes: role of p53 and SIRT1.BRCA2 protein deficiency exaggerates doxorubicin-induced cardiomyocyte apoptosis and cardiac failure Does oxidative stress modulate left ventricular diastolic function in asymptomatic subjects with hereditary hemochromatosis?p53 functions in endothelial cells to prevent radiation-induced myocardial injury in mice The dual topoisomerase inhibitor A35 preferentially and specially targets topoisomerase 2α by enhancing pre-strand and post-strand cleavage and inhibiting DNA religation Cardiac side effects of anticancer treatments: new mechanistic insights Decreased expression level of apoptosis-related genes and/or proteins in skeletal muscles, but not in hearts, of growth hormone receptor knockout mice Decreased levels of proapoptotic factors and increased key regulators of mitochondrial biogenesis constitute new potential beneficial features of long-lived growth hormone receptor gene-disrupted mice.Protection against doxorubicin-induced myocardial dysfunction in mice by cardiac-specific expression of carboxyl terminus of hsp70-interacting protein ERKs/p53 signal transduction pathway is involved in doxorubicin-induced apoptosis in H9c2 cells and cardiomyocytes Topoisomerase 2β: a promising molecular target for primary prevention of anthracycline-induced cardiotoxicity.Doxorubicin-induced death in tumour cells and cardiomyocytes: is autophagy the key to improving future clinical outcomes?Regulator of G protein signaling 6 mediates doxorubicin-induced ATM and p53 activation by a reactive oxygen species-dependent mechanism Regulation of Cellular Metabolism and Hypoxia by p53.Doxorubicin-induced cardiotoxicity: direct correlation of cardiac fibroblast and H9c2 cell survival and aconitase activity with heat shock protein 27.MiR-24-BIM-Smac/DIABLO axis controls the sensitivity to doxorubicin treatment in osteosarcoma.RGS Proteins in Heart: Brakes on the Vagus.Acute doxorubicin cardiotoxicity is associated with p53-induced inhibition of the mammalian target of rapamycin pathway.G-protein inactivator RGS6 mediates myocardial cell apoptosis and cardiomyopathy caused by doxorubicin.The Positive Effects of Exercise in Chemotherapy-Related Cardiomyopathy.

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P2860

Targeted disruption of p53 attenuates doxorubicin-induced cardiac toxicity in mice.

http://www.wikidata.org/entity/Q46597560

description

2005 nî lūn-bûn

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2005年の論文

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年學術文章

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2005年學術文章

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name

Targeted disruption of p53 attenuates doxorubicin-induced cardiac toxicity in mice.

@en

Targeted disruption of p53 attenuates doxorubicin-induced cardiac toxicity in mice.

@nl

type

label

Targeted disruption of p53 attenuates doxorubicin-induced cardiac toxicity in mice.

@en

Targeted disruption of p53 attenuates doxorubicin-induced cardiac toxicity in mice.

@nl

prefLabel

Targeted disruption of p53 attenuates doxorubicin-induced cardiac toxicity in mice.

@en

Targeted disruption of p53 attenuates doxorubicin-induced cardiac toxicity in mice.

@nl

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Molecular and Cellular Biochemistry

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Targeted disruption of p53 attenuates doxorubicin-induced cardiac toxicity in mice.

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Paul M Hwang

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Satoaki Matoba

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Yukitaka Shizukuda

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P2860

Insulin-like growth factor-1 induces Mdm2 and down-regulates p53, attenuating the myocyte renin-angiotensin system and stretch-mediated apoptosis.

Pacing-induced heart failure in dogs enhances the expression of p53 and p53-dependent genes in ventricular myocytes.

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