Juvenile exposure to anthracyclines impairs cardiac progenitor cell function and vascularization resulting in greater susceptibility to stress-induced myocardial injury in adult mice - Wikidata - awgldk - TriplyDB

Juvenile exposure to anthracyclines impairs cardiac progenitor cell function and vascularization resulting in greater susceptibility to stress-induced myocardial injury in adult mice

Juvenile exposure to anthracyclines impairs cardiac progenitor cell function and vascularization resulting in greater susceptibility to stress-induced myocardial injury in adult mice

http://www.wikidata.org/entity/Q24632487

about

Cardiac toxicity of trastuzumab in elderly patients with breast cancer The tell-tale heart: molecular and cellular responses to childhood anthracycline exposure Cardiac stem cells: biology and clinical applications Mitochondrionopathy phenotype in doxorubicin-treated Wistar rats depends on treatment protocol and is cardiac-specific The role of notch in the cardiovascular system: potential adverse effects of investigational notch inhibitors Doxorubicin in vivo rapidly alters expression and translation of myocardial electron transport chain genes, leads to ATP loss and caspase 3 activation Dissecting the Mechanisms of Doxorubicin and Oxidative Stress-Induced Cytotoxicity: The Involvement of Actin Cytoskeleton and ROCK1 Cancer therapy-induced cardiotoxicity: basic mechanisms and potential cardioprotective therapies.Mechanisms of anthracycline cardiotoxicity and strategies to decrease cardiac damage.Heat shock protein 25-enriched plasma transfusion preconditions the heart against doxorubicin-induced dilated cardiomyopathy in mice.p38 MAPK and JNK antagonistically control senescence and cytoplasmic p16INK4A expression in doxorubicin-treated endothelial progenitor cells Preconditioning involves selective mitophagy mediated by Parkin and p62/SQSTM1.The impact of juvenile coxsackievirus infection on cardiac progenitor cells and postnatal heart development Safety and efficacy of aerobic training in patients with cancer who have heart failure: an analysis of the HF-ACTION randomized trial S-diclofenac protects against doxorubicin-induced cardiomyopathy in mice via ameliorating cardiac gap junction remodeling Mitophagy is required for acute cardioprotection by simvastatin.The human amniotic fluid stem cell secretome effectively counteracts doxorubicin-induced cardiotoxicity.Anthracycline-associated cardiotoxicity in survivors of childhood cancer.Cardiotoxicity due to cancer therapy.Physiological activation of Akt by PHLPP1 deletion protects against pathological hypertrophy Plasma high sensitivity troponin T levels in adult survivors of childhood leukaemias: determinants and associations with cardiac function.Apoptosis in Anthracycline Cardiomyopathy Mesenchymal stem cell therapy for doxorubicin cardiomyopathy: hopes and fears Downregulation of doxorubicin-induced myocardial apoptosis accompanies postnatal heart maturation.Recent progress in understanding coxsackievirus replication, dissemination, and pathogenesis.Heat shock factor-1 knockout induces multidrug resistance gene, MDR1b, and enhances P-glycoprotein (ABCB1)-based drug extrusion in the heart.Accumulation of Mitochondrial DNA Mutations Disrupts Cardiac Progenitor Cell Function and Reduces Survival.Increased mitotic rate coincident with transient telomere lengthening resulting from pim-1 overexpression in cardiac progenitor cells.The TGF-β pathway mediates doxorubicin effects on cardiac endothelial cells.Parkin protein deficiency exacerbates cardiac injury and reduces survival following myocardial infarction Testosterone Antagonizes Doxorubicin-Induced Senescence of Cardiomyocytes.Cancer therapy-induced cardiac toxicity in early breast cancer: addressing the unresolved issues.Cardiac side effects of anticancer treatments: new mechanistic insights An engineered bivalent neuregulin protects against doxorubicin-induced cardiotoxicity with reduced proneoplastic potential.Cardiovascular disease following hematopoietic stem cell transplantation: Pathogenesis, detection, and the cardioprotective role of aerobic training Anthracycline Chemotherapy and Cardiotoxicity.Cardiotoxicity of kinase inhibitors: the prediction and translation of preclinical models to clinical outcomes.Regenerative toxicology: the role of stem cells in the development of chronic toxicities.c-kit(+) cells: the tell-tale heart of cardiac regeneration?Mechanisms and management of doxorubicin cardiotoxicity.

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Juvenile exposure to anthracyclines impairs cardiac progenitor cell function and vascularization resulting in greater susceptibility to stress-induced myocardial injury in adult mice

http://www.wikidata.org/entity/Q24632487

description

2010 nî lūn-bûn

@nan

2010 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի փետրվարին հրատարակված գիտական հոդված

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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

@zh-mo

2010年論文

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2010年论文

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name

Juvenile exposure to anthracyc ...... yocardial injury in adult mice

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Juvenile exposure to anthracyc ...... yocardial injury in adult mice

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Juvenile exposure to anthracyc ...... yocardial injury in adult mice

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type

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Juvenile exposure to anthracyc ...... yocardial injury in adult mice

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Juvenile exposure to anthracyc ...... yocardial injury in adult mice

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Juvenile exposure to anthracyc ...... yocardial injury in adult mice

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prefLabel

Juvenile exposure to anthracyc ...... yocardial injury in adult mice

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Juvenile exposure to anthracyc ...... yocardial injury in adult mice

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Juvenile exposure to anthracyc ...... yocardial injury in adult mice

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CIRCULATIONAHA.109.902221

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Juvenile exposure to anthracyc ...... yocardial injury in adult mice

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Asa B Gustafsson

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Chengqun Huang

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Jennifer M Ramil

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Lucy Kim

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Mark A Sussman

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Patricia A Thistlethwaite

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Roberta A Gottlieb

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Shivaji Rikka

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Xiaoxue Zhang

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P2860

Postnatal isl1+ cardioblasts enter fully differentiated cardiomyocyte lineages

Stem cell factor/c-kit signaling mediated cardiac stem cell migration via activation of p38 MAPK

BIOLOGY OF HEMATOPOIETIC STEM CELLS AND PROGENITORS: Implications for Clinical Application

Anthracyclines: molecular advances and pharmacologic developments in antitumor activity and cardiotoxicity

Adult cardiac stem cells are multipotent and support myocardial regeneration

Mobilized bone marrow cells repair the infarcted heart, improving function and survival.

Stem cells in the dog heart are self-renewing, clonogenic, and multipotent and regenerate infarcted myocardium, improving cardiac function.

Cardiotoxicity of chemotherapeutic agents: incidence, treatment and prevention.

Neovascularization of ischemic myocardium by human bone-marrow-derived angioblasts prevents cardiomyocyte apoptosis, reduces remodeling and improves cardiac function.

A clinicopathologic analysis of adriamycin cardiotoxicity.

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675-83

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1921134

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20100968

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