Doxorubicin impairs the insulin-like growth factor-1 system and causes insulin-like growth factor-1 resistance in cardiomyocytes

Insulin-like growth factor-1 (IGF-1) promotes the survival of cardiomyocytes by activating type 1 IGF receptor (IGF-1R). Within the myocardium, IGF-1 action is modulated by IGF binding protein-3 (IGFBP-3), which sequesters IGF-1 away from IGF-1R. Since cardiomyocyte apoptosis is implicated in anthra...

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Veröffentlicht in:	PloS one 2015-05, Vol.10 (5), p.e0124643
Hauptverfasser:	Fabbi, Patrizia, Spallarossa, Paolo, Garibaldi, Silvano, Barisione, Chiara, Mura, Marzia, Altieri, Paola, Rebesco, Barbara, Monti, Maria Gaia, Canepa, Marco, Ghigliotti, Giorgio, Brunelli, Claudio, Ameri, Pietro
Format:	Artikel
Sprache:	eng
Schlagworte:	Acetylcysteine AKT protein Animals Annexin A5 - metabolism Anthracycline Anthracyclines Antioxidants Antioxidants - pharmacology Apoptosis Apoptosis - drug effects Biology Cardiomyocytes Cardiomyopathy Cardiotoxicity Caspase 3 - metabolism Caspase 7 - metabolism Cell Line Conditioning Deoxyribonucleic acid DNA Doxorubicin Doxorubicin - pharmacology Fibroblasts Flow cytometry Heart Heart cells In Situ Nick-End Labeling Insulin Insulin-Like Growth Factor Binding Protein 3 - metabolism Insulin-like growth factor I Insulin-Like Growth Factor I - metabolism Insulin-Like Growth Factor I - pharmacology Insulin-like growth factor-binding protein 3 Insulin-like growth factors Internal medicine Intracellular Space - metabolism Lysates Medicine Myocardium Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Oxidation resistance Oxidative stress p53 Protein Phosphorylation Propidium - metabolism Protein binding Proteins Rats Razoxane Receptor, IGF Type 1 - metabolism Resistance factors Signal Transduction - drug effects Signaling Transcription Tumor proteins Tumor Suppressor Protein p53 - metabolism
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