Heat shock protects cardiac cells from doxorubicin-induced toxicity by activating p38 MAPK and phosphorylation of small heat shock protein 27

Doxorubicin (DOX) and its derivatives are used as chemotherapeutic drugs to treat cancer patients. However, production of DOX-mediated reactive oxygen species (ROS) by prolonged use of these drugs has been found to cause dilative cardiomyopathy and congestive heart failure. Thus various preventive m...

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Bibliographic Details
Published in:	American journal of physiology. Heart and circulatory physiology Vol. 291; no. 6; p. H2680
Main Authors:	Venkatakrishnan, C D, Tewari, Arun K, Moldovan, Leni, Cardounel, Arturo J, Zweier, Jay L, Kuppusamy, Periannan, Ilangovan, Govindasamy
Format:	Journal Article
Language:	English
Published:	United States 01-12-2006
Subjects:	Actins - metabolism Amino Acid Sequence Animals Antibiotics, Antineoplastic - pharmacology Antioxidants - metabolism Apoptosis - drug effects bcl-2-Associated X Protein - genetics bcl-2-Associated X Protein - metabolism Cell Line Doxorubicin - pharmacology Gene Expression Regulation - drug effects Gene Expression Regulation, Enzymologic - drug effects Heat-Shock Proteins - metabolism Heat-Shock Response - physiology HSP27 Heat-Shock Proteins Molecular Sequence Data Myocytes, Cardiac - drug effects Myocytes, Cardiac - pathology Neoplasm Proteins - metabolism p38 Mitogen-Activated Protein Kinases - genetics p38 Mitogen-Activated Protein Kinases - metabolism Phosphorylation Proto-Oncogene Proteins c-bcl-2 - genetics Proto-Oncogene Proteins c-bcl-2 - metabolism Rats Reactive Oxygen Species - metabolism
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