Stabilization of mitochondrial membrane potential prevents doxorubicin-induced cardiotoxicity in isolated rat heart.

[1]  T. Kita,et al.  The targeting of cyclophilin D by RNAi as a novel cardioprotective therapy: evidence from two-photon imaging. , 2009, Cardiovascular research.

[2]  P. Oliveira,et al.  Doxorubicin increases the susceptibility of brain mitochondria to Ca(2+)-induced permeability transition and oxidative damage. , 2008, Free radical biology & medicine.

[3]  L. Matsubara,et al.  Anthracycline-induced cardiotoxicity. , 2008, Cardiovascular & hematological agents in medicinal chemistry.

[4]  K. Wallace.  Adriamycin-induced interference with cardiac mitochondrial calcium homeostasis , 2007, Cardiovascular Toxicology.

[5]  T. Kita,et al.  Real-Time 2-Photon Imaging of Mitochondrial Function in Perfused Rat Hearts Subjected to Ischemia/Reperfusion , 2006, Circulation.

[6]  T. Wallimann,et al.  New insights into doxorubicin-induced cardiotoxicity: the critical role of cellular energetics. , 2006, Journal of molecular and cellular cardiology.

[7]  R. Favory,et al.  Inhibition of mitochondrial permeability transition prevents sepsis-induced myocardial dysfunction and mortality. , 2006, Journal of the American College of Cardiology.

[8]  P. Oliveira,et al.  Depletion of adenine nucleotide translocator protein in heart mitochondria from doxorubicin-treated rats--relevance for mitochondrial dysfunction. , 2006, Toxicology.

[9]  K. Wallace,et al.  Adriamycin-induced oxidative mitochondrial cardiotoxicity , 2006, Cell Biology and Toxicology.

[10]  T. Wallimann,et al.  Acute toxicity of doxorubicin on isolated perfused heart: response of kinases regulating energy supply. , 2005, American journal of physiology. Heart and circulatory physiology.

[11]  R. Favory,et al.  Ventricular Myocyte Caspases Are Directly Responsible for Endotoxin-Induced Cardiac Dysfunction , 2005, Circulation.

[12]  P. Oliveira,et al.  Are the antioxidant properties of carvedilol important for the protection of cardiac mitochondria? , 2005, Current vascular pharmacology.

[13]  L. Gianni,et al.  Anthracyclines: Molecular Advances and Pharmacologic Developments in Antitumor Activity and Cardiotoxicity , 2004, Pharmacological Reviews.

[14]  L. Kevin,et al.  Reduced reactive O2 species formation and preserved mitochondrial NADH and [Ca2+] levels during short-term 17 degrees C ischemia in intact hearts. , 2004, Cardiovascular research.

[15]  S. Javadov,et al.  Mitochondrial permeability transition pore opening during myocardial reperfusion--a target for cardioprotection. , 2004, Cardiovascular research.

[16]  A. Bordoni,et al.  Doxorubicin induces early lipid peroxidation associated with changes in glucose transport in cultured cardiomyocytes. , 2002, Biochimica et biophysica acta.

[17]  A. Halestrap,et al.  Sanglifehrin A Acts as a Potent Inhibitor of the Mitochondrial Permeability Transition and Reperfusion Injury of the Heart by Binding to Cyclophilin-D at a Different Site from Cyclosporin A* , 2002, The Journal of Biological Chemistry.

[18]  U. Christians,et al.  Close Association Between the Reduction in Myocardial Energy Metabolism and Infarct Size: Dose-Response Assessment of Cyclosporine , 2002, Journal of Pharmacology and Experimental Therapeutics.

[19]  Shaoyu Zhou,et al.  Cumulative and irreversible cardiac mitochondrial dysfunction induced by doxorubicin. , 2001, Cancer research.

[20]  G Kaley,et al.  Myocardial glucose uptake is regulated by nitric oxide via endothelial nitric oxide synthase in Langendorff mouse heart. , 2000, Circulation research.

[21]  H. Bruining,et al.  Regional ischemia in hypertrophic Langendorff-perfused rat hearts. , 1999, American journal of physiology. Heart and circulatory physiology.

[22]  I. Al-Nasser.  In vivo prevention of adriamycin cardiotoxicity by cyclosporin A or FK506. , 1998, Toxicology.

[23]  Hung-Yi Wu,et al.  Molecular Mechanisms of Doxorubicin-induced Cardiomyopathy , 1997, The Journal of Biological Chemistry.

[24]  K. Wallace,et al.  Dose-dependent increase in sensitivity to calcium-induced mitochondrial dysfunction and cardiomyocyte cell injury by doxorubicin. , 1996, Journal of molecular and cellular cardiology.

[25]  A. Halestrap,et al.  Protection by Cyclosporin A of ischemia/reperfusion-induced damage in isolated rat hearts. , 1993, Journal of molecular and cellular cardiology.

[26]  K. Wallace,et al.  Selective activation of the sodium-independent, cyclosporin A-sensitive calcium pore of cardiac mitochondria by doxorubicin. , 1993, Toxicology and applied pharmacology.

[27]  A. Allen,et al.  The cardiotoxicity of chemotherapeutic drugs. , 1992, Seminars in oncology.

[28]  R. Mueller,et al.  Doxorubicin toxicity in perfused rat heart. Decreased cell death at low oxygen tension. , 1991, Circulation research.

[29]  B. de Kruijff,et al.  Effects of adriamycin on respiratory chain activities in mitochondria from rat liver, rat heart and bovine heart. Evidence for a preferential inhibition of complex III and IV. , 1987, Biochimica et biophysica acta.

[30]  G. Krishna,et al.  Daunomycin inhibits the uptake of adenine, amino acids, and glucose into cardiac myocytes. , 1987, Toxicology and applied pharmacology.

[31]  P. Boyer.  A model for conformational coupling of membrane potential and proton translocation to ATP synthesis and to active transport , 1975, FEBS letters.