CALL FOR PAPERS Mitochondria in Cardiovascular Physiology and Disease Xanthine oxidase inhibition preserves left ventricular systolic but not diastolic function in cardiac volume overload

نویسندگان

  • James D. Gladden
  • Blake R. Zelickson
  • Jason L. Guichard
  • Mustafa I. Ahmed
  • Danielle M. Yancey
  • Scott Ballinger
  • Mayilvahanan Shanmugam
  • Gopal J. Babu
  • Michelle S. Johnson
  • Victor Darley-Usmar
  • Louis J. Dell’Italia
چکیده

James D. Gladden, Blake R. Zelickson, Jason L. Guichard, Mustafa I. Ahmed, Danielle M. Yancey, Scott Ballinger, Mayilvahanan Shanmugam, Gopal J. Babu, Michelle S. Johnson, Victor Darley-Usmar, and Louis J. Dell’Italia University of Alabama at Birmingham (UAB) Comprehensive Cardiovascular Center, UAB Birmingham, Alabama; Department of Medicine, Division of Cardiovascular Disease, UAB, Birmingham, Alabama; Department of Pathology, UAB, Birmingham, Alabama; UAB Center for Free Radical Biology, UAB, Birmingham, Alabama; Department of Cell Biology and Molecular Medicine, University of Medicine and Dentistry of New Jersey, Newark, New Jersey; and Department of Veterans Affairs Medical Center, Birmingham, Alabama

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Xanthine oxidase inhibition preserves left ventricular systolic but not diastolic function in cardiac volume overload.

Xanthine oxidase (XO) is increased in human and rat left ventricular (LV) myocytes with volume overload (VO) of mitral regurgitation and aortocaval fistula (ACF). In the setting of increased ATP demand, XO-mediated ROS can decrease mitochondrial respiration and contractile function. Thus, we tested the hypothesis that XO inhibition improves cardiomyocyte bioenergetics and LV function in chronic...

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تاریخ انتشار 2013