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WHAT’S THROWING FUEL ON THE FAILING HEART? Altered Energy Metabolism, Oxidative Stress, and Heart Failure Employing a range of customized animal models and ex vivo measurements, Fabio Recchia, MD, PhD, has traced a pathophysiological chain reaction of heart failure mechanisms leading from altered energy substrate selection to sustained functional damage. The ground-breaking central hypothesis of Dr. Recchia et al. is that the decompensated heart switches from free fatty acid oxidation to enhanced glycolysis and glucose oxidation. This, in turn, boosts NADPH supply to superoxide-generating enzymes and accelerates oxidative stress and myocardial damage.

ABOVE Novel experimental models of

heart failure, when probed with exacting hemodynamic and echocardiographic assessments, reveal molecular pathways that may lead to new therapeutic approaches.

In other work, Dr. Recchia’s lab is exploring the cytoprotective and antiapoptotic (but minimally angiogenic) actions of the little-studied vascular endothelial growth factor B (VEGF-B). They are testing the VEGF-B receptor (VEGFR-1) as a potential on/off switch in human cardiomyopathy—an approach that may open a completely new front on the war against heart failure.

HEART | LUNG

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Profile for Temple Health

Temple University School of Medicine - Highlights of Basic and Clinical Research - 2014  

Temple University School of Medicine is pushing the boundaries of science to help reduce the devastating effects of heart and lung disease,...

Temple University School of Medicine - Highlights of Basic and Clinical Research - 2014  

Temple University School of Medicine is pushing the boundaries of science to help reduce the devastating effects of heart and lung disease,...