2 results match your criteria: "University of Illinois at Chicago College of Medicine. dougl@uic.edu.[Affiliation]"

Background: The failing heart displays increased glycolytic flux that is not matched by a commensurate increase in glucose oxidation. This mismatch induces increased anaplerotic flux and inefficient glucose metabolism. We previously found adult transgenic mouse hearts expressing the fetal troponin I isoform, (ssTnI) to be protected from ischemia by increased glycolysis.

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Is the therapeutic window for mitochondrial ROS half-open or half-closed? Mixing mitophagic metaphors.

Circ Res

July 2014

From the Program in Integrative Cardiac Metabolism, Center for Cardiovascular Research (A.N.C., E.D.L.) and Department of Physiology and Biophysics (A.N.C., E.D.L.), University of Illinois at Chicago College of Medicine.

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