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Scott Pattison, Ph.D.



  • Assistant Professor, Basic Biomedical Sciences
  • USD Sanford School of Medicine


  • Postdoctoral Fellow, Molecular Cardio. Biol., Cincinnati Children's Hospital
  • Ph.D., Biomedical Sciences, University of Missouri, Columbia, MO
  • B.A., Biology, Wabash College, Crawfordsville, IN

Current Research: Cardiac disease resulting in heart failure is the leading cause of mortality in the United States. Cardiac hypertrophy, most commonly stimulated by hypertension, is a significant predictor of mortality. Because cardiac hypertrophy can be triggered by many different stimuli, it has been difficult to find a universally applicable mechanism for treatment. Our data show that a gene named Atg7 can stimulate a process known as autophagy. Autophagy is a protein clearance pathway that functions in the degradation of organelles and large protein complexes, including contractile proteins of the heart. Recent works shows that more autophagy signaling can cause atrophy in the heart. Similarly, our pilot data shows that increased Atg7 expression in the heart prevents the heart from hypertrophying in response to a surgical model of severe hypertension. We hypothesize that Atg7-stimulated autophagy will make cardiac cells resistant to hypertrophy from a host of different stimuli. We propose to test whether increasing Atg7 levels in cultured cardiomyocytes effects their growth when different known hypertrophic drugs and genes are added. Testing the effectiveness of increased Atg7 against different hypertrophic stimuli will indicate how broadly applicable upregulating autophagy might be as a future therapy for treating cardiac hypertrophy.