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Konstantinos Drosatos, PhD

Associate Professor, Cardiovascular Sciences
Associate Professor, Center for Translational Medicine
Associate Professor, Alzheimer's Center at Temple
Associate Professor, Center for Metabolic Disease Research
Associate Professor, Neural Sciences

Konstantinos Drosatos
Contact Information

Contact Information



About Me

Research Interests

Our research aims to elucidate the mechanisms that underlie sepsis-induced cardiac energy deprivation and coordinate with clinical scientists to propose potential treatments for improvement of heart function in septic patients. The findings of our studies can be extrapolated to other types of cardiac dysfunction and propose novel therapies for the treatment of heart failure (HF). In addition, we are exploring the cardiac metabolic profile and its contribution in the phenotype of other diseases, such as the Spinal Muscular Atrophy (SMA).

Septic shock follows bacterial infection and is characterized by hypotension, ischemia, multiple organ failure, and increased mortality. Impaired cardiac contractility and diastolic dysfunction occur with sepsis. Cardiac energy production is also reduced due to combined suppression of fatty acid oxidation (FAO) and glucose oxidation. Anti-inflammatory treatment of septic patients has not improved mortality.

Administration of lipopolysaccharide (LPS) mimics the effects of sepsis. LPS-mediated cardiac dysfunction is prevented by treatments that improve FAO, despite persistence of inflammation. Although LPS treatment leads to reduced expression of PPARa and other FA metabolism related genes, the underlying mechanism is unknown. Mechanisms that reduce FAO exclusive of heart failure-related miR changes are ignited by LPS treatment. Binding of LPS to its receptors, TLR4 and CD14, activates the cJun-N-terminal kinase (JNK) pathway. We perform in vitro and in vivo approaches to elucidate the transcriptional mechanism that underlie JNK-mediated down regulation of PPARa gene expression.

The second direction of our research investigates the interchangeable roles of PPARa and PPARy in the induction of cardiac FAO. We showed that genetic and pharmacologic activation of PPARa corrected septic cardiac dysfunction, prevented mitophagy, induced FAO and improves survival despite a reduction in cardiac PPARa. Elucidation of the mechanism via which PPARy compensates for PPARa downregulation and preserves FAO will implicate PPARy as a target for cardiac sepsis treatment. In addition, it may suggest activation of PPARy as a therapeutic approach for other diseases that are associated with reduced PPARa gene expression and FAO levels, such as heart failure and steatosis. Moreover, elucidation of this mechanism can be extrapolated on pan-PPAR agonist-driven accumulation of cardiac lipids, which has been reported.

In addition to our longstanding research goals, we are interested in exploring the novel concept of metabolic dysfunction being involved in the pathogenesis of a neurodegenerative disease, which is designated (SMA). SMA is the major cause for infant mortality and is caused by a gene mutation. The severe phenotype in humans and animal models is characterized by motor neuron loss and muscle atrophy, while cardiac dysfunction has also been reported. We are interested in investigating the metabolic profiles of the heart versus neurons.

Education, Training & Credentials

Educational Background

  • Postdoctoral Research Scientist, Columbia University, 2012
  • PhD, Molecular Biology and Biomedicine, University of Crete, Heraklion, Greece, and Boston University, 2007
  • MSc, Molecular Biology and Biomedicine, University of Crete, Heraklion, Greece, and Boston University, 2002
  • BS, Biology, Aristotle University of Thessaloniki, 2000


  • American Heart Association, Council on Basic Cardiovascular Sciences
  • International Society for Heart Research, North American Section
  • World Hellenic Biomedical Association
  • Hellenic Bioscientific Association in the USA

Honors & Awards

  • Outstanding Early Career Investigator Award, Annual Conference of the American Heart Association, Basic Cardiovascular Sciences Council 2014, Las Vegas, NV
  • New Investigator Travel Award, American Heart Association, Basic Cardiovascular Sciences Conference 2008, Keystone, CO

Digital Bibliography

View NCBI My Bibliography

Book Chapters

Konstantinos Drosatos & Ira J. Goldberg (2014) Lipoproteins: A Source of Cardiac Lipids: Cardiac Energy Metabolism in Health and Disease, Advances in Biochemistry in Health and Disease Volume 11, 2014, pp 15-33 Springer (ed. G. D. Lopaschuk & N.S. Dhall); ISBN: 978-1-4939-1226-1 (Print) 978-1-4939-1227-8 (Online)

Kardassis, D., Drosatos, C. and Zannis, V. I. (2008) Regulation of Genes Involved in the Biogenesis and the Remodeling of HDL, in High-Density Lipoproteins: From Basic Biology to Clinical Aspects (ed C. J. Fielding), Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim, Germany

Zannis, V.I., A. Duka, K. Drosatos, D. Sanoudou, G. Koukos, E. Zanni, D. Kardassis. 2010. Regulation of apoA-I gene expression and prospects to increase plasma apoA-I and HDL levels. In: High Density Lipoproteins, Dyslipidemia, and Coronary Heart Disease. (E.J. Schaefer, ed.) Springer Science + Business Media, LLC, New York, NY

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