Dr. Drosatos works on 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 (FA) and glucose oxidation. Anti-inflammatory treatment of septic patients has not improved mortality. Dr. Drosatos research focuses on the importance of cardiac energy deficiency in cardiac dysfunction during sepsis. Lipopolysaccharide (LPS)-mediated cardiac dysfunction is prevented by treatments that improve FA oxidation (FAO), despite persistence of inflammation. Although LPS treatment leads to reduced expression of PPARα and other FA metabolism related-genes, the underlying mechanism is unknown. Several miRs are linked to chronic heart failure (HF), a condition also associated with impaired FAO. None of these miRs is significantly altered in the hearts of LPS-treated mice. Thus, mechanisms that reduce FAO exclusive of miR-induced changes are ignited by LPS treatment. Binding of LPS to its receptors, TLR4 and CD14, activates the cJun-N-terminal kinase (JNK) pathway. Dr. Drosatos research group perform in vitro and in vivo approaches to investigate the role of JNK in PPARα regulation.