Dr. Steenbergen’s research focuses on mechanisms of ischemic heart disease, and in particular, endogenous mechanisms that can be activated to protect the heart during a subsequent episode of ischemia and reperfusion.
He is interested in identifying signal transduction pathways that are involved in cardioprotection, and understanding how these signaling pathways confer their protective effect.
His lab studies the mechanisms of injury involving ionic dysequilibrium, and has used magnetic resonance spectroscopic techniques to monitor ion concentrations in intact hearts during ischemia and reperfusion. Since infarct size is a major determinant of clinical outcome in patients with ischemic heart disease, the lab hopes that better understanding of these protective mechanisms will lead to the development of better therapies for patients with coronary artery disease and patients undergoing heart surgery.
Learn more about clinical trials at Johns Hopkins Medicine.
Murphy, E. and Steenbergen, C.: Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. Physiol. Rev. 2008; 88: 581-609.
Das, S., Ferlito, M., Kent, O.A., Fox-Talbot, K., Wang, R., Liu, D., Raghavachari, N., Yang, Y., Wheelan, S.J., Murphy, E., Steenbergen, C. Nuclear miRNA regulates the mitochondrial genome in the heart. Circ. Res. 2012; 110: 1596-1603.
Yano, T., Ferlito, M., Aponte, A., Kuno, A., Miura, T., Murphy, E., Steenbergen, C. Pivotal role of mTORC2 and involvement of ribosomal protein S6 in cardioprotective signaling. Circ. Res. 2014; 114: 1268-1280.
Kohr, M.J., Murphy, E., Steenbergen, C. Glyceraldehyde-3-phosphate dehydrogenase acts as a mitochondrial trans-S-nitrosylase in the heart. PLoS One. 2014; 9: e111448.
Sun, J., Nguyen, T., Aponte, A.M., Menazza, S., Kohr, M.J., Roth, D. M. Patel, H.H., Murphy, E., Steenbergen, C. Ischemic preconditioning preferentially increases protein S-nitrosylation in subsarcolemmal mitochondria. Cardiovasc. Res. 2015; 106: 227-236.