Bjoern C. Knollmann, PhD
Division of Clinical Pharmacology
Departments of Pharmacology and Medicine
MedDent Building, Rm C406
3900 Reservoir Road, NW
Washington, DC 20057
Phone: 202 687-7888
Fax: 202 687-2585
Molecules involved in cardiac arrhythmias
My laboratory focuses on mechanisms of cardiac arrhythmias. Another long-term goal of this research is to reveal the underlying biological mechanisms accounting for why women develop drug-induced cardiac arrhythmias at twice the rate found in men. We anticipate that these studies will lead to safer and more effective therapeutic strategies for women and men. Ongoing research examines several key molecules and pathways causing cardiac arrhythmias and sudden death in human disease: 1) Impaired cardiac calcium cycling and electrical remodeling of heart failure, 2) Troponin T mutations associated with hypertrophic cardiomyopathy and 3) Mutations associated with the congenital and drug-induced long QT syndrome. In neither case the mechanisms that lead to sudden cardiac death are fully understood. In my laboratory, comprehensive studies from the molecular level to the whole animal are carried out in order to better understand the mechanisms of arrhythmogenesis. This research may identify therapeutic strategies, which then can be tested in the same model system prior to human studies.
- Knollmann, B.C., Kirchhoff, P., Sirenko, S.G., Degen, H., Greene, A.E., Schober, T., Mackow, J.C., Fabritz, L., Potter, J.D., Morad, M.: FHC-Linked Mutant Troponin T Causes Stress-Induced Ventricular Tachycardia And Ca2+-Dependent Action Potential Remodeling. Circulation Research, 96(4):428-36, 2003.
- Knollmann, B.C., Tranquillo, J., Sirenko, S.G., Henriquez, C., Franz, M.R.: A Microelectrode Study Of The Genesis Of The Monophasic Action Potential By Contact Electrode Technique. Journal of Cardiovascular Electrophysiology, 13(12):1246-1252, 2002.
- Knollmann, B.C., Blatt, S.A., Horton, K, deFreitas, F., Miller, T., Bell, M., Housmans, P.R., Weissman, N.J., Morad, M., Potter, J.D.: Cardiac performance depends on the inotropic state of transgenic mice expressing an FHC-linked Troponin T (I79N) mutation. Journal of Biological Chemistry, 276:10039-10048, 2001.
- Knollmann, B.C., Knollmann, E.C., Weissman, N.J., Jones, L.R., Morad, M.: Remodeling of ionic currents in hypertrophied and failing hearts of transgenic mice overexpressing Calsequestrin. Journal of Physiology, 525(part2):483-498, 2000.
- Drici, M.D., Knollmann, B.C., Wang and W.X., Woosley, R.L.: Cardiac actions of erythromycin: Influence of sex. JAMA 280(20):1774-1776, 1998.