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David A. Kass

Samuel R. Denmeade

Department Affiliation: Primary: Cardiology/Medicine; Secondary: Pharmacology, Biomedical Engineering, and Cellular and Molecular Medicine
Degree: M.D., Yale University School of Medicine
Rank: Professor

Director, Johns Hopkins Institute of CardioScience
Director, Cardiovascular Research NHLBI - T32 Training Program

Director of Research, Johns Hopkins Division of Cardiology
Telephone Number: 410-955-7153
Fax Number: 410-367-2225
E-mail address:
School of Medicine Address: Ross Building, Rm. 858,
720 Rutland Avenue, Baltimore, MD 21205
Kass Lab Website


Molecular Physiology of Myocardial Disease

Dr. Kass' current research interests include his leadership of the Center for Molecular Cardiobiology, where he coordinates basic and translational research at Johns Hopkins University with the aim of paving the road to newer and more effective treatments for cardiovascular disease.  Under the directorship of Dr. Kass, the Center is working to expand its understanding of the causes of heart failure, arrhythmia, and artery disease, and how physicians can treat, cure, and prevent them in the future.  More specifically, Dr. Kass and his colleagues have discovered that the drug, Viagra, can potently influence how the heart responds to abnormal stress.  This work, from Dr. Kass’ lab, has led to a major clinical trial now underway by the National Institute of Health (NIH) and to new studies for treating disorders such as muscular dystrophy.  Additionally, the lab was awarded a new grant from the Muscular Dystrophy Foundation, to study mechanisms for heart disease in patients suffering from Duchennes disease.  As an international leader in the use of pacing devices in heart failure patients, his laboratory is also pioneering research that may ultimately lead to a completely new way to use pacemakers.

Another important new study that was conducted in Dr. Kass’ lab, identified how the vessels in the lung uniquely impact the right heart, and are different in a fundamental way from the arteries in the rest of the body that influence the left heart.  This has important implications for the treatment of heart failure, and patients with a form of hypertension that affects the arteries in the lung.


Representative Publications:

  • Nakamura, T., Ranek, M.J., Lee, D.I., Shalkey Hahn, V., Kim, C., Eaton, P., Kass, D.A.  Prevention of PKG1α oxidation augments cardioprotection in the stressed heart. J Clin. Invest. 2015; Jun;125(6):2468-72.  Pub Med Reference
  • Lee, D.I, Zhu, G., Sasaki, T., Cho, G.S., Hamdani, N., Holewinski, R., Jo, S.H., Danner, T., Zhang, M., Rainer, P.P., Bedja, D., Kirk, J.A., Ranek, M.J., Dostmann, W.R., Kwon, C., Margulies, K.B., Van Eyk, J.E., Paulus, W.J., Takimoto, E., Kass, D.A. Phosphodiesterase 9A controls nitric-oxide-independent cGMP and hypertrophic heart disease. Nature 2015; Mar 26;519(7544):472-6. Pub Med Reference
  • Seo, K., Rainer, P.P., Lee, D.I., Hao, S., Bedja, D., Birnbaumer, L., Cingolani, O.H., Kass, D.A. Hyperactive adverse mechanical stress responses in dystrophic heart are coupled to transient receptor potential canonical 6 and blocked by cGMP-protein kinase G modulation. Circ. Res. 2014; Feb 28;114(5):823-32. Pub Med Reference

  • Kirk, J.A., Holewinski, R.J., Kooij, V., Agnetti, G., Tunin, R.S., Witayavanitkul, N., de Tombe, P.P., Gao, W.D., Van Eyk, J., Kass, D.A. Cardiac resynchronization sensitizes the sarcomere to calcium by reactivating GSK-3β. J Clin. Invest. 2014; Jan;124(1):129-38. Pub Med Reference

  • Chakir, K., Depry, C., Dimaano, V.L., Zhu, W.Z., Vanderheyden, M., Bartunek, J., Abraham, T.P., Tomaselli, G.F., Liu, S.B., Xiang, Y.K., Zhang, M., Takimoto, E., Dulin, N., Xiao, R.P., Zhang, J., Kass, D.A. Galphas-biased beta2-adrenergic receptor signaling from restoring synchronous contraction in the failing heart. Sci Transl Med. 2011; Sept 14;3(100):100ra88. Pub Med Reference

  • Takimoto, E., Champion, H.C., Li, M., Belardi, D., Ren, S., Rodriguez, E.R., Bedja, D., Gabrielson, K.L., Wang, Y., Kass, D.A. Chronic inhibition of cyclic GMP phosphodiesterase 5A prevents and reverses cardiac hypertrophy. Nat Med. 2005; Feb ; 11(2):214-22.  Pub Med Reference


Other graduate programs in which Dr. Dawson participates:

Cellular and Molecular Medicine

Biomedical Engineering