William WeglickiActing Chair, Department of Biochemistry & Molecular Medicine
Professor of Biochemistry and Molecular Medicine
Professor of Medicine (Secondary)
Office Phone: 202-994-0501
Department: Biochemistry and Molecular Medicine
- BS, Loyola College, 1950
- MD, University of Maryland School of Medicine, 1962
Our research team studies mechanisms of cardiovascular injury due to oxidative and nitrosative stress. Some key techniques/models employ tissue culture, antioxidant interventions and long-term treatment with chemotherapy agents, immunohistochemical characterization of apoptosis and inflammation, genetically engineered mice and echocardiography of impaired cardiac function. We identified substance P as a key mediator of inflammation of the heart due to magnesium deficiency, as well as cardioprotection from drugs that block neuropeptide release and the NK1 receptor for substance P. Currently we are studying the role of the neutral endopeoptidase, neprilysin, in amplifying neurogenic inflammation during hypomagnesemia; our lab is the first to report inhibition of this enzyme, which is critical for degrading excess substance P, due to the oxidative/nitrosative stress of hypomagnesemia. Recently we reported on the cardiotoxicity of tyrosine kinase inhibiting chemotherapeutic agents; this work resulted in funding of an NHLBI grant entitled “EGFR Tyrosine Kinase Inhibition-Induced Cardiomyopathy.” These recent studies may have translational relevance to the newly evolving joint cardiology-oncology emphasis on treating cardiovascular disease in long term cancer survivors.
View publications by this faculty member from January 1, 2013 - present
Mak, I.-T, Kramer, J.H., Chmielinska, J.J, Spurney, C.F., Weglicki, W.B. The EGFR TKI, erlotinib, causes hypomagnesemia, oxidative stress and cardiac dysfunction: attenuation by substance P-receptor blockade. J. Cardiovasc. Pharmacol. In Press. 2014.
Weglicki, W.B., Mak, I-T., Chmielinska, J.J., Spurney, C.F., Kramer. J.H. Hypomagnesemia-induced neurogenic inflammation and cardiac dysfunction during experimental Mg deficiency. In: Proceedings of the 13th International Magnesium Symposium. Merida, Yucatan, Mexico. In Press. 2014.
McCaffrey, T.A., Tziros, C., Lewis, J., Katz, R., Siegel, R., Weglicki,W., Kramer, J., Mak, I-T., Toma, I.,Chen, L., Benas, E., Lowitt, A., Rao, S., Witkins, L., Lian, Y., Lai, Y.,Yang, Z., Fu, S.W. Genomic Profiling Reveals the Potential Role of TCL1A and MDR1 Deficiency in Chemotherapy-Induced Cardiotoxicity. Int. J. Biol. Sci. 9(4):350-360, 2013.
Mak, I.-T, Kramer, J.H., Chen X., Chmielinska, J.J, Spurney, C.F., Weglicki, W.B. Mg-supplementation Attenuates Ritonavir-induced Hyperlipidemia, Oxidative Stress and Cardiac Dysfunction in Rats. Am. J. Physiol. Regul. Integr. Comp. Physiol. 305: R1102–R1111, 2013.
Weglicki, W.B. Hypomagnesemia and Inflammation: Clinical and Basic Aspects. Ann. Rev. of Nutrition 32:4.1-4.17;2012. (in press).
Weglicki, W.B. Kramer, J.H., Spurney, C.F., Chmielinska, J.J., Mak, I.T. The EGFR Tyrosine Kinase Inhibitor Tyrphostin AG-1478 Causes Hypomagnesemia and Cardiac Dysfunction. Can. J. of Physiol. & Pharmacol. (accepted 1/20/2012) (in press).
Mak I.T. Chmielinska, J.J, Kramer, J.H. Spurney, C.F., Weglicki, W.B. Loss of neutral endopeptidase activity contributes to neutrophil activation and cardiac dysfunction during chronic hypomagnesemia: Protection by substance P receptor blockade. Exp. & Clin. Cardiol. 16(4):121-124, 2011.
Weglicki, W.B., Mak, I.-T., Chmielinska, J.J., Tejero-Taldo, M.I., Komarov, A., Kramer, J.H. The role of Magnesium Deficiency in Cardiovascular and Intestinal Inflammation. Magnes. Res. 23(4):199-206, 2010. PMID # 20971697
Kramer, J.H., Spurney, C., Iantorno, M., Tziros, C., Mak, I-T., Tejero-Taldo, M.I., Chmielinska, J.J., Komarov, A.M., Weglicki, W.B. Neurogenic inflammation and cardiac dysfunction due to hypomagnesemia in a rodent model. Am. J. Med. Sci. 338: 22-27, 2009.
Weglicki, W.B., Chmielinska, J.J., Tejero-Taldo, M.I., Kramer, J.H., Spurney, C., Viswalingham, K., Lu, B., Mak, I.-T. Neutral endopeptidase inhibition enhances substance P mediated inflammation due to hypomagnesemia. Magnes. Res. 22: 1-7, 2009.
Mak, I. T., Chmielinska, J.J., Kramer, J.H., Weglicki. W.B. AZT-Induced cardiovascular toxicity - attenuation by Mg-supplementation. Cardiovascular Toxicol. 9(2): 78-85,2009.
Weber, KT, Weglicki, W.B. and Simpson, RU. Macro- and Micronutrients Dyshomeostais in the Adverse Structural Remodeling of Myocardium. Cardiovasc. Res. 81(3): 500-508, 2009
Additional publications published before January 1, 2013 may be available within Himmelfarb Library's database.
Industry Relationships and Collaborations
This faculty member (or a member of their immediate family) has reported a financial interest with the healthcare related companies listed below. These relations have been reported to the University and, when appropriate, management plans are in place to address potential conflicts.