Faculty Directory

I. Tong Mak

I. Tong Mak

Research Professor of Biochemistry and Molecular Medicine
Research Professor of Medicine (Secondary)

Office Phone: 202-994-2865
Email: Email
Department: Biochemistry and Molecular Medicine


  • BS, University of Wyoming, 1974
  • MS, Michigan State University, 1977
  • PhD, University of Wisconsin, 1982


There are 2-3 separate research projects ongoing in our laboratory, all in the general areas of cardiovascular oxidative inflammation and therapy. (1) HAART-mediated Cardiac Dysfunction and Protective Efficacy of Magnesium (PI): This project focuses on currently used anti-HIV agents (including NRTIs, NNRTIs and protease inhibitors) -mediated systemic oxidative events (e.g. neutrophil and endothelial activation, inflammatory cytokines) leading to cardiovascular dysfunction (by echocardiography) and pathology and potential protective mechanisms of Mg. Both cultured endothelial cells and relevant rodent models are used. The role of iron, calcium, and the protective efficacy and mechanisms of Mg are investigated. (2) EGFR Tyrosine Kinase Inhibition - Induced Cardiomyopathy (Co-I): This project focuses on if chronic erlotinib (an anti-cancer agent) treatment may induce hypomagnesemia and subsequent intestinal and cardiac inflammation/dysfunction in rats; and 2) if the TKI-induced systemic pathogenesis and cardiac dysfunction can be attenuated by the clinically-used Substance P receptor blocker. (3) Aortic Valve Inflammation Due To Hypomagnesemia (Co-PI, NIH RO1 submitted): The goal of this proposal is to investigate if chronic hypomagnesemia contributes to the development of aortic valve (AV) inflammation and calcification. Furthermore, we also investigate the role of the neurogenic peptide substance-P-mediated oxidative stress and determine if Mg supplementation may reverse aortic valve pathogenesis. This project involves molecular assessment of key osteogenic mediators, along with relevant inflammatory infiltrates in the isolated aortic valves leading to valve calcification.


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 WB, Kramer JH, Chmielinska JJ, Spurney CF, Mak IT. “The EGFR tyrosine kinase inhibitor tyrphostin AG-1478 causes hypomagnesemia and cardiac Dysfunction.” Can. J. of Physiol. & Pharmacol. (accepted 1/20/2012)

Weglicki WB, Chmielinska, JJ Tejero-Taldo MI, Kramer, Mak IT. Cardiovascular and intestinal responses to oxidative and nitrosative stress during prolonged magnesium deficiency. Am J Med Sci 342: 125-128. 2011

Mak IT, Chmielinska JJ, Kramer JH, Spurney CF, Weglicki WB. 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.

Mak IT, Chmielinska JJ, Kramer JH, Weglicki WB. AZT-induced oxidative cardiovascular toxicity—attenuation by Mg-supplementation. Cardiovasc. Toxicol. 2009; 9(2):78-85.

Mak IT, Kramer JH, Chmielinska JJ et al. Inhibition of neutral endopeptidase potentiates neutrophil activation during Mg-deficiency in the rat. Inflammation Res. 57: 300-305, 2008.

Mak IT, Chmielinska JJ, Torres A, Weglicki WB. D-propranolol attenuates lysosomal iron accumulation and oxidative injury in endothelial cells. J Pharmacol Exp Ther. 317:522-508, 2006.

Mak IT, Weglicki WB. Potent antioxidant properties of 4-OH-propranolol. J Pharmacol Exp Ther.; 308: 85-90, 2005.

Tejero-Taldo MI, Chmielinska JJ, Gonzalez G, Mak IT, Weglicki WB. N-Methyl-D-aspartate receptor blockade inhibits cardiac inflammation in the Mg-deficient rat. J Pharm. Exp. Ther. 2004; 311: 8-13.

Mak IT, Goldfarb MG, Weglicki WB, Haudenschild CC. Cardiac pathologic effects of AZT in Mg-deficient mice. Cardiovasc. Toxicol 4: 169-178, 2004.

Dickens BF, Weglicki WB, Boehme P, Mak IT. Antioxidant and lysosomotropic properties of acridine-propranolol: Protection against oxidative endothelial injury. J. Mol Cell Cardiol. 34: 129-137, 2002.

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.

  • None