Timothy L Domeier, PhD


Tim Domeier, PhD, is Assistant Professor of Medical Pharmacology and Physiology at the University of Missouri School of Medicine. His laboratory investigates how the intracellular concentration of calcium changes within heart muscle during heart disease. Calcium is arguably the most important signaling ion throughout the body, With each heartbeat, calcium in the cardiac muscle cell cycles dramatically, changing from very low levels during diastole (the heart's relaxation time) to high levels during systole (the heart's contraction time). In the normal heart these calcium signals exhibit precise timing, which orchestrates the coordinated contraction of all muscle cells and ensures proper pumping of blood. Interestingly, not only is calcium critical to the beating of the heart, but also an important signal for the growth and death of cardiac muscle. A major research focus of Dr. Domeier's laboratory is to investigate the dynamic movement of calcium in individual heart muscle cells. Using a combination of biochemical, electrophysiological, genetic, and pharmacological approaches with a technique called confocal laser scanning fluorescence microscopy, his laboratory monitors the function of calcium channels, calcium pumps, and calcium transporters in individual heart cells. These methods allow the laboratory to decode when and where calcium changes within the muscle cell, and gain comprehensive insight into how calcium is used as the signal to activate myofilaments (in collaboration with Dr. Kerry McDonald), regulate mitochondrial function, and activate various cell signaling pathways (in collaboration with Dr. Chris Baines). The laboratory monitors how calcium signaling changes in various forms of heart disease, including aging (in collaboration with Dr. Steve Segal), muscular dystrophy (in collaboration with Dr. Dongsheng Duan), cardiomyopathy (in collaboration with Dr. Maike Krenz), hypertrophy, and heart failure (in collaboration with Dr. Craig Emter). During heart disease, muscle cells are unable to properly regulate calcium, which predisposes the heart to contractile dysfunction, arrhythmia, and sudden cardiac death. The goal of Dr. Domeier's laboratory is to uncover the mechanisms by which calcium homeostasis is altered with disease, and rapidly translate new research findings into novel treatments for patients with cardiac disease.

Academic Information

Associate Professor


One Hospital Drive
Columbia, MO 65212
United States

P. 573-884-1213

Research Interests

  • Cardiovascular Physiology
  • Calcium Homeostasis
  • Cardiac Aging
  • Cardiomyopathy and Cardiac Failure

Areas of Expertise

  • Cardiovascular Physiology
  • Muscle Cell Physiology
  • Intracellular Calcium Regulation
  • Single- and Multi-photon fluorescence microscopy

Education & Training


2010, Rush University
2008, Loyola University - Chicago

Post-Graduate School

2006, PhD, Cellular and Molecular Physiology, Yale University

Awards & Honors

  • Dorsett L. Spurgeon MD Distinguished Medical Research Award
  • University of Missouri Faculty Scholar
  • NIH Career Development Award
  • NIH Individual Postdoctoral National Research Service Award
  • American Heart Association Postdoctoral Fellowship
  • NIH Individual Predoctoral National Research Service Award
  • Yale University Prize Teaching Fellowship
  • University of Nebraska Regents Scholar


  • Jones JL, Peana D, Veteto AB, Lambert MD, Nourian Z, Karasseva NG, Hill MA, Lindman BR, Baines CP, Krenz M, Domeier TL. TRPV4 increases cardiomyocyte calcium cycling and contractility yet contributes to damage in the aged heart following hypoosmotic stress. Cardiovasc Res. 2018 Jun 20.
  • Hiemstra JA, Veteto AB, Lambert MD, Olver TD, Ferguson BS, McDonald KS, Emter CA, Domeier TL. Chronic low-intensity exercise attenuates cardiomyocyte contractile dysfunction and impaired adrenergic responsiveness in aortic-banded mini-swine. J Appl Physiol (1985). 2018 Apr 1;124(4):1034-1044.
  • Peana D, Domeier TL. Cardiomyocyte Ca2+ homeostasis as a therapeutic target in heart failure with reduced and preserved ejection fraction. Curr Opin Pharmacol. 2017 Apr;33:17-26.
  • Genovese NJ, Domeier TL, Telugu BP, Roberts RM. Enhanced Development of Skeletal Myotubes from Porcine Induced Pluripotent Stem Cells. Sci Rep. 2017 Feb 6;7:41833.
  • Wang X, Nichols L, Grunz-Borgmann EA, Sun Z, Meininger GA, Domeier TL, Baines CP, Parrish AR. Fascin2 regulates cisplatin-induced apoptosis in NRK-52E cells. Toxicol Lett. 2017 Jan 15;266:56-64.
  • Yue, Y., Binalsheikh, I.M., Leach, S.B., Domeier, T.L., and Duan, D. Prospect of gene therapy for cardiomyopathy in hereditary muscular dystrophy. Expert Opinion on Orphan Drugs. 2016; 4(2):169-183
  • Hiemstra, J.A., Lee, D.I., Chakir, K., Gutiérrez-Aguilar, M., Marshall, K.D., Zgoda, P.J., Cruz-Rivera, N., Dozier, D.G., Ferguson, B.S., Heublein, D.M., Burnett, J.C., Scherf, C., Ivey, J.R., Minervini, G., McDonald, K.S., Baines, C.P., Krenz, M, Domeier, T.L., and Emter, C.A. Saxagliptin and Tadalafil Differentially Alter Cyclic Guanosine Monophosphate (cGMP) Signaling and Left Ventricular Function in Aortic-Banded Mini-Swine. J Am Heart Assoc. 2016 Apr 20;5(4)
  • Jia, G., Habibi, J., DeMarco, V.G., Martinez-Lemus, L.A., Ma, L., Whaley-Connell, A.T., Aroor, A.R., Domeier, T.L., Zhu, Y., Meininger, G.A., Barrett Mueller, K., Jaffe, I.Z., and Sowers, J.R. Endothelial Mineralocorticoid Receptor Deletion Prevents Diet-Induced Cardiac Diastolic Dysfunction in Females. Hypertension. 2015 Dec;66(6):1159-67
  • Nance, M.E., Whitfield, J.T., Zhu, Y., Gibson, A.K., Hanft, L.M., Campbell, K.S., Meininger, G.A., McDonald, K.S., Segal, S.S., and Domeier, T.L. Attenuated sarcomere lengthening of the aged murine left ventricle observed using two-photon fluorescence microscopy. Am J Physiol Heart Circ Physiol. 2015 Sep;309(5):H918-25
  • Bostick, B., Habibi, J., DeMarco, V.G., Jia, G., Domeier, T.L., Lambert, M.D., Aroor, A.R., Nistala, R., Bender, S.B., Garro, M., Hayden, M.R., Ma, L., Manrique Acevedo, C., and Sowers, J.R. Mineralocorticoid Receptor Blockade Prevents Western Diet-induced Diastolic Dysfunction in Female Mice. Am J Physiol Heart Circ Physiol. 2015 May 1;308(9):H1126-35
  • Clay, S.A.*, Domeier, T.L.*, Hanft, L.M., McDonald, K.S., Krenz, M. Elevated calcium transients and increased myofibrillar power generation cause cardiac hypercontractility in a model of Noonan Syndrome with Multiple Lentigines. Am J Physiol Heart Circ Physiol. 2015 May 1;308(9):H1086-95
  • Socha, M.J., Boerman, E.M., Behringer, E.J., Shaw, R.L., Domeier, T.L., Segal, S.S. Advanced age protects microvascular endothelium from aberrant Ca2+ influx and cell death induced by hydrogen peroxide. J Physiol. 2015 May 1;593(9):2155-69
  • Domeier, T.L., Roberts, C.J., Gibson, A.K., Hanft, L.M., McDonald, K.S., Segal, S.S. Dantrolene suppresses spontaneous Ca2+ release without altering excitation-contraction coupling in cardiomyocytes of aged mice. Am J Physiol Heart Circ Physiol. 2014 Sep 15;307(6):H818-29
  • Hiemstra, J.A., Gutiérrez-Aguilar, M., Marshall, K.D., McCommis, K.S., Zgoda, P.J., Cruz-Rivera, N., Jenkins, N.T., Krenz, M. *Domeier, T.L. *, Baines, C.P. * , Emter, C.A. * A new twist on an old idea part 2: cyclosporine preserves normal mitochondrial but not cardiomyocyte function in mini-swine with compensated heart failure. Physiol Rep. 2014 Jun 24;2(6)
  • Gutiérrez-Aguilar, M., Douglas, D.L., Gibson, A.K., Domeier, T.L., Molkentin, J.D., Baines, C.P. Genetic manipulation of the cardiac mitochondrial phosphate carrier does not affect permeability transition. J Mol Cell Cardiol. 2014 Jul;72:316-25