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Elizabeth D. Luczak, Ph.D.
Assistant Professor of Medicine
Research Interests: Heart failure; Cardiac arrhythmias
Dr. Luczak earned her Ph.D. at the University of Colorado Boulder, training with Dr. Leslie Leinwand. She joined the Anderson lab as a postdoctoral fellow in 2009. She is primarily interested in the molecular mechanisms of the development of heart failure and cardiac arrhythmias. The lab recently discovered CaMKII as a resident mitochondria protein, and its inhibition in mitochondria is beneficial in several cardiac disease models. Her current research interests focus on describing a role for CaMKII in mitochondria and metabolism regulation in the heart, and its role in the transition to heart failure.
- Assistant Professor of Medicine
Departments / Divisions
- Medicine - Cardiovascular
- B.S., University of Minnesota (Minneapolis) (Minnesota) (2002)
- Ph.D., University of Colorado (Boulder) (Colorado) (2007)
Research & Publications
Research in the Anderson laboratory focuses on cellular signaling and ionic mechanisms that cause heart failure, arrhythmias and sudden cardiac death, major public health problems worldwide. Our primary focus is on the multifunctional Ca2+ and calmodulin-dependent protein kinase II (CaMKII). Our laboratory identified CaMKII as an important pro-arrhythmic and pro-cardiomyopathic signal. These studies have provided proof of concept evidence motivating active efforts in biotech and the pharmaceutical industry to develop therapeutic CaMKII inhibitory drugs to treat heart failure and arrhythmias.
CaMKII is activated by increased intracellular Ca2+ and oxidation. Diverse ‘upstream’ signals, including catecholamines and the renin-angiotensin-aldosterone pathway increase CaMKII activity. CaMKII is multifunctional because it has multiple ‘downstream’ targets. CaMKII catalyzed phosphorylation in myocardium appears to coordinate activity of many or most voltage-gated ion channels, Ca2+ homeostatic proteins and gene transcription events.
Under physiological conditions, CaMKII is important for excitation-contraction coupling and fight or flight increases in heart rate. However, myocardial CaMKII is excessively activated during disease conditions where it contributes to loss of intracellular Ca2+ homeostasis, membrane hyperexcitability, premature cell death, and hypertrophic and inflammatory transcription. These downstream targets appear to contribute coordinately and decisively to heart failure and arrhythmias. Recently, we have developed evidence that CaMKII also participates in asthma.
Lab Website: Anderson Lab
Selected PublicationsView all on Pubmed
Rasmussen TP, Wu Y, Joiner ML, Koval OM, Wilson NR, Luczak ED, Wang Q, Chen B, Gao Z, Zhu Z, Wagner BA, Soto J, McCormick ML, Kutschke W, Weiss RM, Yu L, Boudreau RL, Abel ED, Zhan F, Spitz DR, Buettner GR, Song LS, Zingman LV, Anderson ME. Inhibition of MCU forces extramitochondrial adaptations governing physiological and pathological stress responses in heart. (2015) Proc Natl Acad Sci U S A 21;112(29):9129-34. PMID: 26153425
Wu Y, Rasmussen TP, Koval OM, Joiner ML, Hall DD, Chen B, Luczak ED, Wang Q, Rokita AG, Wehrens XH, Song LS, Anderson ME. The mitochondrial uniporter controls fight or flight heart rate increases. (2015) Nature Communications 6:6081.PMID: 25603276
Luczak ED, Anderson ME. CaMKII oxidative activation and the pathogenesis of cardiac disease. (2014) Journal of Molecular and Cellular Cardiology 73:112-6. PMID:24530899
Luo M, Guan X, Luczak ED, Lang D, Kutschke W, Gao Z, Yang J, Glynn P, Sossalla S, Swaminathan PD, Weiss RM, Yang B, Rokita AG, Maier LS, Efimov IR, Hund TJ, Anderson ME. (2013) Diabetes increases mortality after myocardial infarction by oxidizing CaMKII. Journal of Clinical Investigation 123(3):1262-74. PMID: 23426181
Joiner ML, Koval OM, Li J, He BJ, Allamargot C, Gao Z, Luczak ED, Hall DD, Fink BD, Chen B, Yang J, Moore SA, Scholz TD, Strack S, Mohler PJ, Sivitz WI, Song LS, Anderson ME. (2012) CaMKII determines mitochondrial stress responses in heart. Nature 491(7423):269-73. PMID: 23051746