Department of Internal Medicine
Cardiovascular Medicine Faculty
Medical School:
University of Minnesota
Residency:
Stanford University
Fellowship:
Stanford University
The University of Iowa
Mark E. Anderson, M.D., Ph.D.
Professor of Medicine and Physiology
Head, Department of Internal Medicine
Associate Director, Cardiovascular Research Center
Dr. Anderson is clinically trained as a cardiac electrophysiologist. His research is focused on cellular signaling and ionic mechanisms that cause heart failure and sudden cardiac death. Work from the Anderson laboratory led to current concepts about the role of the multifunctional Ca2+/calmodulin dependent protein kinase II (CaMKII) as a central signal contributing to myocardial dysfunction and arrhythmias. The laboratory work ranges from molecular structure activity analysis of CaMKII to systems physiology using genetically modified mice. The main research themes pursued by the Anderson laboratory are 1. Oxidative activation of CaMKII; 2. CaMKII signaling to ion channels; 3. The role of CaMKII in inflammation; 4. The role of CaMKII in cardiac pacemaker cells; 5. The role of CaMKII in cell survival.
Honors, Awards, and Organizations
- American Society of Clinical Investigation
- Established Investigator, American Heart Association
- Association of American Physicians
- Director, Fondation Leducq Transatlantic Network, “Alliance for CaMKII signaling”
Recent Publications
- Dzhura I, Wu Y, Colbran RJ, Balser JR, Anderson ME. Calmodulin kinase determines calcium-dependent facilitation of L-type calcium channels. Nature Cell Biol 2000; 2:173-177.
- Zhang R, Khoo MSC, Wu Y, Dzhura I, Ni G, Vishnivetskaya TA, Grueter C, Madu EC, Gurevich VV, Colbran RJ, Anderson ME. Calmodulin kinase II inhibition protects against structural heart disease. Nature Med 2005; 11:409-417. Published with an accompanying editorial.
- Anderson ME, Higgins, LS, Schulman H. Disease mechanisms and emerging therapies: Protein kinases and their inhibitors in myocardial disease. Nature Clin Prac 2006; 3:437-445.
- Erickson JR, Joiner MA, Guan X, Kutschke W, Yang J, Oddis CV, Bartlett RK, Lowe JS, O’Donnell S, Aykin-Burns N, Zimmerman MC, Zimmerman K, Ham A-JL, Weiss RM, Spitz DR, Shea MA, Colbran RJ, Mohler PJ, Anderson ME. Direct oxidation results in Ca2+ independent activation of CaMKII. Cell 2008; 133:462-474. Published with accompanying editorial.
- Thiel W, Chen B, Hund T, Koval O, Purihit A, Song L-S, Mohler PJ, Anderson ME. Calmodulin kinase II is required for proarrhythmic defects in Timothy Syndrome. Circulation 118:2225-2234, 2008. Published with accompanying editorial.
- Singh MV, Kapoun A, Higgins L, Kutschke W, Thurman JM, Singh M, Yang J, Guan X, Lowe J, Mohler PJ, Weiss RM, Zimmerman K, Zhang R, Yull FE, Blackwell TS, Anderson ME. CaMKII triggers cell membrane injury by inducing complement factor B in cardiomyocytes. J. Clinical Invest. In press, 2009.
- Wu Y, Gao Z, Chen B, Koval O, Singh M, Guan X, Hund T, Kutschke WJ, Sarma S, Grumbach I, Wehrens X, Mohler P, Song L, Anderson M. Calmodulin kinase II is required for fight or flight sinoatrial node physiology. [Commentary on this work: Sci Signaling 2:ec130, 2009] Proc Natl Acad Sci. 106:5972-5977, 2009.
Links of Interest
- Transatlantic CaMKII Alliance website (Fondation Leducq)