Internal Medicine

Mark E. Anderson, MD, PhD

Portrait

Chair & Department Executive Officer of Internal Medicine
Director, Francois M. Abboud Cardiovascular Research Center
Professor of Internal Medicine  - Cardiovascular Medicine
Professor of Molecular Physiology and Biophysics

Contact Information

Primary Office: SE308 GH General Hospital
Iowa City, IA 52242

Lab: 2270C CBRB
Iowa City, IA 52242

Email: mark-e-anderson@uiowa.edu
Web: Dr. Anderson's Laboratory
Web: Transatlantic CaMKII Alliance website (Fondation Leducq)

Education

BA, Biology, Macalester College, St. Paul, Minnesota
PhD, Physiology, University of Minnesota, Minneapolis, Minnesota
MD, University of Minnesota, Minneapolis, Minnesota

Internal Medicine Internship, Internal Medicine, Stanford University, Stanford, California
Residency, Internal Medicine Residency, Stanford University, Stanford, California
Fellowship, Cardiology Fellowship, Stanford University, Stanford, California
Fellowship, Clinical Cardiac Electrophysiology Fellowship, Stanford University, Stanford, California

Licensure and Certifications

Iowa Medical License, University of Iowa Carver College of Medicine
Tennessee Medical License , Vanderbilt University
Passed Internal Medicine and Cardiovascular Recertification Exam
Clinical Cardiac Electrophysiology Boards
Cardiovascular Medicine Boards
Internal Medicine Boards
National Board Examinations (parts I-III)

Education/Training Program Affiliations

Biosciences Graduate Program
Free Radical and Radiation Biology Graduate Program
Interdisciplinary Graduate Program in Translational Biomedicine
Medical Scientist Training Program

Research Summary

Our research focuses on cellular signaling and ionic mechanisms that cause heart failure, arrhythmias and sudden cardiac death, major public health problems worldwide. Work from our laboratory contributed to current concepts about the role of the multifunctional Ca2+ calmodulin dependent protein kinase II (CaMKII) as a central signal promoting myocardial dysfunction and arrhythmias by actions on ion channels, Ca2+ homeostatic proteins, transcription factors and mitochondria. These studies motivated current efforts in biotech and pharma to develop CaMKII inhibitory drugs for cardiovascular indications. We identified the molecular mechanism for CaMKII activation by ROS and its enzymatic reversal by methionine sulfoxide reductase A (MsrA). Our studies have shown that CaMKII oxidation drives diverse pathological phenotypes in cardiovascular diseases, diabetes and asthma, suggesting CaMKII inhibition may emerge as a targeted antioxidant strategy for treating ROS-related diseases.

Center, Program and Institute Affiliations

Cardiovascular Research Center

Date Last Modified: 10/28/2013 - 14:22:08