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Mark Chapleau, PhD

Professor of Internal Medicine-Cardiovascular Medicine
Photo of Mark Chapleau, PhD
Mark Chapleau, PhD - University of Iowa
Primary Office
629 Medical Research Center
Iowa City, IA 52242

Current Positions

  • Professor of Internal Medicine-Cardiovascular Medicine
  • Professor of Molecular Physiology and Biophysics

Education

  • PhD, Physiology, Louisiana State University Medical Center, New Orleans, Louisiana
  • Postdoctoral Fellow, University of Iowa College of Medicine, Iowa City, Iowa

Graduate Program Affiliations

Center, Program and Institute Affiliations

Research Interests

  • Dr. Chapleau's research focuses on mechanisms of autonomic regulation in health and disease including effects of aging, hypertension, hypercholesterolemia, cardiomyopathy, myocardial infarction (MI), heart failure, and muscular dystrophy. Key hypotheses involve the roles of acid-sensing ion channels in sensory transduction, reactive oxygen species and angiotensin in sensory and sympathetic signaling, and oxidative stress in autonomic dysregulation. Experimental approaches include assessment of the cellular and molecular basis of sensory transduction and neuronal excitability in baroreceptor and sympathetic neurons using patch-clamp, imaging, and molecular techniques; recording of baroreceptor and sympathetic nerve activity in vivo; and assessment of cardiovascular and autonomic function in conscious mice using radiotelemetry.

Selected Publications

  • Chapleau, M. W., Rotella, D. L., Reho, J. J., Rahmouni, K. & Stauss, H. M. (2016). Chronic vagal nerve stimulation prevents high-salt diet-induced endothelial dysfunction and aortic stiffening in stroke-prone spontaneously hypertensive rats. American journal of physiology. Heart and circulatory physiology 311 (1) H276-85. PMID: 27208157.
  • Chu, Y., Lund, D. D., Doshi, H., Keen, H. L., Knudtson, K. L., Funk, N. D., Shao, J. Q., Cheng, J., Hajj, G. P., Zimmerman, K. A., Davis, M. K., Brooks, R. M., Chapleau, M. W., Sigmund, C. D., Weiss, R. M. & Heistad, D. D. (2016). Fibrotic Aortic Valve Stenosis in Hypercholesterolemic/Hypertensive Mice. Arterioscler Thromb Vasc Biol. DOI: 10.1161/atvbaha.115.306912.
  • Sabharwal, R., Rasmussen, L., Sluka, K. A. & Chapleau, M. W. (2016). Exercise prevents development of autonomic dysregulation and hyperalgesia in a mouse model of chronic muscle pain. Pain 157 (2) 387-98. DOI: 10.1097/j.pain.0000000000000330.
  • Singh, M. V., Cicha, M. Z., Meyerholz, D. K., Chapleau, M. W. & Abboud, F. M. (2015). Dual Activation of TRIF and MyD88 Adaptor Proteins by Angiotensin II Evokes Opposing Effects on Pressure, Cardiac Hypertrophy, and Inflammatory Gene Expression. Hypertension 66 (3) 647-56. DOI: 10.1161/hypertensionaha.115.06011.
  • Prasad, A. M., Morgan, D. A., Nuno, D. W., Ketsawatsomkron, P., Bair, T. B., Venema, A. N., Dibbern, M. E., Kutschke, W. J., Weiss, R. M., Lamping, K. G., Chapleau, M. W., Sigmund, C. D., Rahmouni, K. & Grumbach, I. M. (2015). Calcium/calmodulin-dependent kinase II inhibition in smooth muscle reduces angiotensin II-induced hypertension by controlling aortic remodeling and baroreceptor function. J Am Heart Assoc 4 (6) e001949. DOI: 10.1161/jaha.115.001949.
  • Chapleau, M. W. (2014). Contributions of skeletal muscle myopathy to heart failure: novel mechanisms and therapies. Introduction. Exp Physiol 99 (4) 607-8. DOI: 10.1113/expphysiol.2013.074294.
  • Raven, P. B. & Chapleau, M. W. (2014). Blood pressure regulation XI: overview and future research directions. Eur J Appl Physiol 114 (3) 579-86. DOI: 10.1007/s00421-014-2823-z.
  • Sabharwal, R. & Chapleau, M. W. (2014). Autonomic, locomotor and cardiac abnormalities in a mouse model of muscular dystrophy: targeting the renin-angiotensin system. Exp Physiol 99 (4) 627-31. DOI: 10.1113/expphysiol.2013.074336.
  • Singh, M. V., Chapleau, M. W., Harwani, S. C. & Abboud, F. M. (2014). The immune system and hypertension. Immunol Res 59 (1-3) 243-53. DOI: 10.1007/s12026-014-8548-6.
  • Lu, Y., Whiteis, C. A., Sluka, K. A., Chapleau, M. W. & Abboud, F. M. (2013). Responses of glomus cells to hypoxia and acidosis are uncoupled, reciprocal and linked to ASIC3 expression: selectivity of chemosensory transduction. J Physiol 591 (4) 919-32. DOI: 10.1113/jphysiol.2012.247189.