Todd Camenisch

Research Focus Group Membership: 
Research Focus Group 3

PhD, University of North Carolina at Chapel Hill, 1998, Microbiology/Immunology
BS, University of Arizona, Tucson, 1991, Microbiology/Immunology
P.D., Mayo Clinic, Arizona, 1998-2001, Biochemistry & Mol Biol

College Affiliations: 

College of Pharmacy

Research Interests: 

Investigating the integration between extracellular matrix and growth factor receptor signaling during heart morphogenesis.

Environmental Health Research & Expertise: 

My research program centers upon developmental cardiovascular biology stemming from my good fortune to have trained in mouse genetic engineering and producing the first model for patent ductus arteriosus in the mouse(1). Our use of molecular and cellular techniques combined with mouse functional genomics is revealing novel discoveries in regards to heart and coronary vessel development. The significance of this work relates to the fact that cardiovascular-heart defects are the most common congenital defects diagnosed in infants in this country. A 2007 American Heart Association publication reports the incidence of congenital heart defects at 5% for births in the United States. In addition, we firmly propose that cardiovascular disease in adults has developmental origins. Therefore, we are not only defining developmental cardiac events and causes of congenital defects, but also etiology of cardiovascular connective tissue diseases. In this regard, we have identified that exposure to environmental arsenic in drinking water contributes to altered heart structures, hypertension, and cardiac hypertrophy. We are poised to decipher the molecular and cellular mechanisms of arsenic developmental cardiotoxicity as we have previously established  the roles for TGFb(6,13), VEGF(5,9,11) and ErbB signaling(3,7) as well as hyaluronan matrix in heart structure formation and disease(4,7,11,14). We have recently discovered a signaling node through Map3-Kinases that integrates many of these signals to mediate the correct signal transduction for normal heart formation(12). We have also discovered that arsenic exposure disrupts developmental EMT impacting cardiac physiology (14,15). Our efforts will lead to improved diagnostics and be applied to develop novel repair strategies to improve the health of children and adults with congenital heart defects as well as risk reduction or prevention in arsenic vulnerable populations. My collective research program constitutes a critically important amalgamation of molecular and developmental biology, genetics, protein chemistry and eventually pediatric medicine. We have contributed several seminal papers to the field and are recognized as leaders in this area with the contribution of chapter 6 to the 2010 publication of the second edition of Heart Development and Regeneration.

Select Publications


Huang, T., J. V. Barnett, and T. D. Camenisch, "Cardiac epithelial-mesenchymal transition is blocked by monomethylarsonous acid (III).", Toxicol Sci, vol. 142, issue 1, pp. 225-38, 2014 Nov. PubMed PMCID: PMC4334812  PMID: 25145660
Sollome, J. J., E. Thavathiru, T. D. Camenisch, and R. R. Vaillancourt, "HER2/HER3 regulates extracellular acidification and cell migration through MTK1 (MEKK4).", Cell Signal, vol. 26, issue 1, pp. 70-82, 2014 Jan. PubMed PMCID: PMC3869707  PMID: 24036211


Allison, P., T. Huang, D. Broka, P. Parker, J. V. Barnett, and T. D. Camenisch, "Disruption of canonical TGFβ-signaling in murine coronary progenitor cells by low level arsenic.", Toxicol Appl Pharmacol, vol. 272, issue 1, pp. 147-53, 2013 Oct 1. PubMed PMCID: PMC3972124  PMID: 23732083


Druwe, I. L., J. J. Sollome, P. Sanchez-Soria, R. N. Hardwick, T. D. Camenisch, and R. R. Vaillancourt, "Arsenite activates NFκB through induction of C-reactive protein.", Toxicol Appl Pharmacol, vol. 261, issue 3, pp. 263-70, 2012 Jun 15. PubMed PMCID: PMC3598891  PMID: 22521605


Azhar, M., K. Brown, C. Gard, H. Chen, S. Rajan, D. A. Elliott, M. V. Stevens, T. D. Camenisch, S. J. Conway, and T. Doetschman, "Transforming growth factor Beta2 is required for valve remodeling during heart development.", Dev Dyn, vol. 240, issue 9, pp. 2127-41, 2011 Sep. PubMed PMCID: PMC3337781  PMID: 21780244