Stewart, Alexandre


Alexandre Stewart, PhD is the Director of the Laboratory of Translational Genomics at the Ruddy Canadian Cardiovascular Genetics Centre. He is also Full Professor in the Department of Medicine and in the Department of Biochemistry, Microbiology and Immunology, and Member of the Collaborative Program in Human and Molecular Genetics, and of the Faculty of Graduate and Post-doctoral Studies, at the University of Ottawa.


Before joining the University of Ottawa Heart Institute, Dr. Stewart was Assistant Professor of Medicine at the University of Pittsburgh Cardiovascular Institute. He received his post-doctoral training at the University of California, San Francisco, and his PhD from the Department of Anatomy and Organismal Biology at the University of Chicago. Before his PhD training, he obtained an MSc degree in Physiology and a BScH degree in Biology at the University of Ottawa.

Dr. Stewart is a founding member of the international CARDIoGRAM consortium comprising Genome-Wide Associations Studies (GWAS) of > 20 centres in eight countries for the discovery of genetic risk of coronary artery disease (CAD). In 2014, Dr. Stewart was awarded Investigator of the Year by the University of Ottawa Heart Institute.

Research & Clinical Interests 

Lowering cholesterol and blood pressure via current therapies markedly reduces the incidence of cardiac events. Known genetic variants for cardiovascular disease confer a similar risk burden as elevated cholesterol or blood pressure, but are independent of these risk factors, pointing to additional cellular pathways and potentially significant venues for intervention in CAD. Dr. Stewart’s research is directed at elucidating these mechanisms with the vision to devise new therapies to further improve prevention and outcomes. 


See current publications list at PubMed.
See Research Gate profile
See Google Scholar profile.

Selected publications:

  1. Almontashiri NAM, Antoine D, Zhou X, Vilmundarson RO, Zhang SX, Hao KN, Chen HH, Stewart AFR. 9p21.3 coronary artery disease risk variants disrupt tead transcription factor-dependent tgfβ regulation of p16 expression in human aortic smooth muscle cells. Circulation, 2015; 132(21):1969-78.
  2. Chen HH, Keyhanian K, Zhou X, Vilmundarson RO, Almontashiri NAM, Cruz SA, Pandey NR, Yap NL, Ho T, Stewart CA, Huang H, Hari A, Geoffrion M, McPherson R, Rayner KJ, Stewart AFR. IRF2BP2 reduces macrophage inflammation and susceptibility to atherosclerosis. Circulation Research, 2015; 117(8):671-83.
  3. Amontashiri NA, Vilmundarson RO, Ghasemzadeh N, Dandona S, Roberts R, Quyyumi AA, Chen HH, Stewart AF. Plasma PCSK9 levels are elevated with acute myocardial infarction in two independent retrospective angiographic studies. PLoS One. 2014 Sep 2;9(9):e106294. 
  4. Almontashiri NA, Chen HH, Mailloux RJ, Tatsuta T, Teng AC, Mahmoud AB, Ho T, Stewart NA, Rippstein P, Harper ME, Roberts R, Willenborg C, Erdmann J; CARDIoGRAM Consortium, Pastore A, McBride HM, Langer T, Stewart AF. SPG7 variant escapes phosphorylation-regulated processing by AFG3L2, elevates mitochondrial ROS, and is associated with multiple clinical phenotypes. Cell Rep. 2014 May 8;7(3):834-47. 
  5. Fan M, Dandona S, McPherson R, Allayee H, Hazen SL, Wells GA, Roberts R, Stewart AF. Two chromosome 9p21 haplotype blocks distinguish between coronary artery disease and myocardial infarction risk. Circ Cardiovasc Genet. 2013 Aug;6(4):372-80. 
  6. Almontashiri NA, Fan M, Cheng BL, Chen HH, Roberts R, Stewart AF. Interferon-γ activates expression of p15 and p16 regardless of 9p21.3 coronary artery disease risk genotype. J Am Coll Cardiol. 2013 Jan 15;61(2):143-7. 

Share This