Zam Kassiri (PhD, University of Toronto)

Associate Professor
474 Heritage Mediacal Research Center 
University of Alberta
Edmonton, Alberta
Canada T6G 2S2 

Tel: 780 492-9283
Lab: 780 492-8673

Research Description

The extracellular matrix (ECM) is a network structure that mediates the interconnection between different cells and vasculature within an organ. ECM also serves as a reservoir for a number of cytokines and growth factors, which remain inactive until released from the ECM and bind to their receptors. My lab is interested in the contribution of the ECM to progression of cardiovascular diseases. Maintaining the integrity of the ECM is crucial for structure stability as well as the function of an organ. ECM is a dynamic entity and its homeostasis is maintained by a balance in the function of two groups of proteins, matrix metalloproteinases (MMPs) that degrade ECM structural proteins, and their inhibitors, Tissue inhibitor of metalloproteinases (TIMPs). We are also interested in other proteases that can directly or indirectly influence ECM remodeling in diseases, such as a disintegrin and metalloproteinases (ADAMs). We use genetically modified mice that lack individual TIMPs, MMPs, or ADAMs, as global or cell-specific deletions. We subject these mice to models of human heart diseases (myocardial infarction/heart attack, pressure overload, agonist-induced hypertrophic cardiomyopathy); and/or vascular diseases (aortic aneurysm, hypertension, atherosclerosis) to determine the specific functions in each disease.   

A few of the questions that our lab aims to address are:

  • As we have discovered novels functions for the ECM regulatory proteins, how can they be manipulated/targeted as a therapeutic approach for treating heart disease?
  • How can ECM-cell connection alter the cell fate following injury (myocytes versus fibroblasts)?
  • What alternate (non ECM-dependent) functions do ECM regulatory proteins possess?
  • How are the MMPs-TIMPs and ADAMs all interconnected in the healthy heart and arteries, and how is this interaction altered in disease?


  • Heart & Stroke Foundation Maverick Researcher (2011)
  • Alberta Innovates-Health Solution (AHFMR) - Scholar (2010-2017)
  • Canadian Cardiovascular Society (CCS) Young Investigator Award – Basic Science Category (2010)
  • New Investigator of Heart and Stroke Foundation of Canada (July 2008-June 2013)
  • Post-doctoral fellowship, TACTICS, 2005-2007
  • Post-doctoral fellowship, Heart and Stroke Foundation of Canada, 2003-2005
  • Doctoral scholarship, Heart and Stroke Foundation of Canada, 1999-2000

Selected publications

  • Sakamuri S, Takawale A, Basu R, Fedak PMW, Sergio C, Freed D, Oudit GY, Kassiri Z*. Structural and nonstructural ECM remodeling in LVAD hearts. Translational Research, 172:30-44, 2016. Abstract
  • Fan D, Takawale A, Shen M, Wang W, Wang X, Basu R, Oudit GY, Kassiri Z*. Cardiomyocyte ADAM17 is essential in post-myocardial infarction recovery by triggering angiogenesis. Circulation: Heart Failure. 8(5):970-9, 2015. Abstract
  • Shen M, Lee J, Basu R, Sakamuri S, Wang X, Fan D, Kassiri Z*. Divergent Role of Matrix Metalloproteinase 2 in Pathogenesis of Thoracic Aortic Aneurysm. Arteriosclerosis, Thrombosis and Vascular Biology, 35(4):888-98, 2015. Received an Editorial. Abstract
  • Takawale A, Fan D, Basu R, Shen M, Parajuli N, Wang W, Wang X, Oudit GY, Kassiri Z*. Myocardial recovery from ischemia-reperfusion is compromised in the absence of tissue inhibitor of metalloproteinase 4. Circulation: Heart Failure, 7(4):652-62 (PMID: 24842912), 2014. Abstract
  • Lee J, Shen M, Parajuli N, Oudit GY, McMurtry MS, Kassiri Z*. Gender-dependent aortic remodeling in patients with bicuspid aortic valve-associated thoracic aortic aneurysm. Journal of Molecular of Medicine. 92(9):939-49. 2014 (PMID: 24893666). Abstract
  • Fan D, Takawale A, Basu R, Patel V, Lee J, Kandalam V, Wang X, Oudit GY, Kassiri Z*. Differential role of TIMP2 and TIMP3 in cardiac hypertrophy, fibrosis and diastolic dysfunction. Cardiovascular Research; 103(2):268-80 2014 (PMID: 24692173). Received an Editorial. Abstract
  • Wang Z, Famulski K, Lee J, Das SK, Wang X, Halloran P, Oudit GY, Kassiri Z*. Divergent roles of TIMP2 and TIMP3 in early renal tubulointerstitial injury. Kidney International. 85(1):82-93. 2014. Abstract
  • Basu R, Lee J, Morton JS, Takawale A, Fan D, Kandalam V, Wang X, Davidge ST, Kassiri Z*. TIMP3 is the primary TIMP to regulate agonist-induced vascular remodeling and hypertension. Cardiovascular Research. 98(3):360-71, 2013. Abstract
  • Basu R, Fan D, Kandalam V, Das SK, Lee J, Wang X, Baldwin T, Oudit GY, Kassiri Z*. Loss of tissue inhibitor of metalloproteinse-3 leads to abdominal aortic aneurysm formation in response to Angiotensin II: broad MMP inhibition rather than specific MMP inhibition as an effective treatment approach. Journal of Biological Chemistry, 287(53):44083-96, 2012. Abstract
  • Basu R, Lee J, Wang Z, Fan D, Patel VB, Das SK, Liu GC, John R, Scholey JW, Oudit GY, Kassiri Z*. Loss of TIMP3 selectively exacerbates diabetic nephropathy. American Journal of Physiology: Renal Physiology, 303(9):F1341-52, 2012. Abstract
  • Kandalam V, Basu R, Abraham T, Wang X, Awad A, Wang W, Lopaschuk GD, Maeda N, Oudit GY, Kassiri Z*. Early activation of matrix metalloproteinases underlies the exacerbated systolic and diastolic dysfunction in mice lacking TIMP3 following myocardial infarction. American Journal of Physiology: Heart and Circulatory Physiology. 299(4):H1012-23, 2010. Abstract
  • Kandalam V, Basu R, Abraham T, Wang X, Soloway P, Jaworski D, Oudit GY, Kassiri Z*. TIMP2-deficiency accelerates adverse post-myocardial infarction remodeling because of enhanced MT1-MMP activity despite lack of MMP2 activation. Circulation Research, 5; 106(4):796-808, 2010. Abstract