Dr. Mansoor Husain
Director | University Health Network
Toronto, ON, CANADA
As a specialist in cardiovascular disease and nuclear cardiology, Dr. Husain brings outstanding clinical and research credentials to UHN
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Biography
Dr. Mansoor Husain was Director of Research at the Peter Munk Cardiac Centre at UHN and Director of the Heart & Stroke/Richard Lewar Centre of Excellence at the University of Toronto. In addition, he was affiliated with the McEwen Centre for Regenerative Medicine and recently served as President of the Canadian Hypertension Society.
Dr. Husain was awarded the Gold Medal in Medicine for his MD degree from the University of Alberta in 1986. His subsequent clinical and research training was completed at St. Michael's Hospital, UHN, MIT and Harvard Medical School. His own research program focuses on molecular regulation of vascular smooth muscle cell proliferation and differentiation, cardiovascular tissue-specific transgene regulation for studies of molecular pathophysiology, and collaborative studies of genetic and experimental models of cardiovascular disease. His program also involves research in clinical and experimental cardiovascular imaging and trials in acute cardiac care.
Industry Expertise (4)
Research
Health Care - Services
Health Care - Providers
Health and Wellness
Areas of Expertise (6)
Clinical Research
Heart Research
Research Management
Vascular Smooth Muscle Cell Biology
Vasomotor Physiology
Transgenic Mouse Models of Cardiovascular Disease
Education (1)
University of Alberta: Doctor of Medicine (MD), Medicine 1986
Gold Medalist Alpha Omega Alpha
Media Appearances (1)
Mansoor Husain, Director, Toronto General Research Institute
Research Media Ltd online
2013-02-14
Toronto General Hospital has a long history of ground-breaking discoveries. Mansoor Husain, Director of its research arm, details some of the exciting developments emanating from the Institute
Articles (5)
Perlecan Heparan Sulfate Proteoglycan Is a Critical Determinant of Angiogenesis in Response to Mouse Hind-Limb Ischemia
PubMed.gov
2014-06-01
Perlecan is a heparan sulfate proteoglycan (HSPG) constituent of the extracellular matrix with roles in cell growth, differentiation, and angiogenesis. The role of the HS side chains in regulating in vivo angiogenesis after hind-limb ischemia is unknown.
Enhanced proliferation and altered calcium handling in RGS2-deficient vascular smooth muscle cells
PubMed.gov
2014-05-01
Abstract Context: Regulator of G-protein signaling-2 (RGS2) inhibits Gq-mediated regulation of Ca2+ signalling in vascular smooth muscle cells (VSMC). Objective: RGS2 knockout (RGS2KO) mice are hypertensive and show arteriolar remodeling.
p27 protein protects metabolically stressed cardiomyocytes from apoptosis by promoting autophagy
PubMed.gov
2014-06-01
p27(Kip1) (p27), a key regulator of cell division, has been implicated in autophagy of cancer cells. However, its role in autophagy, the evolutionarily conserved catabolic process that enables cells to remove unwanted proteins and damaged organelles, had not been examined in the heart. Here we report that ectopic delivery of a p27 fusion protein (TAT-p27) was sufficient to induce autophagy in neonatal rat ventricular cardiomyocytes in vitro, under basal conditions and after glucose deprivation.
http://www.ncbi.nlm.nih.gov/pubmed/24725934
PubMed.gov
2014-04-01
The role of Group X secreted phospholipase A2 (GX-sPLA2) during influenza infection has not been previously investigated. We examined the role of GX-sPLA2 during H1N1 pandemic influenza infection in a GX-sPLA2 gene targeted mouse (GX(-/-)) model and found that survival after infection was significantly greater in GX(-/-) mice than in GX(+/+) mice.
Antiatherothrombotic effects of dipeptidyl peptidase inhibitors
PubMed.gov
2014-05-01
Atherothrombotic cardiovascular events are a leading cause of morbidity and mortality in patients with type 2 diabetes (T2D). A number of factors beyond hyperglycemia contribute to this increased risk of cardiovascular events in T2D, including elevated blood pressure, dyslipidemia, inflammation, endothelial dysfunction, and enhanced platelet activation.
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