Scott Heximer (He/Him)
PhD
Professional Memberships
- Canadian Society for Atherosclerosis Thrombosis and Vascular Biology (Past-President)
As a graduate student, Dr. Heximer was part of the research team that discovered the RGS2 gene in Dr. Donald Forsdyke’s laboratory at Queen’s University [Siderovski et al. (1994) DNA Cell Biol]. He was the first to propose that RGS2 was a selective inhibitor of Gq signaling, and together with collaborators Dr. Ken Blumer (WUSTL) and Dr. John Hepler (Emory), proved this novel hypothesis [Heximer et al. (1997) PNAS]. Dr. Heximer’s groundbreaking follow-up work on the Rgs2 knockout mouse strain showed that RGS2 is a key regulator of VSMC signaling and blood pressure [Heximer et al, (2003) JCI]. As a young professor at the University of Toronto, Dr. Heximer’s research broadened to RGS4 and RGS5 as signal integrators in heart and blood vessels. He showed RGS4 is an important regulator of parasympathetic signaling, GIRK channel activity, and heart rate regulation in the sinoatrial node [Cifelli et al. (2008) Circ. Res.]. These works sparked further discoveries that implicate RGS4 dysfunction in the pathogenesis of atrial fibrillation and sick sinus node syndrome [Guasch et al. (2015) JACC]. Together with colleagues at the Ted Rogers Centre for Heart Failure, Dr. Heximer’s recent work aims to understand fibroblast heterogeneity and the potential role for unique cardiac fibroblast subpopulations in preclinical models of heart disease. His group identified changes in the proteome and transcriptome of cardiac fibroblasts located in the “healthy” tissue regions of ischemic hearts. Dr. Heximer’s group aims to understand the mechanisms by which these relative healthy regions are remodeled as damaged hearts decompensate into heart failure.
My laboratory is seeking research-motivated graduate and undergraduate students who want to work in a high-energy research environment within the Ted Rogers Centre for Heart Research. Our work explores the mechanistic implications of fibroblast activation in damaged hearts and seeks to identify new therapeutic strategies for the prevention of heart disease through manipulation of fibroblast signalling and function. We use cutting-edge molecular and biochemical techniques to study heart disease pathogenesis in preclinical models and human patient samples.
Faculty Appointments
Associate Professor, Department of Physiology
Member, Translational Biology and Engineering Program, Ted Rogers Centre for Heart Research