Mannix Auger-Messier, Ph. D.
Diabetes, Obesity, and Cardiovascular Complications Axis
Centre de recherche du CHUS
Department of Medicine | Division of Cardiology
Faculty of Medicine and Health Sciences
Université de Sherbrooke
Phone | 819 564-5239
E-Mail | Mannix.Auger-Messier@USherbrooke.ca
Elucidating the Molecular Basis of Heart Failure for a Better Treatment
The prevalence of heart failure continues to rise not only as a consequence of the prolonged life expectancy of men and women but also of the modern advances in interventional cardiology. Patients suffering from heart failure face increased complications, morbidity, and poor long-term prognosis. In addition to its social and personal tolls, heart failure also imposes an enormous economic burden to our healthcare system. Thus, improved and novel strategies for the treatment of heart failure are highly desirable.
In 2011, Doctor Auger-Messier joined the Division of Cardiology at the Université de Sherbrooke - Department of Medicine, and launched an independent research program aimed at discovering the molecular mechanisms underlying heart disease progression. Doctor Auger-Messier’s laboratory exploits a wide range of approaches ranging from molecular pharmacology to physiopathology studies of the heart in genetically modified mouse models.
His laboratory focuses on elucidating the mechanisms of action of MAPK p38, ADAP, and apelin/APJ signaling modules in cardiomyocytes. In the future, discoveries made in Doctor Auger-Messier’s laboratory are expected to lead to the development of novel diagnostic and therapeutic approaches that will modify the management and treatment of heart failure.
- Operating grant (2013-2017) from the Canadian Institutes of Health Research (CIHR); Principal investigator
- Discovery grant (2013-2018) from the Natural Sciences and Engineering Research Council of Canada (NSERC); Principal investigator
- Operating grant (2014-2016) from a donation of Merck, Sharpe & Dohme; Designated principal investigator
- Auger-Messier et al., (2013) Unrestrained p38 MAPK activation in Dusp1/4 double-null mice induces cardiomyopathy. Circ Res. 112(1): 48-56
Know-How & Opportunities for Collaboration
- Hypertrophy, dilation and heart failure
- Signaling mechanisms in cardiomyocytes
- Cardiac function measurement in transgenic mouse models
- Cardiomyopathy-induced murine models by specialized microsurgery techniques