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THE AUBERT G. LAB

Our research aims to understand the concepts and mechanisms which underly the metabolic basis of cardiovascular disease.

SULFONYLUREA RECEPTOR

October 1, 2018

SUR2 (Abcc9) is the regulatory component of the major ATP-sensitive potassium (KATP) in the myocardium.  Notably, human mutations in the ABCC9 gene, which encodes SUR2, are known to cause diverse cardiac phenotypes including dilated cardiomyopathy. These findings support the hypothesis that loss of functional SUR2 in the adult heart contributes to the progressive pathologic metabolic and functional remodeling that leads to end-stage heart failure. We study the effect of the absence or overexpression of SUR2 on cardiomyocyte metabolism and heart function in response to pressure overload, and delineate which SUR2 subunit is crucial for cardiomyocyte metabolic regulation.  The rationale is to better understand SUR2 regulation of cardiomyocyte metabolism as a new target to manipulate cardiac energy expenditure in heart failure.  

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HFPEF AND OBESITY

October 1, 2018

Heart Failure with preserved ejection fraction (HFpEF) is the most common phenotype of heart failure and approximatively 50% of patient with HFpEF are obese. Independently of other risk factors, obese people are at increased risk of heart failure with a greater attributable risk of obesity to HFpEF than heart failure with reduced ejection fraction (HFrEF). Alarmingly, new treatment strategies have lagged significantly behind the growing prevalence of heart failure and recent clinical study have failed to prove benefits to HFpEF patients of drugs effective in HFrEF. Thus, HFpEF is one of the largest unmet needs in cardiovascular medicine and there is an extensive need for new therapeutic strategies that target the fundamental derangement that occurs in the development of HFpEF. The pathophysiology of HFpEF is complex, and this syndrome has been increasingly characterized as heterogenous. A better phenotyping of patients into common pathophysiological groups has been proposed as a tool to better treat HFpEF. Obesity-related HFpEF display unique clinical and pathophysiological feature and could be considered as a specific HFpEF phenotype.  We are studying this unique phenotype as it pertain to obesity, microbioma, circulating short chain fatty acid (SCFA), parasympathetic activity and cardiac diastolic function.

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OPEN POSITION

October 1, 2018

A full time funded postdoc position is available starting December 1st 2018
Our Research focus on cardiometabolism and the role of cardiac metabolism plasticity in health and disease. We routinely use hIPSC, CRSIPR, mice model of heart disease, proteomics and metabolomics.  
Applicants must have a Ph.D. in Biology, Physiology, Biochemistry or a related discipline and demonstrated a strong interest in the understanding of the metabolic basis of disease. A strong  team working ability is mandatory. A background in either, analysis of -omics dataset, CRISPR or hIPSC is preferred.

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CONTACT US

Thanks for your interest in our research. Get in touch with us for any questions or comments regarding our work and publications. We’d love to hear from you.

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