Biocommunication in Cardiometabolic Medicine

Research topic

Cardiovascular disease, type 2 diabetes, and obesity often co-occur in the same individual, within a specific condition known as (cardio)metabolic syndrome. This condition affects more than a quarter of the world’s population and 90% of people with type 2 diabetes. Metabolic syndrome encompasses physiological and metabolic abnormalities (insulin resistance, hypertension, dyslipidemia, obesity) that increase the risk of cardiovascular events (3 times higher), type 2 diabetes (5 times higher), and all-cause mortality (1.5 times higher) (Mottillo et al., J Am Coll Cardiol, 2010). It goes hand in hand with the sharp increase in the prevalence of diabetes, which is estimated to affect 537 million people worldwide (IDF Atlas, 2022), and the rise in mortality from cardiovascular diseases, which account for 30% of all causes of death globally (GBD 2015 Mortality and Causes of Death Collaborators, Lancet, 2016). However, the pathophysiological mechanisms underlying the development of metabolic syndrome and its associated risk factors remain poorly understood.
The Unit’s project focuses on biocommunication between the cardiovascular/renal axis and metabolic tissues, building on the results generated and expertise acquired during the previous five-year period. In the research areas outlined below, the common denominator will be metabolic dysfunction in animals, whether of genetic origin (Zucker and ZDF) or nutritional origin (fructose diet or HFD), or in humans. In this specific context, research will focus on the mechanisms involved in certain cardiovascular dysfunctions (fibrosis, calcification), as well as in metabolic alterations (adipose tissue inflammation and β-cell function).

Three areas are therefore being developed:

  • Cardiac fibrosis and vascular calcification in metabolic dysfunction:

Our goal is to better understand the molecular mechanisms involved in the development of cardiac fibrosis (extracellular matrix, microbiota) and vascular calcification (cytokines, RAGE pathway) that occur during metabolic dysfunction, whether or not associated with hypertension and kidney failure.

  • Biocommunication between adipose tissue and pancreatic β-cells in metabolic dysfunction:

Our goal is to investigate how factors produced by visceral and peripancreatic adipose tissue (lipid derivatives, cytokines, chemokines, and miRNAs) may influence the function of pancreatic β-cells during the development of type 2 diabetes.

  • Screening and evaluation of new compounds of therapeutic interest:

Our goal here is to identify either naturally occurring substances or synthetically derived compounds that may have beneficial effects against the metabolic and/or cardiovascular disorders associated with type 2 diabetes.