Biocommunication in Cardio-Metabolic Health

Research topic

Cardiovascular disease, type 2 diabetes, and obesity are often associated in the same individual, in a specific context known as (cardio)metabolic syndrome. This syndrome 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 affects 537 million people worldwide (IDF Atlas, 2022), and the increase in mortality from cardiovascular disease, which accounts for 30% of deaths worldwide (GBD 2015 Mortality and Causes of Death Collaborators, Lancet, 2016). However, the pathophysiological mechanisms underlying the development of metabolic syndrome and associated risk factors are still 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 developed below, the common denominator will be metabolic dysfunction in animals, whether genetic (Zucker and ZDF) or nutritional (fructose diet or HFD) in origin, or in humans. In this particular context, research will focus on the mechanisms involved in certain cardiovascular dysfunctions (fibrosis, calcification), as well as metabolic alterations (inflammation of adipose tissue 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 renal failure.

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

Our objective is to investigate how factors produced by visceral and peripancreatic adipose tissue (lipid derivatives, cytokines, chemokines, miRNA) can influence the functioning 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 synthetic compounds that could have beneficial effects against the metabolic and/or cardiovascular disorders associated with type 2 diabetes.