Mechanisms involved in the prevention of cardiac fibrosis through a low-salt diet in metabolic syndrome
Project funded in 2018 by the French Society of Nutrition (20,000 euros) and by the Fondation de l’Avenir in 2022 (36,000 euros).
Metabolic syndrome is characterized by the presence of at least three of the following factors: abdominal obesity, dyslipidemia, high blood pressure, and impaired glucose tolerance, all of which increase the risk of cardiovascular and metabolic diseases. Our team investigates the metabolic and cardiovascular/renal consequences of metabolic syndrome using a rat model fed a fructose-enriched diet (Oudot et al., Kidney Int, 2013; Rugale et al., Ann Cardiol Angiol, 2013). When this diet is combined with an angiotensin II infusion, the animals develop insulin resistance and hypertension, similar to metabolic syndrome in humans, along with the development of cardiac fibrosis (Jover et al., Biochim Biophys Acta, 2017), which causes diastolic dysfunction. Interestingly, these abnormalities can be prevented when sodium is completely removed from the animals’ diet to provide a strict sodium-restricted diet.
Our goal is to study the mechanisms involved in preventing cardiac fibrosis in metabolic syndrome through a low-sodium diet, in order to open up new therapeutic and/or diagnostic avenues for better managing the cardiac dysfunction resulting from this fibrosis. We had previously identified that innate immunity is modulated in this model. We are now exploring two new pathways: the role of adaptive immunity and the gut microbiota, as well as the role of the endothelial-mesenchymal transition. In particular, we are studying proteins newly identified in the laboratory as potential targets for cardiac fibrosis.
People involved in the project:
- Caroline Desmetz, MCU (project manager)
- Anne-Dominique Lajoix, PU
- Solène Darlet, Research Technician
- Mohammed Mimouni, Ph.D. candidate
