Fibrosis: integration of mechanical cues in cardiac remodelling

Myocardial infarction and local cell death result in formation of a scar that is essential for mechanical reinforcement of the damaged heart wall. At later times however, progressive fibrosis of adjoining tissue compromises heart function and contributes to subsequent heart failure. The cardiac fibroblasts are the main cell type that mediates fibrosis via conversion to myofibroblasts and extracellular matrix remodelling. Recent studies have suggested that, in healthy hearts, forces distribution is primarily uniaxial, whereas in injured hearts, increases in multi-axial components would be predictive of fibrosis.

This project will study the contribution of force distribution in fibrosis, both in vitro and in animal models of myocardial remodelling. To study this problem in vitro, Nicoals Baeyens recently developed a new methodology in which primary cardiac fibroblasts, suspended in 3D fibrin gels, replace the fibrin with tensed cell-derived matrix over about a week, mimicking the process at stake during myocardial infarction.


Physiology and Pharmacology Laboratory
Faculty of Medicine

Created on September 5, 2018