FibroThera aims to fight against myocardial infarction (MI)-induced heart failure, a major human health problem with high socio-economic implications. In this project, we will abandon the traditional focus on protein-coding genes, but rather explore the noncoding RNA-mediated regulatory pathways.
FibroThera concept is based on the assumption that identifying the ncRNA specifically involved in MI-induced heart failure will increase the probability of finding new druggable therapeutic targets with clinical applicability, which can improve the quality of life in ischemic heart disease patients.
FibroThera will characterize the dynamics of cells contributing to fibrosis during post-MI cardiac repair and will propose solutions for limiting the adverse remodelling after MI.

 

The specific objectives of FibroThera are to: 

(i) Define the pro-fibrotic cell types sequentially involved in the post-MI repair and identify ncRNA candidates for modulation of cardiac fibrosis;
(ii) Identify cell-specific changes induced by Mesenchimal Stromal Cell therapy in fibrosis signalling cascades activated after MI;
(iii) Explore the function of activated fibroblasts and provide insights into the molecular mechanisms of cardiac fibrosis;
(iv) Explore miR-210-controlled pathways that interferes with MI-induced cardiac fibrosis in human and mouse samples.

 

In reaching these objectives, the team will work under the direct coordination of a highly specialized researcher in the field of ncRNA and will greatly benefit from his extensive network of collaborators. We will use innovative in vitro and in vivo models, high throughput RNA sequencing methods and relevant human samples for data validation.