This study identifies the TF-FVIIa-PAR2 signalling complex as the main driver of inflammatory macrophage activity after myocardial infarction, leading to excessive fibrosis and cardiac dysfunction. Targeted blockade of this signalling pathway by genetic or antibody-based approaches reduces inflammation, promotes reparative macrophages and improves cardiac function and survival. This points to a promising new therapeutic option for the treatment of ischaemic heart disease.
Link to the publication: Macrophage-Expressed Coagulation Factor VII Promotes Adverse Cardiac Remodeling (Garlapati et al., Circulation Reseach, 2024)
Link to the news: New insights into the mechanisms of venous thrombosis harbour therapeutic potential
