Possible target for preventing fibrotic scar formation following acute myocardial infarction

Bone morphogenetic protein 1 (BMP1) was originally isolated from bone with other BMPs due to its affinity for heparin. While all other BMPs are members of the Transforming Growth Factor β (TGFβ) superfamily of growth factors, BMP1 is not an authentic member of the BMP protein family. Together with mammalian Tolloid Like protein 1 (mTLL-1) and mTLL-2, BMP1 comprise a small group of zinc- and calcium-dependent proteinases. Acute myocardial infarction (AMI) is the leading cause of death in developed countries which accounts for 13% of deaths worldwide. It was recently shown that inhibition of BMP1-3 reduces progression of fibrosis in chronic kidney disease and suggested that BMP1-3 is an important molecule for fibrogenesis. We hypothesize that inhibition of BMP1-3 represents future of therapeutic interventions in the heart tissue fibrosis following AMI. This novel approach aims to acquire the first candidate specific treatment for recuperating the heart function in patients with AMI.