Bone morphogenetic protein 1.3 inhibition decreases scar formation and supports cardiomyocyte survival after myocardial infarction

• DOI: 10.1038/s41467-021-27622-9
• Publication Date: 2022-01-10T11:02:59Z
• Authors: Slobodan Vukicevic; Andrea Colliva; Vera Kufner; Valentina Martinelli; Silvia Moimas; Simone Vodret; Viktorija Rumenovic; Milan Milosevic; Boris Brkljacic; Diana Delic-Brklj...; Ricardo Correa; Mauro Giacca; Manuel Maglione; Tatjana Bordukalo...; Ivo Dumic-Cule; Serena Zacchigna
• Keywords: Cardioprotection; Cardiac Fibrosis; Myofibroblast

Despite the high prevalence of ischemic heart diseases worldwide, no antibody-based treatment currently exists. Starting from evidence that a specific isoform Bone Morphogenetic Protein 1 (BMP1.3) is particularly elevated in both patients and animal models myocardial infarction, here we assess whether its inhibition by monoclonal antibody reduces cardiac fibrosis. We find this collagen deposition cross-linking, paralleled enhanced cardiomyocyte survival, vivo primary cultures cells. Mechanistically, show anti-BMP1.3 inhibits Transforming Growth Factor β pathway, thus reducing myofibroblast activation inducing cardioprotection through BMP5. Collectively, these data support therapeutic use antibodies to prevent apoptosis, reduce preserve function after ischemia.