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

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

Automated summary

This study demonstrates that the inhibition of the specific isoform of Bone Morphogenetic Protein 1 (BMP1.3) by a monoclonal antibody can reduce cardiac fibrosis and provide cardioprotection through inhibiting the Transforming Growth Factor beta pathway and inducing BMP5. It suggests the therapeutic potential of anti-BMP1.3 antibodies in preventing cardiomyocyte apoptosis, reducing collagen deposition, and preserving cardiac function after ischemia.