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

Slobodan Vukicevic, Andrea Colliva, Vera Kufner, Valentina Martinelli, Silvia Moimas, Simone Vodret, Viktorija Rumenovic, Milan Milosevic, Boris Brkljacic, Diana Delic-Brkljacic, Ricardo Correa, Mauro Giacca, Manuel Maglione, Tatjana Bordukalo-Niksic, Ivo Dumic-Cule and Serena Zacchigna ()
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Slobodan Vukicevic: University of Zagreb School of Medicine
Andrea Colliva: International Centre for Genetic Engineering and Biotechnology
Vera Kufner: University of Zagreb School of Medicine
Valentina Martinelli: International Centre for Genetic Engineering and Biotechnology
Silvia Moimas: International Centre for Genetic Engineering and Biotechnology
Simone Vodret: International Centre for Genetic Engineering and Biotechnology
Viktorija Rumenovic: University of Zagreb School of Medicine
Milan Milosevic: University of Zagreb School of Medicine
Boris Brkljacic: University Hospital Dubrava, University of Zagreb School of Medicine
Diana Delic-Brkljacic: Clinical Hospital Sisters of Mercy, University of Zagreb School of Medicine
Ricardo Correa: International Centre for Genetic Engineering and Biotechnology
Mauro Giacca: Surgery and Health Sciences, University of Trieste
Manuel Maglione: Center of Operative Medicine, Medical University of Innsbruck
Tatjana Bordukalo-Niksic: University of Zagreb School of Medicine
Ivo Dumic-Cule: University of Zagreb School of Medicine
Serena Zacchigna: International Centre for Genetic Engineering and Biotechnology

Nature Communications, 2022, vol. 13, issue 1, 1-11

Abstract: Abstract 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 β 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.

Date: 2022
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DOI: 10.1038/s41467-021-27622-9

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