Bone morphogenetic protein 1.3 inhibition decreases scar formation and supports cardiomyocyte survival after myocardial infarction (CROSBI ID 309725)
Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija
Podaci o odgovornosti
Vukičević, Slobodan ; Colliva, Andrea ; Kufner, Vera ; Martinelli, Valentina ; Moimas, Silvia ; Vodret, Simone ; Rumenović, Viktorija ; Milošević, Milan ; Brkljačić, Boris ; Delić-Brkljačić, Diana ; Correa, Ricardo ; Giacca, Mauro ; Maglione, Manuel ; Bordukalo Nikšić, Tatjana ; Dumić-Čule, Ivo ; Zacchigna, Serena
engleski
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 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.
BMP1.3 ; antibody ; ishemic heart disease ; collagen
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Podaci o izdanju
Povezanost rada
Temeljne medicinske znanosti