Autores: Leonardo Martins, Weslley Wallace Amorim, Marcos Fernandes Gregnani, Ronaldo de Carvalho Araújo, Fatimunnisa Qadri, Michael Bader & João Bosco Pesquero.
Abstract - Objective and design: After traumatic skeletal muscle injury, muscle healing is often incomplete and produces extensive fibrosis. Bradykinin (BK) reduces fibrosis in renal and cardiac damage models through the B2 receptor. The B1 receptor expression is induced by damage, and blocking of the kallikrein-kinin system seems to affect the progression of muscular dystrophy. We hypothesized that both kinin B1 and B2 receptors could play a differential role after traumatic muscle injury, and the lack of the B1 receptor could produce more cellular and molecular substrates for myogenesis and fewer substrates for fibrosis, leading to better muscle healing.