Ontology highlight
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.Material and methods
To test this hypothesis, tibialis anterior muscles of kinin receptor knockout animals were subjected to traumat
SUBMITTER: Martins L
PROVIDER: S-EPMC10499706 | biostudies-literature | 2023 Aug
REPOSITORIES: biostudies-literature