| Grant number: | 17/24051-4 |
| Support Opportunities: | Regular Research Grants |
| Duration: | February 01, 2018 - January 31, 2020 |
| Field of knowledge: | Biological Sciences - Morphology - Anatomy |
| Principal Investigator: | Maria Julia Marques |
| Grantee: | Maria Julia Marques |
| Host Institution: | Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil |
| Associated researchers: | Elaine Minatel ; Humberto Santo Neto ; Samara Camaçarí de Carvalho |
Abstract
Duchenne muscular dystrophy (DMD) is a progressive degenerative disease that affects skeletal and cardiac muscles, leading to death due to cardiorespiratory failure. Although there is no cure for this disease, recent gene and drug therapies are being able to slow down the progression of the disease, improving life quality and duration. So far, corticoids, such as deflazacort, are still the choice therapy for DMD but, due to their side-effects, there is an urgent need for alternative therapies. We previously demonstrated positive effects of omega-3 in the mdx mice model of DMD. Omega-3 is already in use to treat several inflammatory diseases, in humans. Considering that corticoid therapy is still the best choice, we combined omega-3 and deflazacort and the promising results motivated us to go further on omega-3 mechanisms and effects. In the present study, we will evaluate the G protein-coupled receptors GPR40 and GPR120, which are free fatty acid receptors suggested to mediate omega-3 effects in other systems, and the roles of autophagy, as potential targets of omega-3 and deflazacort, in the diaphragm, quadriceps and cardiac muscles of the dystrophin-deficient mdx mouse. (AU)
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