Muscle fibrosis was evident in our CKD mice and PLA treatment significantly reduced the mRNA levels of TGF- β1 and its downstream targets in their muscle and renal tissues.
Our findings suggest that TGF-beta1 is involved in CMD muscle fibrosis, but differently from what we observed in DMD muscles as it seems not to be the major player in connective tissue proliferation.
Expression of transforming growth factor-beta 1 in the early stages of Duchenne muscular dystrophy may be critical in initiating muscle fibrosis and antifibrosis treatment could slow progression of the disease, increasing the utility of gene therapy.