Search

Collagen I is the most abundant type of intramuscular collagen. Lysyl oxidase promotes collagen cross-link formation, which helps stabilize the extracellular matrix. Furthermore, matrix metalloproteinases, responsible for collagen degradation, maintain typical muscle structure and function through remodeling. Although it is well known that aging leads to delayed recovery of muscle fibers, the impact of aging on the remodeling of intramuscular collagen is not well understood. In this study, we investigated the impact of aging on collagen remodeling during muscle injury recovery using young and old mouse models. Muscle injury was induced in the right tibialis anterior (TA) muscle of male C57BL/6J mice [aged 21 weeks (young) and 92 weeks (old)] using intramuscular cardiotoxin injection, with the left TA serving as a sham with saline injection. Following a one-week recovery period, aging was found to delay the recovery of the fiber cross-sectional area. The intensity and area of immunoreactivity for collagen I were significantly increased in old mice compared to young mice post-injury. Additionally, Lox expression and the number of LOX (+) cells in the extracellular matrix significantly increased in old mice compared to young mice post-injury. Furthermore, Mmp9 and MMP9 expression levels after muscle injury were higher in old mice than in young mice. These results suggest that muscle injury in old mice can lead to increased collagen I accumulation, enhanced collagen cross-link formation, and elevated MMP9 expression compared to young mice. [ABSTRACT FROM AUTHOR]