Muscle atrophy induced by SOD1G93A expression does not involve the activation of caspase in the absence of denervation.

摘要: The most remarkable feature of skeletal muscle is the capacity to adapt its morphological, biochemical and molecular properties in response several factors. Nonetheless, under pathological conditions, loses adaptability, leading atrophy or wasting. Several signals might function as physiopathological triggers atrophy. However, specific mechanisms underlying atrophic phenotype different conditions remain be fully elucidated. In this paper, we address involvement caspases induction experimental models amyotrophic lateral sclerosis (ALS) expressing mutant SOD1G93A transgene either locally ubiquitously. We demonstrate that SOD1G93A-mediated independent from caspase activity. particular, expression promotes a reduction phosphatidylinositol 3-kinase/Akt pathway associated with activation forkhead box O3. contrast, occurs later causally linked motor neuron degeneration, which exacerbation shift fiber-type composition. This study suggests induced by toxic effect apoptotic markers caspase-mediated apoptosis process activated upon denervation.