Trimetazidine Improves Mitochondrial Dysfunction in SOD1^G93A Cellular Models of Amyotrophic Lateral Sclerosis through Autophagy Activation.

ABSTRACT: Amyotrophic Lateral Sclerosis (ALS) is considered the prototype of motor neuron disease, characterized by motor neuron loss and muscle waste. A well-established pathogenic hallmark of ALS is mitochondrial failure, leading to bioenergetic deficits. So far, pharmacological interventions for the disease have proven ineffective. Trimetazidine (TMZ) is described as a metabolic modulator acting on different cellular pathways. Its efficacy in enhancing muscular and cardiovascular performance has been widely described, although its molecular target remains elusive. We addressed the molecular mechanisms underlying TMZ action on neuronal experimental paradigms. To this aim, we treated murine SOD1^G93A-model-derived primary cultures of cortical and spinal enriched motor neurons, as well as

SUBMITTER: Salvatori I 

PROVIDER: S-EPMC10970050 | biostudies-literature | 2024 Mar

REPOSITORIES: biostudies-literature