The mitochondria-targeted antioxidant AntiOxCIN4 mitigates cardiac oxidative/nitrosative stress in the amyotrophic lateral sclerosis SOD1G93A mouse
Débora Mena, Fernando Cagide, Sofia Benfeito, Katarzyna Michalik, Luís Grilo, Daniela F. Silva, Paulo Pinheiro, Elisabete Ferreiro, José Teixeira, Filomena Silva, Fernanda Borges, Paulo J. Oliveira, Ana I. Duarte · FENS Forum 2024
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease, defined by motor neuron loss, muscle paralysis, and death. ALS individuals often present alterations in cardiovascular function that may evolve into heart failure and death. Mitochondrial dysfunction and oxidative stress are key players in ALS pathophysiology. Thus, improving mitochondrial function and/or antioxidant capacity constitute promising therapeutic strategies to delay ALS progression. We hypothesized that mitochondria-targeted antioxidant AntiOxCIN4 can reduce cardiac oxidative/nitrosative stress in SOD1G93A ALS mice