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In macrophages isolated from mouse myocardium after infarction and in bone marrow-derived macrophages (BMDMs) exposed to ACs in vitro, the concentration of intracellular fatty acids and mitochondrial oxygen consumption upregulated -oxidation and OXPHOS, leading to the generation of NAD+ and promoting the activation of SIRT1 (a sirtuin) that targets PPAR activity and genes related to mitochondrial biogenesis [71, 72]

Here, we investigated for the first time the therapeutic efficacy of the GLP-1R agonist semaglutide in a mouse model of INAD

Antioxidant glutathione neutralises reactive oxygen species that generate oxidative stress in the brain and elsewhere in the body

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