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L G Mantovani reports support for the present manuscript from the Italian Ministry of Health to Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Istituto Auxologico Italiano, Milano, Italy

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63 Prolonged skeletal muscle inactivity promotes mitochondrial dysfunction, resulting in increase in mitochondrial ROS production and leading to protracted oxidative stress and disturbed redox signaling, 64 which can exacerbate IR through multiple pathways such as JNK and NF-B pathways (Fig

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