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This study employed a comprehensive proteomic and metabolomic analysis to characterize adaptive cellular mechanisms of priority pathogensEscherichia coli, Klebsiella pneumoniae, Enterococcus faecium, and Staphylococcus aureusunder sub-inhibitory concentrations of antibiotics

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Mdivi-1 treatment also effectively inhibited mitochondrial fission regulatory protein markers, Drp1(Ser616) phosphorylation, and mitochondrial fission protein 1 (Fis1) in skeletal muscles from D2-mdx mice, which resulted in reduced content of damaged and fragmented mitochondria

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