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Editor’s summary Pulmonary fibrosis has limited therapeutic options, and a better understanding of the underlying biology of the disease could lead to previously unrecognized therapeutic targets. Ziehr et al. investigated monocarboxylate transporters (MCTs) 1 and 4 and their role in myofibroblast differentiation in experimental models of pulmonary fibrosis. In human cell models of pulmonary fibrosis, inhibition of MCT1 or MCT4 reduced myofibroblast differentiation.
Abstract The growth of antimicrobial resistance (AMR) has highlighted an urgent need to identify bacterial pathogenic functions that may be targets for clinical intervention. Although severe bacterial infections profoundly alter host metabolism, prior studies have largely ignored alterations in microbial metabolism in this context.
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