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Furthermore, from a purely conceptual standpoint, one might postulate that metabolic reprogramming signals carried by these exosomes could disrupt the metabolic plasticity of recipient cells, blocking their adaptive transition from oxidative phosphorylation to glycolysis and thereby imprisoning cells in a metabolic phenotype highly sensitive to cuproptosis ( We must strongly emphasize that this exosome-mediated cuproptosis propagation network is currently entirely conceptual and lacks direct empirical evidence in ARDS models