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Prolyl hydroxylase-1 negatively regulates IkappaB kinase-beta, giving insight into hypoxia-induced NFkappaB activity

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For instance, nanotherapeutics engineered to inhibit ACSL4 (a key mediator of ferroptosis) while activating regulatory T cells (Treg)which modulate excessive immune responsescould synergistically address both oxidative stress and immune dysregulation, two core drivers of asthma progression

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