A schematic illustrating how iron levels influence cell fate and lung repair in the alveoli. In iron deficiency, alveolar epithelial cells experience metabolic stress, resulting in mitochondrial dysfunction and decreased surfactant production. This stress reduces their capacity to self-renew and differentiate. In alveolar macrophages, stress triggers premature senescence and impairs iron recycling, which weakens phagocytosis and immune responses, leading to immune exhaustion during chronic iron deficiency. Conversely, under normal iron levels, alveolar cells manage iron flux, reducing senescence and ferroptosis, while maintaining immune function. Iron overload causes oxidative stress, mitochondrial dysfunction, ferroptosis, epithelial loss, and tissue damage, impairing regeneration and differentiation. Excess iron in macrophages hampers antimicrobial activity, promotes inflammation and fibrosis, and raises the risk of chronic lung disease. Created in BioRender.