ReviewJournal of inflammation research2026
Macrophage Phenotypic Plasticity and Inflammatory Mechanisms in Hyperoxia-Induced Lung Injury.
Review in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
4 authors.
Funding
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Abstract
Hyperoxia-induced lung injury is a prominent inflammatory complication encountered in neonatal and adult critical care, contributing to acute lung injury and bronchopulmonary dysplasia. Although oxidative stress is a primary initiating factor, accumulating evidence suggests that dysregulated immune responses, particularly those mediated by macrophages, critically influence disease progression and resolution. Macrophages exhibit remarkable phenotypic plasticity in response to hyperoxic stress, extending beyond the conventional pro-inflammatory and anti-inflammatory polarization framework. Recent advances, including single-cell transcriptomic analyses, have revealed substantial heterogeneity among macrophage subsets, highlighting inflammatory, metabolically reprogrammed, senescent, and pyroptotic phenotypes in hyperoxic lung injury. These phenotypic shifts are tightly regulated by inflammatory signaling pathways, immunometabolic alterations, and cellular stress responses. In this review, we summarize current evidence regarding macrophage phenotypic plasticity in hyperoxia-induced lung injury, with a focus on key inflammatory pathways, metabolic reprogramming, inflammasome activation, and emerging cell fate programs such as pyroptosis and cellular senescence. We further discuss macrophage-mediated intercellular communication with epithelial and endothelial cells and its contribution to persistent inflammation and impaired lung repair. By integrating these findings, this review aims to provide updated insights into macrophage-driven inflammatory mechanisms and to highlight potential avenues for therapeutic modulation in hyperoxic lung injury.
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