ReviewFrontiers in cell and developmental biology2026
Ferroptosis in smoke inhalation injury: from mechanisms to potential therapeutic targets.
Review in Frontiers in cell and developmental biology, 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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10 authors.
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Abstract
Smoke inhalation injury (SII) is a prevalent yet underrecognized cause of acute respiratory failure and longer-term airway-alveolar remodeling after fires, wildfires, and industrial accidents. Beyond inflammation and generic oxidative stress, accumulating evidence supports ferroptosis as a mechanistically distinct, self-amplifying axis that can sustain epithelial/endothelial damage, barrier breakdown, and maladaptive repair. Ferroptosis is driven by iron-dependent phospholipid peroxidation and collapse of membrane redox homeostasis, and in SII is promoted by iron dyshomeostasis including heme/hemoglobin-derived iron and ferritinophagy, PUFA-phospholipid remodeling, and failure of antioxidant checkpoints centered on the System Xc
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