Necroptosis in asthma: a critical driver of immune dysregulation and airway remodeling

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Asthma is characterized by chronic inflammation and structural remodeling, which are inadequately explained by the traditional Th2 immunity model.
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Necroptosis, a regulated form of cell death, plays a significant role in asthma by driving inflammation and airway remodeling.
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Triggers such as allergens and pollutants activate necroptosis in specific cell types, leading to the release of damage-associated molecular patterns.
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The asthmatic airway environment promotes necroptosis due to oxidative stress and the presence of inflammatory cytokines.
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Current evidence on necroptosis in asthma primarily comes from preclinical models, highlighting a gap in translating findings to human disease.

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