This work establishes the type 2 inflammation-ALOX15-15(S)-HETE-PPAR-γ axis as a key driver of impaired tissue remodeling in ECRSwNP through TGF-β1 suppression. These findings provide novel mechanistic insights into the inflammation-metabolism-remodeling interplay in CRSwNP and highlight promising therapeutic targets for this refractory condition.
Li et al. (2026) studied this question.