Transcriptome sequencing study of pyroptosis pathways related to chronic obstructive pulmonary disease
Chronic obstructive pulmonary disease (COPD) is characterized by persistent airway inflammation and progressive airflow limitation. In this transcriptome sequencing study, we established cellular models of COPD using bronchial epithelial cells to elucidate the molecular events linking increased NOD1 expression to inflammatory cell death (pyroptosis). Transcriptomic and functional analyses revealed that NOD1 promotes pyroptosis in COPD via the FOXA1-NLRP3 signaling axis, with the PI3K-Akt pathway mediating these effects. Mechanistically, NOD1 suppresses FOXA1, leading to upregulation of NLRP3 and enhanced release of pro-inflammatory cytokines IL-18 and IL-1beta. Knockdown of NOD1 alleviated pyroptosis and improved cell survival, effects that were reversed by NLRP3 overexpression. In conclusion, our transcriptome sequencing findings identify the NOD1-FOXA1-NLRP3 axis as a key driver of pyroptosis in COPD, advancing our understanding of the disease's pathogenesis and highlighting potential molecular targets for therapeutic intervention.