Moreover, Itch expression was increased in lung tissues, whereas TXNIP was markedly reduced in lung tissues, bronchoalveolar lavage fluid cells, and peripheral blood mononuclear cells from patients with COPD.<h4>Conclusion</h4>Accordingly, CS-induced oxidative stress promotes Itch-mediated TXNIP degradation, leading to NF-κB-driven inflammation in macrophages and potentially contributing to COPD pathogenesis. Here, ITCH is linked to chronic obstructive pulmonary disease.