Do-Umehara, H.C. et al. Sci. Adv. 6, eabb7238 (2020)
Persistent inflammation in the lung epithelium has been linked to the development of chronic obstructive pulmonary disease (COPD), but the factors regulating the inflammatory response in COPD remain largely unknown. Several animal models of COPD are available, but the development of new experimental models could expand our understanding of COPD pathogenesis.
A new study describes the generation of mice with lung epithelial cell–specific loss of function of Miz1, a transcriptional repressor of NF-κB signaling. The mice developed a COPD-like phenotype with progressive alveolar destruction, airway remodeling and increased inflammation, which could be rescued by NF-κB/RelA haploinsufficiency. These findings suggest that the loss of Miz1 contributes to COPD pathogenesis by triggering NF-κB–dependent inflammation.