EXPERIMENTAL MODEL

Miz1-deficient mice develop COPD

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.

Author information

Affiliations

Authors

Corresponding author

Correspondence to Alexandra Le Bras.

Rights and permissions

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Le Bras, A. Miz1-deficient mice develop COPD. Lab Anim 49, 290 (2020). https://doi.org/10.1038/s41684-020-0645-7

Download citation

Search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing