Epithelial cell–specific loss of function of Miz1 causes a spontaneous COPD-like phenotype and up-regulates Ace2 expression in mice

作者：Hanh Chi Do-Umehara, Cong Chen, Qiao Zhang, Alexander V. Misharin, Hiam Abdala‐Valencia, S. Marina Casalino‐Matsuda, Paul A. Reyfman, Kishore R. Anekalla, Francisco J. González-González, Marc A. Sala, Chao Peng, Ping Wu, Catherine C. L. Wong, Ravi Kalhan, Ankit Bharat, Harris Perlman, Karen M. Ridge, Jacob I. Sznajder, Peter H. S. Sporn, Navdeep S. Chandel, Jindan Yu, Xiang‐Dong Fu, Irina Petrache, Rubin M. Tuder, G. R. Scott Budinger, Jing Liu · 发表于：Science Advances · 年份：2020 · DOI：10.1126/sciadv.abb7238 · 被引用次数：23 · 研究领域：Chronic Obstructive Pulmonary Disease (COPD) Research、Neonatal Respiratory Health Research、Neuroscience of respiration and sleep

-deficient mice. Miz1 protein levels are reduced in the lungs from patients with COPD, and in the lungs of mice exposed to chronic cigarette smoke. Our data suggest that Miz1 down-regulation-induced sustained activation of NF-κB-dependent inflammation in the lung epithelium is sufficient to induce progressive lung and airway destruction that recapitulates features of COPD, with implications for COVID-19.