Published November 2, 2020 - More info
Chronic obstructive pulmonary disease (COPD) involves aberrant airway inflammatory responses to cigarette smoke (CS) that are associated with epithelial cell dysfunction, cilia shortening, and mucociliary clearance disruption. Exposure to CS reduced cilia length and induced autophagy in vivo and in differentiated mouse tracheal epithelial cells (MTECs). Autophagy-impaired (
Hilaire C. Lam, Suzanne M. Cloonan, Abhiram R. Bhashyam, Jeffery A. Haspel, Anju Singh, J. Fah Sathirapongsasuti, Morgan Cervo, Hongwei Yao, Anna L. Chung, Kenji Mizumura, Chang Hyeok An, Bin Shan, Jonathan M. Franks, Kathleen J. Haley, Caroline A. Owen, Yohannes Tesfaigzi, George R. Washko, John Quackenbush, Edwin K. Silverman, Irfan Rahman, Hong Pyo Kim, Ashfaq Mahmood, Shyam S. Biswal, Stefan W. Ryter, Augustine M.K. Choi
Original citation: J Clin Invest. 2013;123(12):5212–5230. https://doi.org/10.1172/JCI69636
Citation for this corrigendum: J Clin Invest. 2020;130(11):6189. https://doi.org/10.1172/JCI143863
During the preparation of this manuscript, two panels of Figure 9B were inadvertently duplicated, resulting in an incorrect image for the ES group. The correct panel is below.
The authors regret the error.
See the related article at Histone deacetylase 6–mediated selective autophagy regulates COPD-associated cilia dysfunction.