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Cited by 257

The DOI matches its Crossref record; 87 of the 87 references it cites were found in a registry or an index.

Mitochondrial iron chelation ameliorates cigarette smoke–induced bronchitis and emphysema in mice

Open access
Cloonan, Suzanne M, Glass, Kimberly, Laucho-Contreras, Maria E, Bhashyam, Abhiram R, Cervo, Morgan, Pabón, Maria A, Konrad, Csaba, Polverino, Francesca, Siempos, Ilias I, Perez, Elizabeth, Mizumura, Kenji, Ghosh, Manik C, Parameswaran, Harikrishnan, Williams, Niamh C, Rooney, Kristen T, Chen, Zhi-Hua, Goldklang, Monica P, Yuan, Guo-Cheng, Moore, Stephen C, Demeo, Dawn L, Rouault, Tracey A, D'Armiento, Jeanine M, Schon, Eric A, Manfredi, Giovanni, Quackenbush, John, Mahmood, Ashfaq, Silverman, Edwin K, Owen, Caroline A, Choi, Augustine M K·2016·Nature Medicine
DOI 10.1038/nm.4021
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Abstract

Chronic obstructive pulmonary disease (COPD) is linked to both cigarette smoking and genetic determinants. We have previously identified iron-responsive element–binding protein 2 (IRP2) as an important COPD susceptibility gene and have shown that IRP2 protein is increased in the lungs of individuals with COPD. Here we demonstrate that mice deficient in Irp2 were protected from cigarette smoke (CS)-induced experimental COPD. By integrating RNA immunoprecipitation followed by sequencing (RIP-seq), RNA sequencing (RNA-seq), and gene expression and functional enrichment clustering analysis, we identified Irp2 as a regulator of mitochondrial function in the lungs of mice. Irp2 increased mitochondrial iron loading and levels of cytochrome c oxidase (COX), which led to mitochondrial dysfunction and subsequent experimental COPD. Frataxin-deficient mice, which had higher mitochondrial iron loading, showed impaired airway mucociliary clearance (MCC) and higher pulmonary inflammation at baseline, whereas mice deficient in the synthesis of cytochrome c oxidase, which have reduced COX, were protected from CS-induced pulmonary inflammation and impairment of MCC. Mice treated with a mitochondrial iron chelator or mice fed a low-iron diet were protected from CS-induced COPD. Mitochondrial iron chelation also alleviated CS-induced impairment of MCC, CS-induced pulmonary inflammation and CS-associated lung injury in mice with established COPD, suggesting a critical functional role and potential therapeutic intervention for the mitochondrial-iron axis in COPD.

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Metadata

Authors
Cloonan, S. M., Glass, K., Laucho-Contreras, M. E., Bhashyam, A. R., Cervo, M., Pabón, M. A., Konrad, C., Polverino, F., Siempos, I. I., Perez, E., Mizumura, K., Ghosh, M. C., Parameswaran, H., Williams, N. C., Rooney, K. T., Chen, Z.-H., Goldklang, M. P., Yuan, G.-C., Moore, S. C., Demeo, D. L., Rouault, T. A., D'Armiento, J. M., Schon, E. A., Manfredi, G., Quackenbush, J., Mahmood, A., Silverman, E. K., Owen, C. A., & Choi, A. M. K.
Venue
Nature Medicine
Publisher
Springer Science and Business Media LLC
Published
2016-01-11
Volume
22
Issue
2
Pages
163-174
ISSN
  • 1078-8956 (ISSN-L)
  • 1546-170X
DOI
10.1038/nm.4021
OpenAlex
W2255333206
Cited by
257
References
87
FWCI
22.77
Type
journal article
Language
en
Open access
green

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