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 accessAbstract
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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Citations
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1 retracted
Mitochondrial Localization and Function of Heme Oxygenase-1 in Cigarette Smoke–Induced Cell Death
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Self-citationDela Cruz, C. S., & Kang, M.-J. (2018) · Mitochondrion · doi:10.1016/j.mito.2017.12.001 · Cited by 255
“Later studies have revealed that mitochondrial NFPs are recognized by high-affinity formyl peptides receptors (FPRs) (Dahlgren et al., 2016).”
Cellular Metabolism in Lung Health and Disease
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Healy, C., Munoz-Wolf, N., Strydom, J., Faherty, L., Williams, N. C., Kenny, S., Donnelly, S. C., & Cloonan, S. M. (2021) · Respiratory Research · doi:10.1186/s12931-021-01722-y · Cited by 78
Self-citationSmoking-induced iron dysregulation in the lung
Zhang, W. Z., Butler, J. J., & Cloonan, S. M. (2019) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2018.07.024 · Cited by 62
Self-citationZhang, V., Nemeth, E., & Kim, A. (2019) · Pharmaceuticals · doi:10.3390/ph12010030 · Cited by 57
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
- Published
- 2016-01-11
- Volume
- 22
- Issue
- 2
- Pages
- 163-174
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W2255333206
- Cited by
- 257
- References
- 87
- FWCI
- 22.77
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
