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Respiratory disorders

Ironing out smoking-related airway disease

Nature volume 531, pages 586–587 (2016)Cite this article

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Lack of the protein IRP2 in mice prevents organelles called mitochondria from accumulating toxic levels of iron in response to smoke exposure. This discovery links environmental and genetic risk factors for a chronic lung disease.

Since 2008, chronic lower-respiratory diseases have been the third most common cause of death in the United States1 — the most prevalent of these being chronic obstructive pulmonary disease (COPD). The name COPD encompasses a complex range of traits associated with irreversible airflow obstruction. These include destruction of the lungs' alveoli (emphysema), excessive mucus production in the airways (chronic bronchitis) and defects in a process called mucociliary clearance, in which cellular protrusions called cilia move mucus out of the lung, along with entrapped irritants. Initially thought to be a smokers' disease, many risk factors for COPD are now known, both environmental and genetic2,3,4. Writing in Nature Medicine, Cloonan et al.5 reveal how one genetic risk factor, increased expression of iron-responsive element-binding protein 2 (IRP2), contributes to disease by modulating iron levels in organelles called mitochondria, ultimately affecting the ability of cilia to protect the lungs from environmental pollutants and pathogens.

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Figure 1: Regulation of mucociliary clearance in chronic obstructive pulmonary disease (COPD).

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Authors and Affiliations

  1. Thomas J. Mariani is in the Division of Neonatology and the Pediatric Molecular and Personalized Medicine Program, University of Rochester Medical Center, Rochester, New York 14642, USA.,

    Thomas J. Mariani

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  1. Thomas J. Mariani
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Correspondence to Thomas J. Mariani.

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Mariani, T. Ironing out smoking-related airway disease. Nature 531, 586–587 (2016). https://doi.org/10.1038/nature17309

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