Lung fibrosis enters the iron age†.

Iron is an essential nutrient for numerous cellular processes. However, excess iron in the lung (e.g. inhaled in pollution/cigarette smoke) can be harmful, acting as a catalyst in the formation of free radicals. Pulmonary iron content is therefore tightly regulated and alterations in iron metabolism have been associated with chronic lung disease. In particular, patients with idiopathic pulmonary fibrosis have been reported to have numerous aspects of dysfunctional iron metabolism in the lung, including increased iron levels, presence of iron-laden macrophages and iron-induced oxidative stress. In a recent issue of The Journal of Pathology, Ali et al showed a mechanistic link between iron accumulation and pulmonary fibrosis pathology. Using mouse models of iron overload, the authors showed that increased iron levels resulted in reduced lung function and worse pulmonary fibrosis upon lung injury by bleomycin. Treatment with inhaled iron chelator deferoxamine ameliorated pulmonary fibrosis and prevented lung function decline in vivo. This study highlights the importance of iron homeostasis in the lung and provides evidence of pulmonary iron overload contributing to the development and progression of pulmonary fibrosis.