| Abstract: | Idiopathic Pulmonary Fibrosis (IPF) is a form of interstitial lung disease (ILD), which is characterized by progressive dyspnea and a decline in lung function. The exact cause of IPF is unknown, however, a prevailing theory is that recurrent microinjuries to alveolar type II (AEC2) cells results in an altered dysfunctional phenotype, which drives the pathogenesis of the disease. In conjunction with this, iron has also been suggested to play a role in the development of IPF, with recent studies showing alterations of iron levels in the lungs of individuals with IPF. This study aimed to investigate whether iron is altered in in vivo and in vitro experimental models of IPF. Here, we show that iron levels decline in AEC2 cells isolated from experimental IPF models. These reduced intracellular iron levels were associated with AEC2 cell dysfunction and altered expression levels of cell senescence markers. Furthermore, restoration of iron in AEC2 cells was also shown to prevent bleomycin-induced mortality and injury in vivo . These findings highlight the potential role iron dyshomeostasis plays in driving disease pathogenesis and presents the manipulation of iron levels through iron supplementation as an interesting potential therapeutic target. |
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