A new study has assessed the role of iron overload and ferroptosis in the pathogenesis of idiopathic pulmonary fibrosis (IPF).
The study, published in Redox Biology, observed that iron accumulation and ferroptosis lead to fibroblast activation in IPF, and that ferroptosis inhibitors could be an effective treatment approach.
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They then observed that treatment with liproxstatin-1 inhibited the accumulation of lipid peroxides and ameliorated bleomycin- and LPS-induced ferroptosis and the subsequent development of fibrosis in the mice. Furthermore, the iron chelator deferoxamine inhibited fibroblast activation and reduced collagen deposition in the mice with bleomycin-induced fibrosis.
The authors attribute these effects to the prevention of iron accumulation in both the early inflammatory phase and the fibrotic phase, indicating both ferroptosis and iron homeostasis are essentially involved in the onset and progression of pulmonary fibrosis.
The evidence obtained suggests that treatment strategies that target ferroptosis and disorders of iron homeostasis could be effective in diseases associated with iron overload, including pulmonary fibrosis.
Pei Z, Qin Y, Fu X, et al. Inhibition of ferroptosis and iron accumulation alleviates pulmonary fibrosis in a bleomycin model. Redox Biol. Published online November 2022. doi:10.1016/j.redox.2022.102509