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Critical role for iron accumulation in the pathogenesis of fibrotic lung disease
The Journal of pathology, 2020-05, Vol.251 (1), p.49-62
Ali, Md Khadem
Kim, Richard Y
Brown, Alexandra C
Donovan, Chantal
Vanka, Kanth S
Mayall, Jemma R
Liu, Gang
Pillar, Amber L
Jones‐Freeman, Bernadette
Xenaki, Dikaia
Borghuis, Theo
Karim, Rafia
Pinkerton, James W
Aryal, Ritambhara
Heidari, Moones
Martin, Kristy L
Burgess, Janette K
Oliver, Brian G
Trinder, Debbie
Johnstone, Daniel M
Milward, Elizabeth A
Hansbro, Philip M
Horvat, Jay C
2020
Details
Autor(en) / Beteiligte
Ali, Md Khadem
Kim, Richard Y
Brown, Alexandra C
Donovan, Chantal
Vanka, Kanth S
Mayall, Jemma R
Liu, Gang
Pillar, Amber L
Jones‐Freeman, Bernadette
Xenaki, Dikaia
Borghuis, Theo
Karim, Rafia
Pinkerton, James W
Aryal, Ritambhara
Heidari, Moones
Martin, Kristy L
Burgess, Janette K
Oliver, Brian G
Trinder, Debbie
Johnstone, Daniel M
Milward, Elizabeth A
Hansbro, Philip M
Horvat, Jay C
Titel
Critical role for iron accumulation in the pathogenesis of fibrotic lung disease
Ist Teil von
The Journal of pathology, 2020-05, Vol.251 (1), p.49-62
Ort / Verlag
Chichester, UK: John Wiley & Sons, Ltd
Erscheinungsjahr
2020
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
Increased iron levels and dysregulated iron homeostasis, or both, occur in several lung diseases. Here, the effects of iron accumulation on the pathogenesis of pulmonary fibrosis and associated lung function decline was investigated using a combination of murine models of iron overload and bleomycin‐induced pulmonary fibrosis, primary human lung fibroblasts treated with iron, and histological samples from patients with or without idiopathic pulmonary fibrosis (IPF). Iron levels are significantly increased in iron overloaded transferrin receptor 2 (Tfr2) mutant mice and homeostatic iron regulator (Hfe) gene–deficient mice and this is associated with increases in airway fibrosis and reduced lung function. Furthermore, fibrosis and lung function decline are associated with pulmonary iron accumulation in bleomycin‐induced pulmonary fibrosis. In addition, we show that iron accumulation is increased in lung sections from patients with IPF and that human lung fibroblasts show greater proliferation and cytokine and extracellular matrix responses when exposed to increased iron levels. Significantly, we show that intranasal treatment with the iron chelator, deferoxamine (DFO), from the time when pulmonary iron levels accumulate, prevents airway fibrosis and decline in lung function in experimental pulmonary fibrosis. Pulmonary fibrosis is associated with an increase in Tfr1+ macrophages that display altered phenotype in disease, and DFO treatment modified the abundance of these cells. These experimental and clinical data demonstrate that increased accumulation of pulmonary iron plays a key role in the pathogenesis of pulmonary fibrosis and lung function decline. Furthermore, these data highlight the potential for the therapeutic targeting of increased pulmonary iron in the treatment of fibrotic lung diseases such as IPF. © 2020 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Sprache
Englisch
Identifikatoren
ISSN: 0022-3417
eISSN: 1096-9896
DOI: 10.1002/path.5401
Titel-ID: cdi_proquest_journals_2395700626
Format
–
Schlagworte
airway hyperresponsiveness
,
airway inflammation
,
airway remodeling
,
Airway Remodeling - drug effects
,
Animal models
,
Animals
,
Bleomycin
,
Bleomycin - pharmacology
,
Cell Proliferation
,
Cells, Cultured
,
collagen
,
Deferoxamine
,
Extracellular matrix
,
Extracellular Matrix - drug effects
,
Extracellular Matrix - pathology
,
Fibroblasts
,
Fibroblasts - drug effects
,
Fibroblasts - pathology
,
Fibrosis
,
Homeostasis
,
Humans
,
Idiopathic Pulmonary Fibrosis - drug therapy
,
Idiopathic Pulmonary Fibrosis - metabolism
,
Idiopathic Pulmonary Fibrosis - pathology
,
IPF
,
Iron
,
Iron - metabolism
,
Lung - drug effects
,
Lung - pathology
,
Lung diseases
,
lung function
,
Macrophages
,
Macrophages - drug effects
,
Macrophages - pathology
,
Mice, Knockout
,
Pathogenesis
,
Patients
,
Phenotypes
,
Pulmonary fibrosis
,
Respiratory function
,
Respiratory tract
,
Therapeutic targets
,
Transferrins
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