ReviewFrontiers in immunology2025
Iron homeostasis and macrophage polarization in pulmonary fibrosis: mechanisms and therapeutic perspectives.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed.
- The inflammatory-autophagy-NETs axis in renal fibrosis: mechanistic crosstalk and pathological feed-forward amplification loops.Molecular and cellular biochemistry · 2026Review
- Iron and the lung: emerging roles of iron metabolism in pulmonary disease pathogenesis and therapy.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Si Ni Powder enhances chemotherapy efficacy in sleep-deprived breast cancer via modulation of the tumor microenvironment.Translational cancer research · 2026Article
- Review
- Iron homeostasis and macrophage polarization in oral squamous cell carcinoma: mechanisms and therapeutic perspectives.Frontiers in immunology · 2026Review
- Recent understanding of immunometabolic remodeling in pulmonary macrophages: homeostasis, chronic respiratory diseases, and therapeutic targeting.Frontiers in pharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic progressive and fatal interstitial lung disease with limited therapeutic options. Recent evidence highlights dysregulated iron metabolism in macrophages as a critical yet underrecognized driver of disease progression. Excess iron accumulation functions as a signaling cue that promotes macrophage polarization toward the pro-fibrotic M2 phenotype through pathways such as HIF-1α/IL-10/STAT6, contributing to aberrant tissue repair, myofibroblast activation, and excessive extracellular matrix (ECM) deposition. This review synthesizes current findings on the mechanistic interplay between iron homeostasis and macrophage phenotypic switching in IPF and evaluates emerging therapeutic strategies that target iron availability, including iron chelators, ferroportin modulators, and targeted nanocarrier delivery systems. While these approaches show promise, challenges remain regarding specificity, off-target effects, and systemic toxicity. By integrating mechanistic insights with translational advances, this review underscores the therapeutic potential of targeting the macrophage-iron axis and outlines how precision medicine-based interventions may offer novel avenues for effective IPF treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.