ArticleCommunications biology2026
Histone demethylase KDM7A negatively regulates fibrotic macrophage polarization and lung fibrosis progression.
Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed.
- Macrophage polarization plasticity in pulmonary fibrosis: a review from pathogenesis to therapeutic targeting.Inflammopharmacology · 2026Review
- Profibrotic macrophage populations and cell communications in pulmonary fibrosis.Journal of physiology and biochemistry · 2026Review
- From support to homeostatic licensing: the bidirectional fibroblast-macrophage circuit and its central role in tissue homeostasis and fibrosis.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Macrophage polarization shapes immune responses in inflammation and fibrosis, yet the epigenetic mechanisms restraining pathogenic states remain unclear. Here, we identify lysine-specific demethylase 7 A (KDM7A) as an epigenetic suppressor of a profibrotic macrophage (Fib-Mac). Using macrophage assays, single-cell RNA sequencing of Kdm7a-knockout mice, and lung tissue from fibrosis patients, we show that Kdm7a loss drives transcriptional and metabolic reprogramming toward Fib-Mac states. Kdm7a-knockout mice exhibit exacerbated bleomycin-induced lung fibrosis with the expansion of Fib-Mac populations. Mechanistically, we identify toll-like receptor 8 (TLR8) as a suppressor of Fib-Mac polarization whose expression is regulated by KDM7A via the repressive mark H3K27me2 at its enhancer. Notably, macrophage Kdm7a and Tlr8 expression declines with age in male mice, consistent with clinical risk patterns. These findings uncover an epigenetic mechanism restraining disease-driving macrophage states and suggest the KDM7A-TLR8 axis as a potential therapeutic target in fibrotic disorders.
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Registered trials
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