ReviewInternational immunology2021
Macrophages in lung fibrosis.
Review in International immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
69 citing papers in PubMed, 115 citations in OpenAlex.
- Macrophage polarization plasticity in pulmonary fibrosis: a review from pathogenesis to therapeutic targeting.Inflammopharmacology · 2026Review
- Efferocytosis triggered proteomic reprogramming of macrophages reveals CD97 as a novel apoptotic receptor.Cell death and differentiation · 2026Article
- Mapping the dialogue: Decoding alveolar stem-niche interactions.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- 8-oxo-7,8-dihydroguanosine (8-oxo-Guo) drives pulmonary inflammatory pathways through pattern recognition receptors.Redox biology · 2026Article
- Repeated air pollution exposure predisposes to adverse outcomes from acute lung injury.Particle and fibre toxicology · 2026Article
- The transcriptome of CD14The European respiratory journal · 2026Article
- TRPML1 suppresses pulmonary fibrosis by limiting collagen and elastin deposition.The EMBO journal · 2026Article
- Oxidative Stress as a Mechanistic Link Between Severe Respiratory Viral Infection and Pulmonary Fibrosis.Biology · 2026Review
- Molecular and spatial specialization of lung interstitial macrophage subsets: beyond chemokines.Frontiers in immunology · 2026Article
- Interleukin-23 in lung and airway diseases: from pathogenesis to precision-guided therapeutic targeting.Frontiers in pharmacology · 2026Review
- Macrophage Actin Cytoskeleton in Chronic Rejection.Results and problems in cell differentiation · 2026Review
- Decoding fibrosis in nonresolvable COVID-19: a role for myeloid-specific HIF1A deletion.American journal of physiology. Cell physiology · 2025Article
- The clinical utility of elevated monocyte count in patients with fibrotic interstitial lung disease.ERJ open research · 2025Article
- Ex vivo lung-organoid model for aberrant basaloid cell induction and activation.Inflammation and regeneration · 2025Article
- Mitigation of radiation-induced esophageal fibrosis by macrophage-targeted phosphatidylserine-containing liposomes with partial PEGylation.Bioactive materials · 2025Article
- Modulating NLRP3 Inflammasomes in Idiopathic Pulmonary Fibrosis: A Comprehensive Review on Flavonoid-Based Interventions.Cell biochemistry and biophysics · 2025Review
- Research Progress on Anti-fibrotic Effects and Mechanisms of Tetrandrine.Chinese journal of integrative medicine · 2025Review
- M2 macrophage co-culture overrides viscoelastic hydrogel mechanics to promote IL6-dependent fibroblast activation.Cell biomaterials · 2025Article
- Inhibition of sphingosine 1-phosphate receptor 3 ameliorates bleomycin-induced pulmonary fibrosis by suppressing macrophage M2 polarization.Genes & diseases · 2025Article
- Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary fibrosis (PF) is a disease in which excessive extracellular matrix (ECM) accumulation occurs in the lungs, which induces thickening of the alveolar walls, ultimately leading to the destruction of alveolar structures and respiratory failure. Idiopathic PF, the cause of which is unknown, has a poor prognosis with a median survival of 2-4 years after diagnosis. There is currently no known curative treatment. The mechanism underlying PF is thought to be initiated by the dysfunction of type II alveolar epithelial cells, which leads to ECM overproduction through the activation of fibroblasts. In addition, it has been suggested that a variety of cells contribute to fibrotic processes. In particular, clinical and basic research findings examining the roles of macrophages suggest that they may be pivotal regulators of PF. In this review, we discuss the characteristics, functions and origins of subsets of macrophages involved in PF, including resident alveolar, interstitial and monocyte-derived macrophages.
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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 OpenQuestion graph.