ReviewAmerican journal of physiology. Cell physiology2023
Monocytes and macrophages: emerging mechanisms and novel therapeutic targets in pulmonary fibrosis.
Review in American journal of physiology. Cell physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 3 of them syntheses that pooled it.
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
53 citing papers in PubMed, 3 syntheses or guidelines pooled it, 71 citations in OpenAlex.
- Molecular Systems Architecture of Fibrotic Lung Microenvironment in Idiopathic Pulmonary Fibrosis.Cells · 2026Pooled it
- The Role of Monocytes in the Natural History of Idiopathic Pulmonary Fibrosis: A Systematic Literature Review.International journal of molecular sciences · 2025Pooled it
- The Intriguing Connection Between the Gut and Lung Microbiomes.Pathogens (Basel, Switzerland) · 2024Pooled it
- Antifibrotic monocyte activation by nanoparticles resolves murine pulmonary fibrosis.Biomaterials · 2026Article
- Precision nanomedicine for pulmonary diseases: from molecular targeting to clinical translation.Signal transduction and targeted therapy · 2026Review
- Ginseng as a Functional Food Intervention for Interstitial Lung Disease: A Review of the Benefits and Molecular Mechanisms.Food science & nutrition · 2026Review
- Norcantharidin attenuates amiodarone-induced pulmonary fibrosis via modulating miRNA-30a/GSK-3β/β-catenin and oxidative-inflammatory pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Unlocking the potential of mRNA nanomedicines for comprehensive fibrosis therapy.Molecular therapy. Nucleic acids · 2026Review
- Cell-specific gene expression plasticity in response to hypoxia promotes high-altitude adaptive evolution.Science China. Life sciences · 2026Article
- The transcriptome of CD14The European respiratory journal · 2026Article
- Inactivation Rap2a in Endothelial Cell Prevents Pulmonary Fibrosis by Regulating Immune Microenvironment Through MAP4K4-VCAM1 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Flavin adenine dinucleotide increases antioxidant availability and protects neonatal C57Bl6 lungs from high oxygen induced lung injury.American journal of physiology. Cell physiology · 2026Article
- Emerging Therapies in Pulmonary Fibrosis.Pulmonary therapy · 2026Review
- Assessment of mosaic loss of chromosome Y in pulmonary fibrosis reveals limited association with susceptibility or disease severity.BMJ open respiratory research · 2026Article
- Pulmonary fibrosis: evolving therapeutic pipeline.BMJ medicine · 2026Review
- Article
- CAR T cell therapy for fighting IPF: perspectives on a living drug.Frontiers in immunology · 2026Review
- Influenza A Virus after Radiotherapy Amplifies Lung Injury and Monocyte-derived Macrophage Responses.American journal of respiratory cell and molecular biology · 2026Article
- Article
- FTO inhibition attenuates renal fibrosis by downregulating ferroptosis activator ACSL4 and profibrotic factor TGFBI.iScience · 2025Article
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary fibrosis results from a plethora of abnormal pathogenetic events. In idiopathic pulmonary fibrosis (IPF), inhalational, environmental, or occupational exposures in genetically and epigenetically predisposed individuals trigger recurrent cycles of alveolar epithelial cell injury, activation of coagulation pathways, chemoattraction, and differentiation of monocytes into monocyte-derived alveolar macrophages (Mo-AMs). When these events happen intermittently and repeatedly throughout the individual's life cycle, the wound repair process becomes aberrant leading to bronchiolization of distal air spaces, fibroblast accumulation, extracellular matrix deposition, and loss of the alveolar-capillary architecture. The role of immune dysregulation in IPF pathogenesis and progression has been underscored in the past mainly after the disappointing results of immunosuppressant use in IPF patients; however, recent reports highlighting the prognostic and mechanistic roles of monocytes and Mo-AMs revived the interest in immune dysregulation in IPF. In this review, we will discuss the role of these cells in the onset and progression of IPF, as well as potential targeted therapies.
Indexed as
Identifiers
What OpenQuestion holds
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.