ArticleCell communication and signaling : CCS2018
M2 macrophages promote myofibroblast differentiation of LR-MSCs and are associated with pulmonary fibrogenesis.
Article in Cell communication and signaling : CCS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.
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Who cites it
121 citing papers in PubMed, 194 citations in OpenAlex.
- Macrophage polarization plasticity in pulmonary fibrosis: a review from pathogenesis to therapeutic targeting.Inflammopharmacology · 2026Review
- Amniotic Mesenchymal Stromal Cell Administration Prevents and Stops Lung Fibrosis and Is Associated with Distinct Macrophage Signatures.Pharmaceutics · 2026Article
- BCL9 inhibition promotes fibroblast lipogenesis by regulating macrophage-fibroblast interactions to attenuate pulmonary fibrosis.Signal transduction and targeted therapy · 2026Article
- Vitronectin metabolically programs profibrotic macrophages in 3D cultures and idiopathic pulmonary fibrosis.Science advances · 2026Article
- Convergent Microenvironment Linking Idiopathic Pulmonary Fibrosis and Lung Cancer.Expert reviews in molecular medicine · 2026Review
- Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- An agent-based model suggests how senescent cell behavior and matrix mechanics drive pulmonary fibrosis in aged mice.bioRxiv : the preprint server for biology · 2026Article
- Profibrotic macrophage populations and cell communications in pulmonary fibrosis.Journal of physiology and biochemistry · 2026Review
- Discovery of key regulators in classical monocyte phenotypes linked to COVID-19 severity using single-cell multi-omics sequencing.iScience · 2026Article
- The role of immune cell crosstalk and signaling pathways in the pathogenesis of pulmonary fibrosis.Molecular biology reports · 2026Review
- Article
- From support to homeostatic licensing: the bidirectional fibroblast-macrophage circuit and its central role in tissue homeostasis and fibrosis.Frontiers in immunology · 2026Review
- Monocyte/Macrophage Subsets in the Peripheral Blood, Their Related Cytokines, and Circulating Markers of Fibrosis in Active Takayasu Arteritis and Longitudinal Changes Following Immunosuppressive Therapy.Journal of inflammation research · 2026Article
- Inflammatory Macrophages Associate With Tissue Injury and Fibrosis in a Mouse Model of Tuberculosis.The Journal of infectious diseases · 2025Article
- Intracellular Calcium as a Regulator of Polarization and Target Reprogramming of Macrophages.International journal of molecular sciences · 2025Review
- Radiation meets inflammation: NLRP3 inflammasome at the core of radiation-induced cardiac injury.Journal of translational medicine · 2025Review
- Inhalability and Bioactivity of Spray-Dried versus Pressurized Gas eXpanded Liquid Technology-Processed Yeast Beta-Glucan Microparticles for Anti-Fibrotic Therapies.Advanced healthcare materials · 2025Article
- Dynamic macrophage phenotypes in autoimmune and inflammatory rheumatic diseases.Nature reviews. Rheumatology · 2025Review
- CD206 and dust particles are prognostic biomarkers of progressive fibrosing interstitial lung disease associated with air pollutant exposure.Scientific reports · 2025Article
- Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis.Journal of respiratory biology and translational medicine · 2025Article
61 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIdiopathic pulmonary fibrosis (IPF) is a devastating disease characterized by the histopathological pattern of usual interstitial pneumonia and is associated with a high mortality rate. Recently, lung resident mesenchymal stem cells (LR-MSCs) have been identified as an important contributor to myofibroblast activation in pulmonary fibrosis. Macrophages are also believed to play a critical role in pulmonary fibrosis. However, the underlying connections between LR-MSCs and macrophages in the pathogenesis of pulmonary fibrosis are still elusive.
methodsIn this study, we investigated the interaction between LR-MSCs and macrophages using a bleomycin-induced mouse pulmonary fibrosis model and a coculture system.
resultsHere, we show that blocking pulmonary macrophage infiltration attenuated bleomycin-induced pulmonary fibrosis. In addition, as determined by flow cytometry, we discovered that the recruited macrophages in fibrotic lungs of bleomycin-treated mice were mainly M2 macrophages. In particular, we found that M2, rather than M1 macrophages, promoted myofibroblast differentiation of LR-MSCs. Moreover, we demonstrated that suppression of the Wnt/β-catenin signaling pathway could attenuate myofibroblast differentiation of LR-MSCs induced by M2 macrophages and bleomycin-induced pulmonary fibrosis. Tissue samples from IPF patients confirmed the infiltration of M2 macrophages and activation of Wnt/β-catenin signaling pathway.
conclusionIn summary, this study furthered our understanding of the pulmonary fibrosis pathogenesis and highlighted M2 macrophages as a critical target for treating pulmonary fibrosis.
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