ArticleInternational journal of molecular sciences2024
Single-Cell RNA Sequencing Reveals Monocyte-Derived Interstitial Macrophages with a Pro-Fibrotic Phenotype in Bleomycin-Induced Pulmonary Fibrosis.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Role of Monocytes in the Natural History of Idiopathic Pulmonary Fibrosis: A Systematic Literature Review.International journal of molecular sciences · 2025Pooled it
- Inhibition of macrophage migration inhibitory factor attenuates bleomycin-induced murine pulmonary fibrosis via the MAPK pathway.Respiratory research · 2026Article
- Testosterone protects from metabolic syndrome-associated lung dysfunction in a high-fat diet rabbit model.Endocrinology · 2026Article
- Longitudinal Single-Cell RNA-seq Profiling of Lung Cell Phenotypes, Signaling, and Cross-talk During Fibrosis Resolution.bioRxiv : the preprint server for biology · 2026Article
- Pharmacovigilance study and genetic target prediction analysis of FDA adverse event reporting system for anticancer drug-associated interstitial lung disease.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- A single-cell atlas and Shiny-based framework for murine lung injury and remodeling.Frontiers in bioinformatics · 2026Article
- The gene regulatory networks shaping macrophage plasticity and altered function in fibrosis.Frontiers in immunology · 2026Review
- Decoding macrophage heterogeneity in the pulmonary fibrosis lung cancer transition.Frontiers in immunology · 2026Review
- Microbiome-innate immune crosstalk in acute exacerbation of idiopathic pulmonary fibrosis: an amplification framework.Frontiers in immunology · 2026Review
- From support to homeostatic licensing: the bidirectional fibroblast-macrophage circuit and its central role in tissue homeostasis and fibrosis.Frontiers in immunology · 2026Review
- Toxicity of BEP chemotherapy in germ cell tumors: focus on immune-mediated bleomycin pulmonary toxicity in comparison with EP and VIP regimens.Frontiers in immunology · 2026Review
- Article
- Macrophage Phenotypic Plasticity and Inflammatory Mechanisms in Hyperoxia-Induced Lung Injury.Journal of inflammation research · 2026Review
- Relationship between SPP1 (Osteopontin) and extracellular matrix dynamics: a comprehensive review.Frontiers in medicine · 2025Review
- Immunological mechanisms underlying fibrotic diseases via single-cell technologies.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease with limited effective therapies. Interstitial macrophages (IMs), especially those derived from monocytes, play an unknown role in IPF pathogenesis. By using single-cell RNA sequencing (scRNA-seq), bleomycin (BLM)-induced pulmonary fibrosis mouse lungs were analyzed to characterize the cellular landscape and heterogeneity of macrophages in this model. scRNA-seq was used to identify distinct interstitial macrophage subpopulations in fibrotic lungs, with monocyte-derived macrophages exhibiting a pro-fibrotic gene expression profile enriched in wound healing, extracellular matrix (ECM) remodeling, and pro-fibrotic cytokine production functions. A pseudotime analysis revealed that IMs originated from monocytes and differentiated along a specific trajectory. A cell-cell communication analysis demonstrated strong interactions between monocyte-derived interstitial macrophages (Mo-IMs) and fibroblasts through the transforming growth factor beta (TGFβ), secreted phosphoprotein 1 (SPP1), and platelet-derived growth factor (PDGF) signaling pathways. Flow cytometry validated the presence and expansion of Mo-IMs subpopulations in BLM-treated mice. This study reveals the cellular heterogeneity and developmental trajectory of lung macrophages in early BLM-induced pulmonary fibrosis, highlighting the crucial role of Mo-IMs with a pro-fibrotic phenotype in IPF pathogenesis via interactions with fibroblasts. Targeting these specific macrophage subpopulations and associated signaling pathways may provide novel therapeutic strategies for IPF.
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