ArticleCells2023
A Novel CD206 Targeting Peptide Inhibits Bleomycin-Induced Pulmonary Fibrosis in Mice.
Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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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
35 citing papers in PubMed, 41 citations in OpenAlex.
- Renal denervation attenuates cardiac fibrosis and improves left ventricular function in rats with myocardial infarction.Scientific reports · 2026Article
- Nintedanib Lacks Efficacy in a Spirometry-Confirmed and Bleomycin-Induced Mouse Model of Idiopathic Pulmonary Fibrosis.Basic & clinical pharmacology & toxicology · 2026Article
- Lung injury, oxidative stress, and impaired functioning in a model of prolonged ozone exposure in female mice are associated with macrophage proinflammatory and profibrotic activation and altered bioenergetics.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Macrophages Are Critical Inducers of Bleomycin-Induced Fibrosis in a Systemic Scleroderma Model.The American journal of pathology · 2026Article
- Baricitinib alleviates interstitial lung disease in CIA mice by inhibiting macrophage polarization and increase exosomal miR-126a-3p with anti-fibrotic activityFrontiers in pharmacology · 2026Article
- The immune dysregulation of fibrosis: insights into immune-fibrotic crosstalk and potential therapeutic targets.Frontiers in immunology · 2026Review
- Protective effect of cannabinoid type II receptor ligand on bleomycin-induced pulmonary fibrosis in mice.PloS one · 2026Article
- RP-182 alleviated obstruction-induced renal fibrosis by reprogramming CD206Frontiers in pharmacology · 2026Article
- Influenza A Virus after Radiotherapy Amplifies Lung Injury and Monocyte-derived Macrophage Responses.American journal of respiratory cell and molecular biology · 2026Article
- Modulation of infiltrating CD206The European respiratory journal · 2025Article
- 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
- Article
- CD206 and dust particles are prognostic biomarkers of progressive fibrosing interstitial lung disease associated with air pollutant exposure.Scientific reports · 2025Article
- PET Imaging of CD206 Macrophages in Bleomycin-Induced Lung Injury Mouse Model.Pharmaceutics · 2025Article
- Unpacking the anti-fibrotic arsenal: molecular mechanisms and therapeutic translation of MSC-derived exosomes in pulmonary fibrosis.Frontiers in immunology · 2025Review
- Immunomodulatory biomaterials for treating chronic inflammation at mucosal sites.npj biomedical innovations · 2025Review
- CD206Thorax · 2024Article
- A macrophage-collagen fragment axis mediates subcutaneous adipose tissue remodeling in mice.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Chensinin-1b Alleviates DSS-Induced Inflammatory Bowel Disease by Inducing Macrophage Switching from the M1 to the M2 Phenotype.Biomedicines · 2024Article
- Metabolism-driven glycosylation represents therapeutic opportunities in interstitial lung diseases.Frontiers in immunology · 2024Review
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
Abstract
Activated M2-polarized macrophages are drivers of pulmonary fibrosis in several clinical scenarios, including Idiopathic Pulmonary Fibrosis (IPF). In this study, we investigated the effects of targeting the CD206 receptor in M2-like macrophages with a novel synthetic analogue of a naturally occurring Host Defense Peptide (HDP), RP-832c, to decrease profibrotic cytokines. RP-832c selectively binds to CD206 on M2-polarized bone marrow-derived macrophages (BMDM) in vitro, resulting in a time-dependent decrease in CD206 expression and a transient increase in M1-macrophage marker TNF-α. To elucidate the antifibrotic effects of RP-832c, we used a murine model of bleomycin (BLM)-induced early-stage pulmonary fibrosis. RP-832c significantly reduced fibrosis in a dose-dependent manner, and decreased CD206, TGF-β1, and α-SMA expression in mouse lungs. Similarly, in an established model of lung fibrosis, RP-832c significantly decreased lung fibrosis and significantly decreased inflammatory cytokines TNF-α, IL-6, IL-10, IFN-γ, CXCL1/2, and fibrosis markers TGF-β1 and MMP-13. In comparison with the FDA-approved drugs Nintedanib and Pirfenidone, RP-832c exhibited a similar reduction in fibrosis compared to Pirfenidone, and to a greater extent than Nintedanib, with no apparent toxicities observed. In summary, our findings showed that inhibiting the profibrotic alternatively activated M2-like macrophages using a novel peptide, RP-832c, could reduce BLM-induced pulmonary fibrosis in mice, warranting the therapeutic potential of this peptide for patients with pulmonary fibrosis.
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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.