ArticleEMBO molecular medicine2020
Reprogramming of profibrotic macrophages for treatment of bleomycin-induced pulmonary fibrosis.
Article in EMBO molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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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.
The trial behind it
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Who cites it
48 citing papers in PubMed, 101 citations in OpenAlex.
- Alveolar type II cell therapy ameliorates pulmonary fibrosis by reprogramming macrophage activation.Inflammation and regeneration · 2026Article
- Innate Immune-Cloaked Microgel-Coated Mesenchymal Stromal Cells Reverse Persistent Pulmonary Fibrosis via Reparative Macrophages.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Recent understanding of immunometabolic remodeling in pulmonary macrophages: homeostasis, chronic respiratory diseases, and therapeutic targeting.Frontiers in pharmacology · 2026Review
- von Willebrand Factor Deficiency Inhibits Endothelial-to-Mesenchymal Transition to Attenuate Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2025Article
- Scar wars: the viral menace.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- Transcriptomic Plasticity of Human Alveolar Macrophages Revealed by Single-Cell RNA Sequencing Following Drug Exposure: Implications for Therapeutic Development.International journal of molecular sciences · 2025Article
- Article
- NLRP3 inflammasome-mediated disruption of mitochondrial homeostasis in alveolar macrophages contributes to ozone-induced acute lung inflammatory injury.Acta biochimica et biophysica Sinica · 2025Article
- Folate receptor β performs an immune checkpoint function in activated macrophages.Frontiers in immunology · 2025Article
- The Intersection between Immune System and Idiopathic Pulmonary Fibrosis-A Concise Review.Fibrosis (Hong Kong, China) · 2025Article
- CXCL11 reprograms M2-biased macrophage polarization to alleviate pulmonary fibrosis in mice.Cell & bioscience · 2024Article
- Targeted liposomes for macrophages-mediated pulmonary fibrosis therapy.Drug delivery and translational research · 2024Article
- Study on the efficacy of early treatment with pirfenidone on the lung function of patients with idiopathic pulmonary fibrosis.World journal of clinical cases · 2024Article
- Macrophages and HLA-Class II Alleles in Multiple Sclerosis: Insights in Therapeutic Dynamics.International journal of molecular sciences · 2024Review
- Emerging roles of ferroptosis in pulmonary fibrosis: current perspectives, opportunities and challenges.Cell death discovery · 2024Review
- The guardians of pulmonary harmony: alveolar macrophages orchestrating the symphony of lung inflammation and tissue homeostasis.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- 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
- Advances in macrophage-myofibroblast transformation in fibrotic diseases.Frontiers in immunology · 2024Review
- SGK1 aggravates idiopathic pulmonary fibrosis by triggering H3k27ac-mediated macrophage reprogramming and disturbing immune homeostasis.International journal of biological sciences · 2024Article
- Tumor-specific activation of folate receptor beta enables reprogramming of immune cells in the tumor microenvironment.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
Fibrotic diseases cause organ failure that lead to ~45% of all deaths in the United States. Activated macrophages stimulate fibrosis by secreting cytokines that induce fibroblasts to synthesize collagen and extracellular matrix proteins. Although suppression of macrophage-derived cytokine production can halt progression of fibrosis, therapeutic agents that prevent release of these cytokines (e.g., TLR7 agonists) have proven too toxic to administer systemically. Based on the expression of folate receptor β solely on activated myeloid cells, we have created a folate-targeted TLR7 agonist (FA-TLR7-54) that selectively accumulates in profibrotic macrophages and suppresses fibrosis-inducing cytokine production. We demonstrate that FA-TLR7-54 reprograms M2-like fibrosis-inducing macrophages into fibrosis-suppressing macrophages, resulting in dramatic declines in profibrotic cytokine release, hydroxyproline biosynthesis, and collagen deposition, with concomitant increases in alveolar airspaces. Although nontargeted TLR7-54 is lethal at fibrosis-suppressing doses, FA-TLR7-54 halts fibrosis without evidence of toxicity. Taken together, FA-TLR7-54 is shown to constitute a novel and potent approach for treating fibrosis without causing dose-limiting systemic toxicities.
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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.