ArticleProceedings of the National Academy of Sciences of the United States of America2022
Nanoparticle targeting of de novo profibrotic macrophages mitigates lung fibrosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 91 citations in OpenAlex.
- Materialogenetics: an emerging and promising framework for cell-specific genetic manipulation.Bioactive materials · 2026Article
- Alveolar Macrophages: Development, Respiratory Homeostasis, Signal Pathways, Diseases, and Therapeutic Opportunities.MedComm · 2026Review
- Precision nanomedicine for pulmonary diseases: from molecular targeting to clinical translation.Signal transduction and targeted therapy · 2026Review
- Polyplex of peptide-mannan and RNA for intranasal delivery of TGF-β siRNA in treatment of pulmonary fibrosis.Bioactive materials · 2026Article
- Enhancing anti-fibrotic therapy: nanomedicine approaches to overcome current limitations.Materials today. Bio · 2026Review
- Monocyte-mediated mechanisms in idiopathic pulmonary fibrosis: opportunities for early intervention.Apoptosis : an international journal on programmed cell death · 2026Review
- Nanocarrier-Enabled siRNA Therapy for Pulmonary Fibrosis: Pharmacological Rationale, Delivery Barriers, and Translational Opportunities.International journal of nanomedicine · 2026Review
- Targeted RNA Therapy Reprograms Fibrotic Macrophages to Reverse Pulmonary Fibrosis.Theranostics · 2026Article
- Polypeptide sono-adjuvant for ultrasound-activatable regulation of innate immunity and cancer vaccination therapy.Nature communications · 2025Article
- Macrophage-specific therapy blocks the lung's mechanosensitive immune response to alveolar distension.JCI insight · 2025Article
- Chronic Graft-versus-host Disease, Part 1: How Preclinical Models Shape Our Understanding of Biology and Pave the Way for Future Therapeutic Interventions.Transplantation · 2025Review
- Effects of beta and gamma radiation sterilization on growth factor-loaded nanoparticles: an innovative approach for osteoarticular disorders treatment.Drug delivery and translational research · 2025Article
- Modulating NLRP3 Inflammasomes in Idiopathic Pulmonary Fibrosis: A Comprehensive Review on Flavonoid-Based Interventions.Cell biochemistry and biophysics · 2025Review
- Inhibition of Circadian Rhythm GeneEnvironment & health (Washington, D.C.) · 2025Article
- M2 Macrophages-Based Immunotherapy: A New Therapeutic Approach in Liver Fibrosis.Advanced pharmaceutical bulletin · 2025Review
- Targeting alveolar macrophages: a promising intervention for pulmonary infection and acute lung injury.Cellular & molecular biology letters · 2025Review
- BHLHE40 contributes to allergic asthma progression in mice through NRTN downregulation in macrophages.Communications biology · 2025Article
- YAP/TAZ are crucial regulators of macrophage-mediated pulmonary inflammation and fibrosis after bleomycin-induced injury.The European respiratory journal · 2025Article
- The crucial function of IDO1 in pulmonary fibrosis: From the perspective of mitochondrial fusion in lung fibroblasts and targeted molecular inhibition.Acta pharmaceutica Sinica. B · 2025Article
- 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
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The pathogenesis of lung fibrosis involves hyperactivation of innate and adaptive immune pathways that release inflammatory cytokines and growth factors such as tumor growth factor (TGF)β1 and induce aberrant extracellular matrix protein production. During the genesis of pulmonary fibrosis, resident alveolar macrophages are replaced by a population of newly arrived monocyte-derived interstitial macrophages that subsequently transition into alveolar macrophages (Mo-AMs). These transitioning cells initiate fibrosis by releasing profibrotic cytokines and remodeling the matrix. Here, we describe a strategy for leveraging the up-regulation of the mannose receptor CD206 in interstitial macrophages and Mo-AM to treat lung fibrosis. We engineered mannosylated albumin nanoparticles, which were found to be internalized by fibrogenic CD206+ monocyte derived macrophages (Mo-Macs). Mannosylated albumin nanoparticles incorporating TGFβ1 small-interfering RNA (siRNA) targeted the profibrotic subpopulation of CD206+ macrophages and prevented lung fibrosis. The findings point to the potential utility of mannosylated albumin nanoparticles in delivering TGFβ-siRNA into CD206+ profibrotic macrophages as an antilung fibrosis strategy.
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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 Socratic graph.