ArticleAdvanced materials (Deerfield Beach, Fla.)2024
Nanomaterial-Mediated Reprogramming of Macrophages to Inhibit Refractory Muscle Fibrosis.
Article in Advanced materials (Deerfield Beach, Fla.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- FAP-targeted ROS-responsive nanoparticles delivering siBTF3 modulate the TME to enhance immunotherapy in colorectal cancer.Journal of translational medicine · 2026Article
- Targeting Apolipoprotein E4 rescues photoreceptor degeneration by inhibiting the disease-associated microglia activation in experimental retinal detachment.Journal of neuroinflammation · 2026Article
- Cell-Free DNA-Based Theranostics for Inflammatory Disorders.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Cationic nanoparticles-enabled mouthwash combats precancerous oral mucosal inflammation.Regenerative biomaterials · 2026Article
- Cationic microparticles inhibit local sterile inflammation in tissue injuries.Regenerative biomaterials · 2026Article
- A sandwich-like nanofibrous scaffold with macrophage phenotype transformation and myogenic differentiation for skeletal muscle regeneration.Bioactive materials · 2025Article
- Macrophage polarization: molecular mechanisms, disease implications, and targeted therapeutic strategies.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Orofacial muscles are particularly prone to refractory fibrosis after injury, leading to a negative effect on the patient's quality of life and limited therapeutic options. Gaining insights into innate inflammatory response-fibrogenesis homeostasis can aid in the development of new therapeutic strategies for muscle fibrosis. In this study, the crucial role of macrophages is identified in the regulation of orofacial muscle fibrogenesis after injury. Hypothesizing that orchestrating macrophage polarization and functions will be beneficial for fibrosis treatment, nanomaterials are engineered with polyethylenimine functionalization to regulate the macrophage phenotype by capturing negatively charged cell-free nucleic acids (cfNAs). This cationic nanomaterial reduces macrophage-related inflammation in vitr and demonstrates excellent efficacy in preventing orofacial muscle fibrosis in vivo. Single-cell RNA sequencing reveals that the cationic nanomaterial reduces the proportion of profibrotic Gal3
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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.