ArticleNature medicine2017
MAFB prevents excess inflammation after ischemic stroke by accelerating clearance of damage signals through MSR1.
Article in Nature medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers, 1 of them a synthesis that pooled it.
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Who cites it
137 citing papers in PubMed, 1 synthesis or guideline pooled it, 242 citations in OpenAlex.
- Microglial Responses to MSC-EVs Treatment in Animal and Cellular Models of Ischemic Stroke: a Systematic Review with Meta-analysis.Molecular neurobiology · 2025Pooled it
- Tibial bone compression promotes recovery after brain injury through osteocyte PIEZO1.Nature neuroscience · 2026Article
- Biomimetic nanodelivery of antagomiR-155-5p ameliorates wear particle-induced osteolysis by dual regulation of Gas6/Axl-mediated macrophage inflammation.Journal of orthopaedic translation · 2026Article
- Article
- GPNMB modulates neutrophil extracellular trap formation: therapeutic implications for ischemic stroke.Journal of neuroinflammation · 2026Article
- Nanomedicines and stroke: Advantages in chronic inflammation treatment and neural regeneration.Neural regeneration research · 2026Article
- CD204 regulates microglial/macrophage M1/M2 polarization and alleviates neuroinflammation following intracerebral hemorrhage.Scientific reports · 2026Article
- Nanotechnology for ischemic stroke treatment: addressing challenges across stroke management stages.Frontiers in molecular biosciences · 2026Review
- Inhibition of the TLR4/RAGE pathway by clearance of extracellular HMGB1 is a potential therapeutic target for radiation-damaged salivary glands.Regenerative therapy · 2025Article
- MAFB regulates hematopoietic stem cell proliferation and maintenance.Scientific reports · 2025Article
- TGF-β signaling regulates gene expression, phagocytosis, and cell proliferation and supports glial cell survival in primary rat mixed glial cell cultures.Journal of molecular histology · 2025Article
- Peroxiredoxin 1 inhibits tumorigenesis by activating the NLRP3/GSDMD pathway to induce pyroptosis of colorectal cancer cells.World journal of gastroenterology · 2025Article
- Chemerin 15 enhances microglial phagocytosis to attenuate cerebral ischemia-reperfusion injury through the ChemR23/p38 MAPK pathway.iScience · 2025Article
- Neutrophil/monocyte-targeted dual-ligands modified liposomes delivering puerarin for ischemia stroke treatment.Materials today. Bio · 2025Article
- CKLF1 disrupts microglial efferocytosis following acute ischemic stroke by binding to phosphatidylserine.Cell death and differentiation · 2025Article
- The Role and Phagocytic Mechanisms of Alveolar Macrophages in Inflammatory Responses Induced by Diesel Exhaust Particles.Environmental science & technology · 2025Article
- Peroxiredoxin 1 promotes intestinal inflammation by activating the NLRP3 inflammasome in macrophages through lysosomal disruption in Crohn's disease.Cell death & disease · 2025Article
- HMGB1: A New Target for Ischemic Stroke and Hemorrhagic Transformation.Translational stroke research · 2025Review
- Predictive Model for Early Neurological Deterioration in Acute Ischemic Stroke Utilizing Novel Thrombotic Biomarkers.Brain and behavior · 2025Article
- Repair-associated macrophages increase after early-phase microglia attenuation to promote ischemic stroke recovery.Nature communications · 2025Article
77 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Damage-associated molecular patterns (DAMPs) trigger sterile inflammation after tissue injury, but the mechanisms underlying the resolution of inflammation remain unclear. In this study, we demonstrate that common DAMPs, such as high-mobility-group box 1 (HMGB1), peroxiredoxins (PRXs), and S100A8 and S100A9, were internalized through the class A scavenger receptors MSR1 and MARCO in vitro. In ischemic murine brain, DAMP internalization was largely mediated by MSR1. An elevation of MSR1 levels in infiltrating myeloid cells observed 3 d after experimental stroke was dependent on the transcription factor Mafb. Combined deficiency for Msr1 and Marco, or for Mafb alone, in infiltrating myeloid cells caused impaired clearance of DAMPs, more severe inflammation, and exacerbated neuronal injury in a murine model of ischemic stroke. The retinoic acid receptor (RAR) agonist Am80 increased the expression of Mafb, thereby enhancing MSR1 expression. Am80 exhibited therapeutic efficacy when administered, even at 24 h after the onset of experimental stroke. Our findings uncover cellular mechanisms contributing to DAMP clearance in resolution of the sterile inflammation triggered by tissue injury.
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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.