ArticleAutophagy2023
FOXP3+ macrophage represses acute ischemic stroke-induced neural inflammation.
Article in Autophagy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 90 citations in OpenAlex.
- Serine protease inhibitor from Trichinella spiralis ameliorates diet-induced obesity and adipose tissue inflammation through TIM-3-dependent macrophage reprogramming.PLoS pathogens · 2026Article
- Decoding neuron-specific lineage to identify diagnostic biomarkers and therapeutic targets for ischemic stroke.iScience · 2026Article
- Macrophage immunometabolism in stroke: a view from single-cell and nano technologies.Journal of translational medicine · 2026Review
- Single-cell RNA sequencing in stroke and traumatic brain injury: Current achievements, challenges and future perspectives on transcriptomic profiling.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- The Therapeutic Potential of Mesenchymal Stem Cells in Post-Stroke Depression.International journal of molecular sciences · 2026Review
- Emerging research themes in macrophage-associated research for esophageal cancer: a bibliometric and visualized analysis.Journal of thoracic disease · 2026Article
- TRIM56 Aggravates Cerebral Ischemia-Reperfusion Injury via Inhibiting KLF4-Activated Ferroptosis Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Transcription Factor DDIT3 Regulates Macrophage Function by Inhibiting KLF10 to Attenuate ALI/ARDS Inflammation.Inflammation · 2026Article
- Monocyte-derived macrophages and their roles in ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- Article
- Single-cell and single-nucleus transcriptomics in ischemic stroke: cellular mechanisms and therapeutic implications.Frontiers in neurology · 2026Review
- Insights gained from single-cell sequencing analysis of ischemic stroke.Frontiers in cell and developmental biology · 2026Review
- Immunometabolic control of macrophage plasticity in wound healing: mechanistic insights and therapeutic opportunities.Frontiers in immunology · 2026Review
- Microglial handling of myelin debris and remyelination after ischaemic stroke: recognition, intracellular processing, lipid fate, and oligodendroglial repair.Frontiers in cellular neuroscience · 2026Review
- Exploring Hypoxia-Induced Neuroprotection Mechanisms in Post-Stroke Recovery.Translational stroke research · 2025Review
- BM-MSC-derived migrasomes reverse stroke-induced thymic atrophy and immunosuppression via Pin1 delivery to thymic epithelial cells.Journal of neuroinflammation · 2025Article
- Extracellular vesicles of cancer cells induce FOXP3+ fibroblasts and facilitate tumor invasion via the Wnt3-β-catenin pathway.Oncogene · 2025Article
- Integrative single-cell and machine learning approach to characterize immunogenic cell death and tumor microenvironment in LUAD.Journal of translational medicine · 2025Article
- Review
- Effects of maternal Echinococcus multilocularis infection on colitis susceptibility and gut microbiota of offspring.Parasites & vectors · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proper termination of cell-death-induced neural inflammation is the premise of tissue repair in acute ischemic stroke (AIS). Macrophages scavenge cell corpses/debris and produce inflammatory mediators that orchestrate immune responses. Here, we report that FOXP3, the key immune-repressive transcription factor of Tregs, is conditionally expressed in macrophages in stroke lesion. FOXP3 ablation in macrophages results in detrimental stroke outcomes, emphasizing the beneficial role of FOXP3+ macrophages. FOXP3+ macrophages are distinct from the M1 or M2 subsets and display superactive efferocytic capacity. With scRNAseq and analysis of FOXP3-bound-DNA isolated with CUT & RUN, we show that FOXP3 facilitates macrophage phagocytosis through enhancing cargo metabolism. FOXP3 expression is controlled by macroautophagic/autophagic protein degradation in resting macrophages, while initiation of LC3-associated phagocytosis (LAP) competitively occupies the autophagic machineries, and thus permits FOXP3 activation. Our data demonstrate a distinct set of FOXP3+ macrophages with enhanced scavenging capability, which could be a target in immunomodulatory therapy against AIS.
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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.