ArticleNature communications2015
The HIF-1/glial TIM-3 axis controls inflammation-associated brain damage under hypoxia.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 137 citations in OpenAlex.
- T-cell immunoglobulin and mucin-domain containing-3 orchestrates myeloid dysfunction across brain aging and disease.Neural regeneration research · 2026Article
- Hypoxia-inducible factor-1: A new neuroprotective agent for the treatment of hyperglycemia after stroke.Neural regeneration research · 2026Article
- The Role of Macrophages in the Immune Response to Peritoneal Infection withPathogens (Basel, Switzerland) · 2026Article
- Astrocytes in Multiple Sclerosis: Getting to the Core.International journal of molecular sciences · 2026Review
- The lung-brain axis: elucidating the mechanisms of pulmonary-driven neurological disorders.Journal of neuroinflammation · 2026Review
- Iron Oxide Nanozyme as Reactive Oxygen and Nitrogen Species Scavenger to Regulate Microglial Homeostasis in Stroke.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single-cell sequencing analysis and machine learning model reveal aberrant TIM-3 expression in microglia during Alzheimer's disease progression.Journal of translational medicine · 2026Article
- Spatial protein profiling reveals active roles for astrocytes in the chronic active lesion core during multiple sclerosis.Acta neuropathologica · 2025Article
- The role of coinhibitory receptor-expressing non-T cells in inflammation and immunity: unsung heroes or peripheral players?Experimental & molecular medicine · 2025Review
- The Bidirectional Role of Hypoxia-Inducible Factor 1 Alpha in Vascular Dementia Caused by Chronic Cerebral Hypoperfusion.Molecular neurobiology · 2025Review
- Investigating the impact of camel whey protein hydrolysate on cyp1a1 and keap1/nrf2 expression in hypoxic stress-affected liver tissue of Oreochromis niloticus.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2025Article
- Markers of T cell activation and exhaustion in plasma are associated with persistent symptoms up to 18 months following mild SARS-CoV-2 infection.Frontiers in immunology · 2025Article
- Glutamine metabolism and ammonia death: targeted modulation for enhanced cancer immunotherapy.Frontiers in immunology · 2025Review
- Hypoxia-inducible Factor-1α Pathway in Cerebral Ischemia: From Molecular Mechanisms to Therapeutic Targets.CNS & neurological disorders drug targets · 2025Review
- Blocking of Tim-3 Ameliorates Spinal Cord Ischemia-Reperfusion Injury Through Inhibiting Neuroinflammation and Promoting M1-to-M2 Phenotypic Polarization of Microglia.Immunity, inflammation and disease · 2024Article
- Intrathecal lactate dehydrogenase A inhibitors FX11 and oxamate alleviate chronic constriction injury-induced nociceptive sensitization through neuroinflammation and angiogenesis.The journal of headache and pain · 2024Article
- TIM-3 on myeloid cells promotes pulmonary inflammation through increased production of galectin-3.Communications biology · 2024Article
- Combination of locoregional radiotherapy with a TIM-3 aptamer improves survival in diffuse midline glioma models.JCI insight · 2024Article
- Ozone Improves Oxygenation and Offers Organ Protection after Autologous Blood Transfusion in a Simulated Carbon Dioxide Pneumoperitoneal Environment in a Rabbit Hemorrhagic Shock Model.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2024Article
- Supervised latent factor modeling isolates cell-type-specific transcriptomic modules that underlie Alzheimer's disease progression.Communications biology · 2024Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation is closely related to the extent of damage following cerebral ischaemia, and the targeting of this inflammation has emerged as a promising therapeutic strategy. Here, we present that hypoxia-induced glial T-cell immunoglobulin and mucin domain protein (TIM)-3 can function as a modulator that links inflammation and subsequent brain damage after ischaemia. We find that TIM-3 is highly expressed in hypoxic brain regions of a mouse cerebral hypoxia-ischaemia (H/I) model. TIM-3 is distinctively upregulated in activated microglia and astrocytes, brain resident immune cells, in a hypoxia-inducible factor (HIF)-1-dependent manner. Notably, blockade of TIM-3 markedly reduces infarct size, neuronal cell death, oedema formation and neutrophil infiltration in H/I mice. Hypoxia-triggered neutrophil migration and infarction are also decreased in HIF-1α-deficient mice. Moreover, functional neurological deficits after H/I are significantly improved in both anti-TIM-3-treated mice and myeloid-specific HIF-1α-deficient mice. Further understanding of these insights could serve as the basis for broadening the therapeutic scope against hypoxia-associated brain diseases.
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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.