ReviewCellular and molecular life sciences : CMLS2019
The regulatory role of Toll-like receptors after ischemic stroke: neurosteroids as TLR modulators with the focus on TLR2/4.
Review in Cellular and molecular life sciences : CMLS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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The trial behind it
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Who cites it
52 citing papers in PubMed, 82 citations in OpenAlex.
- Lipid metabolism, microglia, and stroke.Neural regeneration research · 2026Article
- Transcriptomics and Experiments Verified that Astaxanthin Reduces the Apoptosis of Nerve Cells in Ischemic Stroke by Inhibiting the Toll-like Receptor Signaling Pathway.Molecular neurobiology · 2026Article
- Integrated Transcriptomics and Machine Learning Reveal Lipid Metabolism Related Genes in Ischemic Stroke.Journal of molecular neuroscience : MN · 2026Article
- Pan-Cell Death Protein Signature as a Novel Diagnostic and Prognostic Biomarker for Intracerebral Hemorrhage.Journal of proteome research · 2026Article
- Probiotic Supplementation Modulates FGFR2 and TLR4 Signaling and Attenuates Chronic Neuroinflammation in an Experimental Stroke Model.Neurochemical research · 2026Article
- BMSC-Derived Exosomal miR-21a-5p Ameliorates Blood-Brain Barrier Injury and Hemorrhagic Transformation.Molecular neurobiology · 2026Article
- Obstructive Sleep Apnea Syndrome and Ischemic Stroke: Investigating Inflammatory Mechanisms.Nature and science of sleep · 2026Review
- Identification and validation of microglia-associated genes in ischemic stroke using single-cell and bulk RNA-seq.Molecular brain · 2025Article
- Therapeutic potential of calcitriol in cerebral ischemia/reperfusion injury: In vivo and in silico insights into TLR4 and FGFR2 pathways.IBRO neuroscience reports · 2025Article
- Proteoglycan 4 attenuates ischemic post-stroke hemorrhagic transformation and blood-brain barrier disruption.IBRO neuroscience reports · 2025Article
- Late-Stage Activation of Toll-like receptor 3 Alleviates Cognitive Impairment and Neuropathology in an Alzheimer's Disease Mouse Model.Molecular neurobiology · 2025Article
- Altered Lipid Metabolism in CNS Demyelination and Remyelination Are Key Elements Driving Progressive MS.International journal of molecular sciences · 2025Review
- Research status and future perspectives of IL‑27 in the treatment of stroke (Review).International journal of molecular medicine · 2025Review
- Immune genes involved in synaptic plasticity during early postnatal brain development contribute to post-stroke damage in the aging male rat brain.Biogerontology · 2025Article
- Estrogen and progesterone attenuate CD4-positive immune cell traffic to the penumbra region of rat's ischemic stroke brain.Iranian journal of basic medical sciences · 2025Article
- Inflammation-related biomarkers and berberine therapy in post-stroke depression: evidence from bioinformatics, machine learning, and experimental validation.Frontiers in neuroscience · 2025Article
- Association of Serum Macrophage Migration Inhibitory Factor with 3-Month Poor Outcome and Malignant Cerebral Edema in Patients with Large Hemispheric Infarction.Neurocritical care · 2024Article
- DL-3-n-Butylphthalide Ameliorates Post-stroke Emotional Disorders by Suppressing Neuroinflammation and PANoptosis.Neurochemical research · 2024Article
- Potential of Neuroinflammation-Modulating Strategies in Tuberculous Meningitis: Targeting Microglia.Aging and disease · 2024Review
- Neuroactive Steroids, Toll-like Receptors, and Neuroimmune Regulation: Insights into Their Impact on Neuropsychiatric Disorders.Life (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Ischemic stroke is the most common cerebrovascular disease and considered as a worldwide leading cause of death. After cerebral ischemia, different pathophysiological processes including neuroinflammation, invasion and aggregation of inflammatory cells and up-regulation of cytokines occur simultaneously. In this respect, Toll-like receptors (TLRs) are the first identified important mediators for the activation of the innate immune system and are widely expressed in glial cells and neurons following brain trauma. TLRs are also able to interact with endogenous and exogenous molecules released during ischemia and can increase tissue damage. Particularly, TLR2 and TLR4 activate different downstream inflammatory signaling pathways. In addition, TLR signaling can alternatively play a role for endogenous neuroprotection. In this review, the gene and protein structures, common genetic polymorphisms of TLR2 and TLR4, TLR-related molecular pathways and their putative role after ischemic stroke are delineated. Furthermore, the relationship between neurosteroids and TLRs as neuroprotective mechanism is highlighted in the context of brain ischemia.
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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.