ReviewMolecular neurobiology2013
Role of the Toll Like receptor (TLR) radical cycle in chronic inflammation: possible treatments targeting the TLR4 pathway.
Review in Molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 232 papers, 1 of them a synthesis that pooled it.
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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
232 citing papers in PubMed, 1 synthesis or guideline pooled it, 464 citations in OpenAlex.
- Monocytic TLR4 expression and activation in schizophrenia: A systematic review and meta-analysis.PloS one · 2025Pooled it
- Trimetazidine Improves the Outcome of EECP Therapy in Patients with Refractory Angina Pectoris.Medical archives (Sarajevo, Bosnia and Herzegovina) · 2020Trial
- Is increased inflammation in schizophrenia associated with increased cardiovascular risk and the etiopathogenesis of this disorder?Brain, behavior, & immunity - health · 2026Article
- Unifying the hallmarks of major depression through neuroimmune-metabolic-oxidative (NIMETOX) dysregulation: a mechanistic systems framework.Cellular & molecular immunology · 2026Review
- Rhein alleviates acute pancreatitis by inhibiting TMAO-mediated inflammatory signaling pathways and reducing acinar cell injury.Journal of advanced research · 2026Article
- Atmospheric stressors and kidney diseases.Nature reviews. Nephrology · 2026Review
- Immune cell signature in non-ischemic heart failure indicates chronic systemic immune activation with features of immunosenescence.Immunity & ageing : I & A · 2026Article
- Decoding the gut microbiota-mitochondrial-inflammasome axis in cardiovascular disease.Molecular and cellular biochemistry · 2026Review
- Health among sexual and gender minority people affected by armed conflict and forced displacement: Call for a biocultural and minority stress framework.Social science & medicine (1982) · 2026Review
- Bacterial Communities as Modulators of Innate Immune Signalling: An In Vitro Perspective on Toll-Like Receptor Activation.Environmental microbiology reports · 2026Article
- Protection byPharmaceuticals (Basel, Switzerland) · 2026Article
- Increased Toll-Like Receptor-4 Signalling in Breast Tissue of High Fibroglandular Density.Journal of mammary gland biology and neoplasia · 2026Article
- Synergistic interactions of melatonin and glucocorticoids in alleviating allergic airway inflammation.Frontiers in medicine · 2026Article
- Orchestrating immunopathology: the spectrum of programmed cell death pathways co-opted by influenza a virus in pulmonary immunity.Frontiers in immunology · 2026Review
- Gut Microbiome and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Insights into Disease Mechanisms.International journal of molecular sciences · 2025Review
- Bioactive Polysaccharides and Phlorotannins fromJournal of microbiology and biotechnology · 2025Article
- NOX-NOS crosstalk in the liver-brain axis: Novel insights for redox regulation and neurodegenerative diseases.Redox biology · 2025Review
- D-Carvone Mitigating Renal Damage and Enhancing Antioxidant Defense in Lithium Induced Nephrotoxicity.Food science & nutrition · 2025Article
- TLR-4/Notch1/NF-κB pathway modulation by dapagliflozin: a novel mechanism for neuroprotection in hepatic encephalopathy.Metabolic brain disease · 2025Article
- Neuroimmune, metabolic and oxidative stress pathways in major depressive disorder.Nature reviews. Neurology · 2025Review
172 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of the Toll-like receptor 4 (TLR4) complex, a receptor of the innate immune system, may underpin the pathophysiology of many human diseases, including asthma, cardiovascular disorder, diabetes, obesity, metabolic syndrome, autoimmune disorders, neuroinflammatory disorders, schizophrenia, bipolar disorder, autism, clinical depression, chronic fatigue syndrome, alcohol abuse, and toluene inhalation. TLRs are pattern recognition receptors that recognize damage-associated molecular patterns and pathogen-associated molecular patterns, including lipopolysaccharide (LPS) from gram-negative bacteria. Here we focus on the environmental factors, which are known to trigger TLR4, e.g., ozone, atmosphere particulate matter, long-lived reactive oxygen intermediate, pentachlorophenol, ionizing radiation, and toluene. Activation of the TLR4 pathways may cause chronic inflammation and increased production of reactive oxygen and nitrogen species (ROS/RNS) and oxidative and nitrosative stress and therefore TLR-related diseases. This implies that drugs or substances that modify these pathways may prevent or improve the abovementioned diseases. Here we review some of the most promising drugs and agents that have the potential to attenuate TLR-mediated inflammation, e.g., anti-LPS strategies that aim to neutralize LPS (synthetic anti-LPS peptides and recombinant factor C) and TLR4/MyD88 antagonists, including eritoran, CyP, EM-163, epigallocatechin-3-gallate, 6-shogaol, cinnamon extract, N-acetylcysteine, melatonin, and molecular hydrogen. The authors posit that activation of the TLR radical (ROS/RNS) cycle is a common pathway underpinning many "civilization" disorders and that targeting the TLR radical cycle may be an effective method to treat many inflammatory disorders.
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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.