ReviewAntioxidants & redox signaling2011
Toll-like receptors: new players in myocardial ischemia/reperfusion injury.
Review in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
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
47 citing papers in PubMed, 112 citations in OpenAlex.
- Neutrophil-mediated myocardial ischemia-reperfusion injury: mechanisms and potential therapeutic targets.Frontiers in immunology · 2026Review
- Endotoxin Pretreatment Mitigates Myocardial Ischemia-Reperfusion Injury Through Preservation of Mitochondrial Respiration: A Combined Assessment of In Vivo, Ex Vivo, and In Vitro Data.International journal of molecular sciences · 2025Article
- Relationship between inflammatory markers and long-term prognosis in ICU patients with acute non-ST-segment elevation myocardial infarction.Frontiers in cardiovascular medicine · 2025Article
- Treponema pallidum recombinant protein Tp0768 enhances the ability of HUVECs to promote neutrophil chemotaxis through the TLR2/ER stress signaling pathway.Journal of leukocyte biology · 2024Article
- Inhibition of circDGKZ ameliorates myocardial ischemia/reperfusion injury by targeting miR-345-5p/TLR4.ESC heart failure · 2024Article
- TLR4 signalling in ischemia/reperfusion injury: a promising target for linking inflammation, oxidative stress and programmed cell death to improve organ transplantation outcomes.Frontiers in immunology · 2024Review
- Suppression of NLRP3 inflammasome orchestrates the protective efficacy of tiron against isoprenaline-induced myocardial injury.Frontiers in pharmacology · 2024Article
- Mechanism Repositioning Based on Integrative Pharmacology: Anti-Inflammatory Effect of Safflower in Myocardial Ischemia-Reperfusion Injury.International journal of molecular sciences · 2023Article
- The Innate Immune System in Cardiovascular Diseases and Its Role in Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2022Review
- Screening for Regulatory Network of miRNA-Inflammation, Oxidative Stress and Prognosis-Related mRNA in Acute Myocardial Infarction: An in silico and Validation Study.International journal of general medicine · 2022Article
- TLR4-SIRT3 Mechanism Modulates Mitochondrial and Redox Homeostasis and Promotes EPCs Recruitment and Survival.Oxidative medicine and cellular longevity · 2022Article
- Calcium Ionophore-Induced Extracellular Vesicles Mediate Cytoprotection against Simulated Ischemia/Reperfusion Injury in Cardiomyocyte-Derived Cell Lines by Inducing Heme Oxygenase 1.International journal of molecular sciences · 2020Article
- Astragaloside IV protects human cardiomyocytes from hypoxia/reoxygenation injury by regulating miR-101a.Molecular and cellular biochemistry · 2020Article
- Identification of Key Genes Involved in Acute Myocardial Infarction by Comparative Transcriptome Analysis.BioMed research international · 2020Article
- The Protective Effect of rhBNP on Postresuscitation Myocardial Dysfunction in a Rat Cardiac Arrest Model.BioMed research international · 2020Article
- Clemastine Fumarate Protects Against Myocardial Ischemia Reperfusion Injury by Activating the TLR4/PI3K/Akt Signaling Pathway.Frontiers in pharmacology · 2020Article
- Protective effect of miR-20a against hypoxia/reoxygenation treatment on cardiomyocytes cell viability and cell apoptosis by targeting TLR4 and inhibiting p38 MAPK/JNK signaling.In vitro cellular & developmental biology. Animal · 2019Article
- Bioinformatics analysis of gene expression profile data to screen key genes involved in intracranial aneurysms.Molecular medicine reports · 2019Article
- Gene expression profiling analysis to investigate the role of remote ischemic postconditioning in ischemia-reperfusion injury in rats.BMC genomics · 2019Article
- NFkappaB is a Key Player in the Crosstalk between Inflammation and Cardiovascular Diseases.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Innate immune and inflammatory responses have been implicated in myocardial ischemia/reperfusion (I/R) injury. However, the mechanisms by which innate immunity and inflammatory response are involved in myocardial I/R have not been elucidated completely. Recent studies highlight the role of Toll-like receptors (TLRs) in the induction of innate immune and inflammatory responses. Growing evidence has demonstrated that TLRs play a critical role in myocardial I/R injury. Specifically, deficiency of TLR4 protects the myocardium from ischemic injury, whereas modulation of TLR2 induces cardioprotection against ischemic insult. Importantly, cardioprotection induced by modulation of TLRs involves activation of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway, suggesting that there is a crosstalk between TLRs and PI3K/Akt signaling pathways. In addition, TLRs also associate with other coreceptors, such as macrophage scavenger receptors in the recognition of their ligands. TLRs are also involved in the induction of angiogenesis, modulation of stem cell function, and expression of microRNA, which are currently important topic areas in myocardial I/R. Understanding how TLRs contribute to myocardial I/R injury could provide basic scientific knowledge for the development of new therapeutic approaches for the treatment and management of patients with heart attack.
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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.