ArticleBiochimica et biophysica acta2014
Toll-like receptor 3 plays a role in myocardial infarction and ischemia/reperfusion injury.
Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 73 citations in OpenAlex.
- The innate immune receptor NLRX1 is a novel required modulator for mPTP opening: implications for cardioprotection.Basic research in cardiology · 2025Article
- Interplay between Pro-inflammatory Mediators and Oxidative Stressinvolved Recurrent Chronic Heart Failure in Elderly Patients with Coronary Stents.Current medicinal chemistry · 2025Article
- Identification and verification of biomarkers associated with neutrophils in acute myocardial infarction: integrated analysis of bulk RNA-seq, expression quantitative trait loci, and mendelian randomization.Frontiers in molecular biosciences · 2025Article
- Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities.Circulation research · 2024Review
- Inflammation in Myocardial Ischemia/Reperfusion Injury: Underlying Mechanisms and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2023Review
- Lactate promotes endothelial-to-mesenchymal transition via Snail1 lactylation after myocardial infarction.Science advances · 2023Article
- Interaction of Cardiovascular Nonmodifiable Risk Factors, Comorbidities and Comedications With Ischemia/Reperfusion Injury and Cardioprotection by Pharmacological Treatments and Ischemic Conditioning.Pharmacological reviews · 2023Review
- MyD88: At the heart of inflammatory signaling and cardiovascular disease.Journal of molecular and cellular cardiology · 2021Review
- Chemokines in Myocardial Infarction.Journal of cardiovascular translational research · 2021Review
- Article
- Poly(I:C) preconditioning protects the heart against myocardial ischemia/reperfusion injury through TLR3/PI3K/Akt-dependent pathway.Signal transduction and targeted therapy · 2020Article
- Endothelial cell HSPA12B and yes-associated protein cooperatively regulate angiogenesis following myocardial infarction.JCI insight · 2020Article
- MicroRNA‑93 promotes angiogenesis and attenuates remodeling via inactivation of the Hippo/Yap pathway by targeting Lats2 after myocardial infarctionω.Molecular medicine reports · 2020Article
- Nucleic Acid Sensors and Programmed Cell Death.Journal of molecular biology · 2020Review
- MicroRNA-214-5p protects against myocardial ischemia reperfusion injury through targeting the FAS ligand.Archives of medical science : AMS · 2020Article
- Damage-Associated Molecular Patterns in Myocardial Infarction and Heart Transplantation: The Road to Translational Success.Frontiers in immunology · 2020Review
- Innate immunity as a target for acute cardioprotection.Cardiovascular research · 2019Review
- Adenosine 2A Receptor Activation Attenuates Ischemia Reperfusion Injury During Extracorporeal Cardiopulmonary Resuscitation.Annals of surgery · 2019Article
- Immune responses in cardiac repair and regeneration: a comparative point of view.Cellular and molecular life sciences : CMLS · 2019Review
- Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Innate immune and inflammatory responses mediated by Toll like receptors (TLRs) have been implicated in myocardial ischemia/reperfusion (I/R) injury. This study examined the role of TLR3 in myocardial injury induced by two models, namely, myocardial infarction (MI) and I/R. First, we examined the role of TLR3 in MI. TLR3 deficient (TLR3(-/-)) and wild type (WT) mice were subjected to MI induced by permanent ligation of the left anterior descending (LAD) coronary artery for 21days. Cardiac function was measured by echocardiography. Next, we examined whether TLR3 contributes to myocardial I/R injury. TLR3(-/-) and WT mice were subjected to myocardial ischemia (45min) followed by reperfusion for up to 3days. Cardiac function and myocardial infarct size were examined. We also examined the effect of TLR3 deficiency on I/R-induced myocardial apoptosis and inflammatory cytokine production. TLR3(-/-) mice showed significant attenuation of cardiac dysfunction after MI or I/R. Myocardial infarct size and myocardial apoptosis induced by I/R injury were significantly attenuated in TLR3(-/-) mice. TLR3 deficiency increases B-cell lymphoma 2 (BCL2) levels and attenuates I/R-increased Fas, Fas ligand or CD95L (FasL), Fas-Associated protein with Death Domain (FADD), Bax and Bak levels in the myocardium. TLR3 deficiency also attenuates I/R-induced myocardial nuclear factor KappaB (NF-κB) binding activity, Tumor necrosis factor alpha (TNF-α) and Interleukin-1 beta (IL-1β) production as well as I/R-induced infiltration of neutrophils and macrophages into the myocardium. TLR3 plays an important role in myocardial injury induced by MI or I/R. The mechanisms involve activation of apoptotic signaling and NF-κB binding activity. Modulation of TLR3 may be an effective approach for ameliorating heart injury in heart attack patients.
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Registered trials
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