ArticleJournal of cellular and molecular medicine2019
The role of dendritic cells regulated by HMGB1/TLR4 signalling pathway in myocardial ischaemia reperfusion injury.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 36 citations in OpenAlex.
- LILRB4 Recruits SHP-1 to Enhance Oxidative Stress and Apoptosis, Aggravating Myocardial Ischemia-Reperfusion Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- HMGB1-mediated endoplasmic reticulum stress in monocyte-derived dendritic cells regulates CD4+ T cell immune responses in myasthenia gravis.Journal of neuroinflammation · 2026Article
- Intestinal microecology regulates neutrophil recruitment through TLR4/MAPK/CXCR2 signaling pathway to promote liver ischemia/reperfusion injury.Journal of bioenergetics and biomembranes · 2026Article
- Scoping review of preclinical and clinical studies on the role of HMGB1 in heart disease.NPJ cardiovascular health · 2026Article
- What Is-and What Is Not-Immunogenic Cell Death? Functional Definitions, Experimental Standards, and Common Pitfalls.International journal of molecular sciences · 2026Review
- Ferulic acid in combination with ginsenoside Rb1 alleviates myocardial no-reflow by inhibiting platelet HMGB1 release and NET formation.Chinese medicine · 2026Article
- Stem cell-derived extracellular vesicles as immunomodulators: a novel paradigm for post-myocardial infarction repair and regeneration.Frontiers in pharmacology · 2026Review
- Therapeutic targeting of cell death-immune crosstalk in cancer to rewire the tumor immune microenvironment.Molecular cancer · 2025Review
- Myocardial Ischemia/Reperfusion Injury: Molecular Insights, Forensic Perspectives, and Therapeutic Horizons.Cells · 2025Review
- The Ambiguous Role of HMGB1 Across the Hallmarks of Aging: A Narrative Review.Clinical interventions in aging · 2025Review
- Inhibition of HMGB1/NF-κB signaling restores Th17/Treg balance via dendritic cell modulation in liver transplant rejection.Frontiers in immunology · 2025Article
- Myeloid Cells in Myocardial Ischemic Injury: The Role of the Macrophage Migration Inhibitory Factor.Life (Basel, Switzerland) · 2024Review
- The roles of Th cells in myocardial infarction.Cell death discovery · 2024Review
- Inflammation in Myocardial Ischemia/Reperfusion Injury: Underlying Mechanisms and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2023Review
- Hydrogen sulfide alleviates lipopolysaccharide-induced myocardial injury through TLR4-NLRP3 pathway.Physiological research · 2023Article
- The Mechanism of Delayed Ischemic Preconditioning in Alleviating Acute Ischemia/Reperfusion Renal Injury through Treg Mediated by Immature CD11cKidney diseases (Basel, Switzerland) · 2022Article
- Ac2‑26 alleviates hepatic ischemia‑reperfusion injury based on inhibiting the positive feedback loop of HMGB1/TLR4/NF‑κB/neutrophils.Experimental and therapeutic medicine · 2022Article
- HMGB1-Mediated Activation of the Inflammatory-Reparative Response Following Myocardial Infarction.Cells · 2022Review
- Integrated Bioinformatics Analysis and Verification of Gene Targets for Myocardial Ischemia-Reperfusion Injury.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- C1q/TNF-related protein 9 decreases cardiomyocyte hypoxia/reoxygenation-induced inflammation by inhibiting the TLR4/MyD88/NF-κB signaling pathway.Experimental and therapeutic medicine · 2021Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory response plays an important role in ischaemia reperfusion injury (IRI) through a variety of inflammatory cells. Apart from neutrophils, macrophages and lymphocytes, the role of dendritic cells (DCs) in IRI has been noticed. The study was aimed at investigating whether the high-mobility group protein box-1/toll like receptor 4 (HMGB1/TLR4) signalling pathway regulate the migration, adhesion and aggregation of DCs to the myocardium, induce DCs activation and maturation, stimulate the expression of surface costimulatory molecules and participate in myocardial IRI. In vivo, migration, adhesion, and aggregation of DCs was enhanced; the expression of peripheral blood DCs CD80 and CD86, myocardial adhesion molecules were increased; and the infarct size was increased during myocardial ischaemia reperfusion injury myocardial ischemic/reperfusion injury (MI/RI). These responses induced by MI/RI were significantly inhibited by HMGB1 specific neutralizing antibody treatment. Cellular experiments confirmed that HMGB1 promoted the release of inflammatory cytokines through TLR4/MyD88/NF-κB, upregulated CD80 and CD86 expression, mediated the damage of cardiomyocytes and accelerated the apoptosis. Our results indicate that DCs activation and maturation, stimulate the expression of surface costimulatory molecules by promoting the release of inflammatory factors through NF-κB pathway and participate in myocardial IRI.
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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.