ArticleBiochimica et biophysica acta2013
CpG-ODN, the TLR9 agonist, attenuates myocardial ischemia/reperfusion injury: involving activation of PI3K/Akt signaling.
Article in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 68 citations in OpenAlex.
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- Circulating cell-free mitochondrial DNA in diabetes mellitus: Current insights and unexplored frontiers.Journal of diabetes investigation · 2025Review
- DNA sensors in metabolic and cardiovascular diseases: Molecular mechanisms and therapeutic prospects.Immunological reviews · 2025Review
- Regulation of TAR DNA binding protein 43 (TDP-43) homeostasis by cytosolic DNA accumulation.The Journal of biological chemistry · 2024Article
- Sulfate-Reducing Bacteria Induce Pro-Inflammatory TNF-α and iNOS via PI3K/Akt Pathway in a TLR 2-Dependent Manner.Microorganisms · 2024Article
- Short-term toll-like receptor 9 inhibition leads to left ventricular wall thinning after myocardial infarction.ESC heart failure · 2023Article
- The role of circulating cell-free DNA as an inflammatory mediator after stroke.Seminars in immunopathology · 2023Review
- Potential therapeutic strategies for myocardial infarction: the role of Toll-like receptors.Immunologic research · 2022Review
- Post-ischemic Myocardial Inflammatory Response: A Complex and Dynamic Process Susceptible to Immunomodulatory Therapies.Frontiers in cardiovascular medicine · 2021Review
- MAIR-II deficiency ameliorates cardiac remodelling post-myocardial infarction by suppressing TLR9-mediated macrophage activation.Journal of cellular and molecular medicine · 2020Article
- Salvianolic acid B protects against myocardial ischaemia-reperfusion injury in rats via inhibiting high mobility group box 1 protein expression through the PI3K/Akt signalling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Innate Immune Receptors, Key Actors in Cardiovascular Diseases.JACC. Basic to translational science · 2020Review
- Selective nanoparticle-mediated targeting of renal tubular Toll-like receptor 9 attenuates ischemic acute kidney injury.Kidney international · 2020Article
- Overexpression of long non-coding RNA ANRIL promotes post-ischaemic angiogenesis and improves cardiac functions by targeting Akt.Journal of cellular and molecular medicine · 2020Article
- Protective effects of fisetin against myocardial ischemia/reperfusion injury.Experimental and therapeutic medicine · 2020Article
- The Trinity of cGAS, TLR9, and ALRs Guardians of the Cellular Galaxy Against Host-Derived Self-DNA.Frontiers in immunology · 2020Review
- PTEN loss regulates alveolar epithelial cell senescence in pulmonary fibrosis depending on Akt activation.Aging · 2019Article
- Ablation of Toll-like receptor 9 attenuates myocardial ischemia/reperfusion injury in mice.Biochemical and biophysical research communications · 2019Article
- TLR9 is essential for HMGB1-mediated post-myocardial infarction tissue repair through affecting apoptosis, cardiac healing, and angiogenesis.Cell death & disease · 2019Article
- Immune responses in cardiac repair and regeneration: a comparative point of view.Cellular and molecular life sciences : CMLS · 2019Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundToll-like receptors (TLRs) have been implicated in myocardial ischemia/reperfusion (I/R) injury. The TLR9 ligand, CpG-ODN has been reported to improve cell survival. We examined effect of CpG-ODN on myocardial I/R injury.
methodsMale C57BL/6 mice were treated with either CpG-ODN, control-ODN, or inhibitory CpG-ODN (iCpG-ODN) 1h prior to myocardial ischemia (60min) followed by reperfusion. Untreated mice served as I/R control (n=10/each group). Infarct size was determined by TTC straining. Cardiac function was examined by echocardiography before and after myocardial I/R up to 14days.
resultsCpG-ODN administration significantly decreased infarct size by 31.4% and improved cardiac function after myocardial I/R up to 14days. Neither control-ODN nor iCpG-ODN altered I/R-induced myocardial infarction and cardiac dysfunction. CpG-ODN attenuated I/R-induced myocardial apoptosis and prevented I/R-induced decrease in Bcl2 and increase in Bax levels in the myocardium. CpG-ODN increased Akt and GSK-3β phosphorylation in the myocardium. In vitro data suggested that CpG-ODN treatment induced TLR9 tyrosine phosphorylation and promoted an association between TLR9 and the p85 subunit of PI3K. Importantly, PI3K/Akt inhibition and Akt kinase deficiency abolished CpG-ODN-induced cardioprotection.
conclusionCpG-ODN, the TLR9 ligand, induces protection against myocardial I/R injury. The mechanisms involve activation of the PI3K/Akt signaling pathway.
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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.