ArticleBasic research in cardiology2023
Splenic monocytes mediate inflammatory response and exacerbate myocardial ischemia/reperfusion injury in a mitochondrial cell-free DNA-TLR9-NLRP3-dependent fashion.
Article in Basic research in cardiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 28 citations in OpenAlex.
- Toll-like receptor 9-overexpressing red blood cell biomimetic microbubbles adsorb cell-free DNA to relieve steatotic liver ischemia-reperfusion injury.Materials today. Bio · 2026Article
- Sodium bicarbonate attenuates myocardial ischemia-reperfusion injury via activation of the splenic cholinergic anti-inflammatory pathway.JTCVS open · 2026Article
- The spleen-heart crosstalk in cardiovascular disease: integrating neural, immune, and secretory pathways.Acta pharmacologica Sinica · 2026Review
- Preemptive cardioprotection with a small molecule in rodents that suppresses genes predictive of heart failure.Science advances · 2026Article
- Mitochondrial DNA regulation of hepatic ischemia-reperfusion injury and intervention strategies.Journal of translational medicine · 2026Review
- The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities.MedComm · 2026Review
- Organelle stress in NLRP3 inflammasome: a central mediator of neurodegenerative diseases.Molecular neurodegeneration · 2026Review
- Circulating-free DNA: A promising tool for early detection of myocardial infarction.International journal of cardiology. Cardiovascular risk and prevention · 2025Review
- The E3 ubiquitin ligase MARCH9 alleviates pyroptosis by regulating NLPR3 ubiquitination following myocardial ischemia reperfusion.Cellular and molecular life sciences : CMLS · 2025Article
- Revealing Cell-Free Mitochondrial DNA Breakage Patterns as Novel Biomarkers for Sepsis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The spleen in ischaemic heart disease.Nature reviews. Cardiology · 2025Review
- [Asiaticoside alleviates myocardial ischemia-reperfusion injury in rats by inhibiting NLRP3 inflammasome-mediated pyroptosis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Mitochondrial dysfunction in AMI: mechanisms and therapeutic perspectives.Journal of translational medicine · 2025Review
- Cytosolic nucleic acid sensing as driver of critical illness: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2025Review
- pH-responsive cationic polymer-functionalized poly-ε-caprolactone microspheres scavenge cell-free-DNA to alleviate intestinal ischemia/reperfusion injury by inhibiting M1 macrophage polarization.Journal of nanobiotechnology · 2025Article
- Mitochondrial DNA in atherosclerosis research progress: a mini review.Frontiers in immunology · 2025Review
- Cell-free mitochondrial DNA as a pro-inflammatory agent in blood circulation: mechanisms, therapeutic implications, and clinical challenges in immune dysregulation.Frontiers in immunology · 2025Review
- Early and Late Treatment Influence on Chorioretinal Microvasculature in Vogt-Koyanagi-Harada Patients Using Optical Coherence Tomography Angiography.Translational vision science & technology · 2024Article
- Characterizing the immune response to myocardial infarction in pigs.Basic research in cardiology · 2024Article
- A single-chain antibody construct with specificity of a natural IgM antibody reduces hepatic ischemia reperfusion injury in mice.Journal of cellular and molecular medicine · 2024Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The spleen contributes importantly to myocardial ischemia/reperfusion (MI/R) injury. Nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) recruits inflammasomes, initiating inflammatory responses and mediating tissue injury. We hypothesize that myocardial cell-free DNA (cfDNA) activates the splenic NLRP3 inflammasome during early reperfusion, increases systemic inflammatory response, and exacerbates myocardial infarct. Mice were subjected to 40 min of ischemia followed by 0, 1, 5, or 15 min, or 24 h of reperfusion. Splenic leukocyte adoptive transfer was performed by injecting isolated splenocytes to mice with splenectomy performed prior to left coronary artery occlusion. CY-09 (4 mg/kg) was administered 5 min before reperfusion. During post-ischemic reperfusion, splenic protein levels of NLRP3, cleaved caspase-1, and interleukin-1β (IL-1β) were significantly elevated and peaked (2.1 ± 0.2-, 3.4 ± 0.4-, and 3.2 ± 0.2-fold increase respectively, p < 0.05) within 5 min of reperfusion. In myocardial tissue, NLRP3 was not upregulated until 24 h after reperfusion. Suppression by CY09, a specific NLRP3 inflammasome inhibitor, or deficiency of NLRP3 significantly reduced myocardial infarct size (17.3% ± 4.2% and 33.2% ± 1.8% decrease respectively, p < 0.01). Adoptive transfer of NLRP3
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