ArticleJournal of cellular and molecular medicine2019
Microglial Mincle receptor in the PVN contributes to sympathetic hyperactivity in acute myocardial infarction rat.
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, 41 citations in OpenAlex.
- Role of Exercise in Modulating the Brain-Heart Axis in Cardiovascular Diseases.International journal of molecular sciences · 2026Review
- Study on Immune-Related Genes and Clinical Validation of Acute Myocardial Infarction Based on Bioinformatics.Biochemical genetics · 2026Article
- PVN-centered multi-omics and single-cell analyses suggest shared inflammatory and immune features in acute myocardial infarction-associated ventricular arrhythmia and atrial fibrillation.Frontiers in cardiovascular medicine · 2026Article
- Beyond the Heart: The Neuroprotective Potential of Nebivolol in Acute Myocardial Infarction.Life (Basel, Switzerland) · 2025Article
- Sleep fragmentation exacerbates myocardial ischemia-reperfusion injury via hypothalamic paraventricular nucleus-resident OX1R-mediated sympathetic hyperactivity in adult mice.Annals of medicine · 2025Article
- Ventricular Arrhythmias and Myocardial Infarction: Electrophysiological and Neuroimmune Mechanisms.Biomedicines · 2025Review
- Balancing Microglial Density and Activation in Central Nervous System Development and Disease.Current issues in molecular biology · 2025Review
- The effects of hypothalamic microglial activation on ventricular arrhythmias in stress cardiomyopathy.Journal of geriatric cardiology : JGC · 2024Article
- Tanshinone IIA Exerts Cardioprotective Effects Through Improving Gut-Brain Axis Post-Myocardial Infarction.Cardiovascular toxicology · 2024Article
- The association between joint Serum Neurofilament Light Chain and type 2 diabetes with all-cause and cardiovascular mortality in US adults: a longitudinal study of NHANES.BMC endocrine disorders · 2024Article
- IL-1 signaling pathway, an important target for inflammation surrounding in myocardial infarction.Inflammopharmacology · 2024Review
- Proteomic study of left ventricle and cortex in rats after myocardial infarction.Scientific reports · 2024Article
- Genetic determinants of blood pressure and heart rate identified through ENU-induced mutagenesis with automated meiotic mapping.Science advances · 2024Article
- Circulating mitochondria promoted endothelial cGAS-derived neuroinflammation in subfornical organ to aggravate sympathetic overdrive in heart failure mice.Journal of neuroinflammation · 2024Article
- Neutrophil extracellular traps aggravate neuronal endoplasmic reticulum stress and apoptosis via TLR9 after traumatic brain injury.Cell death & disease · 2023Article
- Microglia-Mediated Neuroimmune Response Regulates Cardiac Remodeling After Myocardial Infarction.Journal of the American Heart Association · 2023Article
- Fir(e)ing the Rhythm: Inflammatory Cytokines and Cardiac Arrhythmias.JACC. Basic to translational science · 2023Review
- Noise exposure and its relationship with postinfarction cardiac remodeling: implications for NLRP3 inflammasome activation.Bioengineered · 2022Article
- MCC950 ameliorates ventricular arrhythmia vulnerability induced by heart failure.Bioengineered · 2022Article
- New insights into the central sympathetic hyperactivity post-myocardial infarction: Roles of METTL3-mediated mJournal of cellular and molecular medicine · 2022Article
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant ventricular arrhythmias (VAs) following myocardial infarction (MI) is a lethal complication resulting from sympathetic nerve hyperactivity. Numerous evidence have shown that inflammation within the paraventricular nucleus (PVN) participates in sympathetic hyperactivity. Our aim was to explore the role of Macrophage-inducible C-type lectin (Mincle) within the PVN in augmenting sympathetic activity following MI,and whether NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome/IL-1β axis is involved in this activity. MI was induced by coronary artery ligation. Mincle expression localized in microglia within the PVN was markedly increased at 24 hours post-MI together with sympathetic hyperactivity, as indicated by measurement of the renal sympathetic nerve activity (RSNA) and norepinephrine (NE) concentration. Mincle-specific siRNA was administrated locally to the PVN, which consequently decreased microglial activation and sympathetic nerve activity. The MI rats exhibited a higher arrhythmia score after programmed electric stimulation than that treated with Mincle siRNA, suggesting that the inhibition of Mincle attenuated foetal ventricular arrhythmias post-MI. The underlying mechanism of Mincle in sympathetic hyperactivity was investigated in lipopolysaccharide (LPS)-primed naïve rats. Recombinant Sin3A-associated protein 130kD (rSAP130), an endogenous ligand for Mincle, induced high levels of NLRP3 and mature IL-1β protein. PVN-targeted injection of NLRP3 siRNA or IL-1β antagonist gevokizumab attenuated sympathetic hyperactivity. Together, the data indicated that the knockdown of Mincle in microglia within the PVN prevents VAs by attenuating sympathetic hyperactivity and ventricular susceptibility, in part by inhibiting its downstream NLRP3/IL-1β axis following MI. Therapeutic interventions targeting Mincle signalling pathway could constitute a novel approach for preventing infarction injury.
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