ArticleRedox biology2019
TLR4 participates in sympathetic hyperactivity Post-MI in the PVN by regulating NF-κB pathway and ROS production.
Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.
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Who cites it
62 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.
- The Interaction of Central Nervous System and Acute Kidney Injury: Pathophysiology and Clinical Perspectives.Frontiers in physiology · 2022Pooled it
- Anti-angiogenic effect of exo-LncRNA TUG1 in myocardial infarction and modulation by remote ischemic conditioning.Basic research in cardiology · 2023Trial
- Metabolomics and Mechanistic Approaches Reveal the Synergistic and Attenuating of Rubus chingii Hu on Tripterygium Glycoside Tablets in the Treatment of Rheumatoid Arthritis.Chemistry & biodiversity · 2026Article
- Architecting NIR-II metal supramolecular dyes-illuminating the path to precision medicine.Chemical science · 2026Review
- Artemisinin attenuates 3-nitropropionic acid-induced neurodegeneration via HMGB1/TLR4/NF-κB modulation in a rat model of huntington's disease.Archives of pharmacal research · 2026Article
- Pyridostigmine Attenuated Placental Ischemia-Upregulated Paraventricular Nucleus TLR4-Associated Hypertension in Preeclamptic Rats.Molecular neurobiology · 2026Article
- The role of ubiquitination in the pathogenesis of atrial fibrillation: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Neurocardiac Crosstalk: Sympathetic Remodeling and Arrhythmogenesis After Myocardial Infarction.Current issues in molecular biology · 2025Review
- Beyond the Heart: The Neuroprotective Potential of Nebivolol in Acute Myocardial Infarction.Life (Basel, Switzerland) · 2025Article
- Review
- Exercise Intervention in Autonomic Function, Immunity, and Cardiovascular Health: A Precision Medicine Approach.Journal of cardiovascular development and disease · 2025Review
- Article
- Effect of electroacupuncture on hypertensive and sympathetic excitability mechanism mediated by the paraventricular nucleus of the hypothalamus in spontaneous hypertensive rats.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Ventricular Arrhythmias and Myocardial Infarction: Electrophysiological and Neuroimmune Mechanisms.Biomedicines · 2025Review
- Geniposide Protects Against Myocardial Infarction Injury via the Restoration in Gut Microbiota and Gut-Brain Axis.Journal of cellular and molecular medicine · 2025Article
- Biological engineering approaches for modulating the pathological microenvironment and promoting axonal regeneration after spinal cord injury.Frontiers in neuroscience · 2025Review
- P300-Targeted Acetylome Reveals a Role for HMGB1 Translocation in Central Cardiac Sympathetic Activation Post Myocardial Infarction.Journal of inflammation research · 2025Article
- Inhibition of CB1R in the Hypothalamic Paraventricular Nucleus Ameliorates Hypertension Through Wnt/β-Catenin/RAS Pathway.Cardiovascular toxicology · 2025Article
- mRNA-103 inhibition attenuates autophagy and inflammation in myocardial infarction by regulating the TLR4 pathway.Archives of medical science : AMS · 2025Article
- Tanshinone IIA Exerts Cardioprotective Effects Through Improving Gut-Brain Axis Post-Myocardial Infarction.Cardiovascular toxicology · 2024Article
2 more citing papers are in PubMed but not listed here.
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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
Sympathetic nerve hyperactivity is a primary reason for fatal ventricular arrhythmias (VAs) following myocardial infarction (MI). Pro-inflammatory cytokines produced in the paraventricular nucleus (PVN) post-MI are associated with sympathetic overexcitation; however, the precise mechanism needs further investigation. Our aim was to explore the mechanism of toll-like receptor 4 (TLR4) and its downstream molecular pathway in mediating sympathetic activity post-MI within the PVN. A rat MI model was developed via left anterior descending coronary artery ligation. TLR4 was primarily localized in microglia and increased markedly within the PVN at 3 days in MI rats. Sympathoexcitation also increased, as indicated by high levels of renal sympathetic nerve activity (RSNA) and norepinephrine (NE) concentration. TLR4 knockdown via shRNA microinjection to the PVN resulted in decreased activation of Fos protein (+) neurons in the PVN and peripheral sympathetic nerve activity. TLR4 knockdown also exhibited a lower arrhythmia score following programmed electrical stimulation than those treated with MI surgery only, indicating that the knockdown of TLR4 decreased the incidence of malignant ventricular arrhythmias following MI. LPS-induced inflammatory response was analyzed to explore the underlying mechanism of TLR4 in sympathetic hyperactivity. High levels of NF-κB protein, the pro-inflammatory cytokines IL-1β and TNF-α, and ROS production were observed in the LPS group. PVN-targeted injection of the NF-κB inhibitor PDTC attenuated NF-κB expression and sympathetic activity. Taken together, the results suggested that knockdown of microglial TLR4 within the PVN decreased sympathetic hyperactivity and subsequent VAs post-MI. The downstream NF-κB pathway and ROS production participated in the process. Interventions targeting TLR4 signaling in the PVN may be a novel approach to ameliorate the incidence of VAs post-MI.
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