ArticleJournal of the American Heart Association2023
Microglia-Mediated Neuroimmune Response Regulates Cardiac Remodeling After Myocardial Infarction.
Article in Journal of the American Heart Association, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Research progress on microglial pyroptosis and inflammasomes: a comprehensive analysis.Frontiers in aging neuroscience · 2025Pooled it
- Tissue-Resident Macrophages: Linking Physiology and Inflammation in Infection.Clinical reviews in allergy & immunology · 2026Review
- Transcriptional Remodeling of Microglia After Experimental Myocardial Infarction.International journal of molecular sciences · 2026Article
- Myocardial Inflammation as Key Mediator of Heart-brain Interaction After Myocardial Ischemia/Infarction: Mechanistic Exploration of Post-Myocardial Infarction Cognitive Dysfunction.Current neuropharmacology · 2026Review
- Neural-immune-cardiovascular axis: from mechanistic crosstalk to therapeutic targets in cardiovascular disease.Frontiers in immunology · 2026Review
- 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
- Neurocardiac Crosstalk: Sympathetic Remodeling and Arrhythmogenesis After Myocardial Infarction.Current issues in molecular biology · 2025Review
- Identification of Diagnostic Biomarkers for Myocardial Infarction Using Bioinformatics and Disulfidptosis-Targeted Computational Drug Discovery.Mediators of inflammation · 2025Article
- Multimodal analyses of immune cells during bone repair identify macrophages as a therapeutic target in musculoskeletal trauma.Bone research · 2024Article
- Exploring personalized treatment for cardiac graft rejection based on a four-archetype analysis model and bioinformatics analysis.Scientific reports · 2024Article
- Circulating mitochondria promoted endothelial cGAS-derived neuroinflammation in subfornical organ to aggravate sympathetic overdrive in heart failure mice.Journal of neuroinflammation · 2024Article
- Stellate ganglion, inflammation, and arrhythmias: a new perspective on neuroimmune regulation.Frontiers in cardiovascular medicine · 2024Review
- Limitations of PLX3397 as a microglial investigational tool: peripheral and off-target effects dictate the response to inflammation.Frontiers in immunology · 2023Article
- The Anti-Inflammatory Mediator 17(R)-Resolvin D1 Attenuates Pressure Overload-Induced Cardiac Hypertrophy and Fibrosis.Drug design, development and therapy · 2023Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Sympathetic hyperactivity contributes to pathological remodeling after myocardial infarction (MI). However, the mechanisms underlying the increase in sympathetic activity remain unknown. Microglia are the predominant immune cells in the central nervous system and can regulate sympathetic neuron activity through neuroimmune response in the hypothalamic paraventricular nucleus. The present study aimed to investigate whether microglia-mediated neuroimmune response can regulate sympathetic activity and cardiac remodeling after MI. Methods and Results PLX3397 (pexidartinib) was used to deplete central microglia via intragastric injection or intracerebroventricular injection. After that, MI was induced by ligation of the left anterior descending coronary artery. Our study showed that MI resulted in the activation of microglia in the paraventricular nucleus. Microglia depletion, which was induced by PLX3397 treatment via intragastric injection or intracerebroventricular injection, improved cardiac function, reduced infarction size, and attenuated cardiomyocyte apoptosis, fibrosis, pathological electrical remodeling, and myocardial inflammation after MI. Mechanistically, these protective effects were associated with an attenuated neuroimmune response in the paraventricular nucleus, which contributed to the decrease of sympathetic activity and attenuation of sympathetic remodeling in the heart. However, intragastric injection with PLX3397 obviously depleted macrophages and induced neutrophil and T-lymphocyte disorders in the heart, blood, and spleen. Conclusions Microglia depletion in the central nervous system attenuates pathological cardiac remodeling after MI by inhibiting neuroimmune response and sympathetic activity. Intragastric administration of PLX3397 leads to serious deleterious effects in peripheral immune cells, especially macrophages, which should be a cause for concern in animal experiments and clinical practice.
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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.