ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2023
Activating α7nAChR helps post-myocardial infarction healing by regulating macrophage polarization via the STAT3 signaling pathway.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- The Origin and Application of Cardiomyocyte-Derived Small Extracellular Vesicles: A Systematic Review.International journal of medical sciences · 2026Pooled it
- The effect of remote ischemic preconditioning on postoperative gastrointestinal function recovery in patients undergoing gynecological laparoscopic surgery: a prospective randomized controlled trial.BMC women's health · 2026Trial
- The impact of inflammation, neuromodulation, and gut microbiota on developing cardiac fibrosis and hypertension.Cardiovascular research · 2026Review
- Activation of α7nAChR prevents maladaptive right ventricular remodeling via inhibiting the recruitment of CCR2Respiratory research · 2026Article
- The neuroimmune axis in cardiovascular disease: from immune activation to inflammatory resolution.Frontiers in immunology · 2026Review
- The Neuroimmune Axis in Sepsis: From Pathophysiological Circuits to Precision Neuromodulation.Journal of inflammation research · 2026Review
- Association of Systemic Inflammation Indices With Mortality in Coronary Atherosclerosis Patients With and Without Standard Modifiable Risk Factors.Mediators of inflammation · 2026Article
- α7nAChR alleviates cognitive impairment by promoting autophagy in astrocytes via CaMKK2/AMPK/mTOR pathway in sepsis-associated encephalopathy.Frontiers in immunology · 2026Article
- Targeting α7 Nicotinic Acetylcholine Receptor for Modulating the Neuroinflammation of Dry Eye Disease Via Macrophages.Investigative ophthalmology & visual science · 2025Article
- Mesenchymal stem cells derived exosomes: a new era in cardiac regeneration.Stem cell research & therapy · 2025Review
- Role of Monocyte/Macrophage-Associated Gene Ccl9 in Acute Myocardial Infarction Analysis: Based on Bulk and Single Cell RNA Sequencing Data.Journal of inflammation research · 2025Article
- Activating α7nAChR suppresses systemic inflammation by mitigating neuroinflammation of the medullary visceral zone in sepsis in a rat model.Translational neuroscience · 2024Article
- Nicorandil-Pretreated Mesenchymal Stem Cell-Derived Exosomes Facilitate Cardiac Repair After Myocardial Infarction via Promoting Macrophage M2 Polarization by Targeting miR-125a-5p/TRAF6/IRF5 Signaling Pathway.International journal of nanomedicine · 2024Article
- Cholinergic Polarization of Human Macrophages.International journal of molecular sciences · 2023Review
- Retinal Microenvironment-Protected Rhein-GFFYE Nanofibers Attenuate Retinal Ischemia-Reperfusion Injury via Inhibiting Oxidative Stress and Regulating Microglial/Macrophage M1/M2 Polarization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
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Authors and funding
9 authors at 4 institutions in 1 country.
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Abstract
backgroundMonocytes/macrophages play critical roles in inflammation and cardiac remodeling following myocardial infarction (MI). The cholinergic anti-inflammatory pathway (CAP) modulates local and systemic inflammatory responses by activating α7 nicotinic acetylcholine receptors (α7nAChR) in monocytes/macrophages. We investigated the effect of α7nAChR on MI-induced monocyte/macrophage recruitment and polarization and its contribution to cardiac remodeling and dysfunction.
methodsAdult male Sprague Dawley rats underwent coronary ligation and were intraperitoneally injected with the α7nAChR-selective agonist PNU282987 or the antagonist methyllycaconitine (MLA). RAW264.7 cells were stimulated with lipopolysaccharide (LPS) + interferon-gamma (IFN-γ) and treated with PNU282987, MLA, and S3I-201 (a STAT3 inhibitor). Cardiac function was evaluated by echocardiography. Masson's trichrome and immunofluorescence were used to detect cardiac fibrosis, myocardial capillary density, and M1/M2 macrophages. Western blotting was used to detect protein expression, and the proportion of monocytes was measured using flow cytometry.
resultsActivating the CAP with PNU282987 significantly improved cardiac function and reduced cardiac fibrosis and 28-day mortality after MI. On days 3 and 7 post-MI, PNU282987 reduced the percentage of peripheral CD172a + CD43low monocytes and the infiltration of M1 macrophages in the infarcted hearts, whereas it increased the recruitment of peripheral CD172a + CD43high monocytes and M2 macrophages. Conversely, MLA exerted the opposite effects. In vitro, PNU282987 inhibited M1 macrophage polarization and promoted M2 macrophage polarization in LPS + IFN-γ-stimulated RAW264.7 cells. These PNU282987-induced changes in LPS + IFN-γ-stimulated RAW264.7 cells were reversed by administering S3I-201.
conclusionActivating α7nAChR inhibits the early recruitment of pro-inflammatory monocytes/macrophages during MI and improves cardiac function and remodeling. Our findings suggest a promising therapeutic target for regulating monocyte/macrophage phenotypes and promoting healing after MI.
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