ArticleEuropean heart journal2018
IL-18 cleavage triggers cardiac inflammation and fibrosis upon β-adrenergic insult.
Article in European heart journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers, 1 of them a synthesis that pooled it.
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Who cites it
159 citing papers in PubMed, 1 synthesis or guideline pooled it, 293 citations in OpenAlex.
- Diagnostic and prognostic value of circulating biomarkers in heart failure.Frontiers in cardiovascular medicine · 2025Pooled it
- A SpecificFrontiers in immunology · 2020Trial
- P2X7-NEK7-NLRP3 Axis Drives Cardiac Inflammation and Fibrosis in Isoproterenol-Induced Cardiac Remodeling in Mice.Acta physiologica (Oxford, England) · 2026Article
- Impact of genetic polymorphisms in the interleukin-18 and interleukin-21 genes on the risk and clinical outcomes of multiple sclerosis.BMC neurology · 2026Article
- The impact of inflammation, neuromodulation, and gut microbiota on developing cardiac fibrosis and hypertension.Cardiovascular research · 2026Review
- Dimethyl Fumarate Reverses β-Adrenoceptor-Mediated Myocardial Fibrosis in Mice by Inhibiting Yes-Associated Protein-Regulated Expression of Intermediate-Conductance CaJournal of the American Heart Association · 2026Article
- Distinct immunometabolic signatures of type 1 versus type 2 diabetes in a murine model of myocardial infarction.Cardiovascular diabetology · 2026Article
- IL-18 promotes pancreatic fibrosis via release of IL-4 from pancreatic stellate cells and induces macrophage M2 polarization.Scientific reports · 2026Article
- Temporal Exercise Conditioning Confers Dual-Phase Cardioprotection Against Isoproterenol-Induced Injury in a Rat Model.Antioxidants (Basel, Switzerland) · 2026Article
- Immunometabolic regulation of cardiac macrophages in heart failure with preserved ejection fraction.Frontiers in immunology · 2026Review
- NLRP3 inflammasome in cardiovascular diseases: molecular mechanisms and advances in targeted drug research.Frontiers in immunology · 2026Review
- The mechanism of electrical remodeling in atrial fibrillation and current research status of natural drugs and active ingredients inhibiting atrial electrical remodeling.Frontiers in cardiovascular medicine · 2026Review
- Caspase-1 inhibition mitigates neonatal hyperoxia-induced vascular and cardiopulmonary inflammation in neonatal rats.Clinical science (London, England : 1979) · 2025Article
- Inflammasomes as Potential Therapeutic Targets to Prevent Chronic Active Viral Myocarditis-Translating Basic Science into Clinical Practice.International journal of molecular sciences · 2025Review
- Lung-Derived Small Extracellular Vesicles Containing miR-15a-5p/miR-96-5p Promote Myocardial Fibrosis in Hypertrophic Cardiomyopathy via Targeting SMAD7.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Targeting pyroptosis in myocardial inflammation and fibrosis: molecular mechanisms and therapeutic strategies.Apoptosis : an international journal on programmed cell death · 2025Review
- P2X7 receptor is essential for ST36-attenuated cardiac fibrosis upon beta-adrenergic insult.Purinergic signalling · 2025Article
- Association Between Triglyceride-Glucose Index and Prognosis of Patients with Hypertrophic Cardiomyopathy and Heart Failure with Preserved Ejection Fraction.Anatolian journal of cardiology · 2025Article
- Sympathetic reactivity to physiological stress is associated with expanded cardiac extracellular volume in humans.BMC medicine · 2025Article
- The Genetic Puzzle of the Stress-Induced Cardiomyopathy (Takotsubo Syndrome): State of Art and Future Perspectives.Biomolecules · 2025Review
99 more citing papers are in PubMed but not listed here.
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Authors and funding
20 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aims: Rapid over-activation of β-adrenergic receptor (β-AR) upon stress leads to cardiac inflammation, a prevailing factor that underlies heart injury. However, mechanisms by which acute β-AR stimulation induce cardiac inflammation still remain unknown. Here, we set out to identify the crucial role of inflammasome/interleukin (IL)-18 in initiating and maintaining cardiac inflammatory cascades upon β-AR insult. Methods and results: Male C57BL/6 mice were injected with a single dose of β-AR agonist, isoproterenol (ISO, 5 mg/kg body weight) or saline subcutaneously. Cytokine array profiling demonstrated that chemokines dominated the initial cytokines upregulation specifically within the heart upon β-AR insult, which promoted early macrophage infiltration. Further investigation revealed that the rapid inflammasome-dependent activation of IL-18, but not IL-1β, was the critical up-stream regulator for elevated chemokine expression in the myocardium upon ISO induced β1-AR-ROS signalling. Indeed, a positive correlation was observed between the serum levels of norepinephrine and IL-18 in patients with chest pain. Genetic deletion of IL-18 or the up-stream inflammasome component NLRP3 significantly attenuated ISO-induced chemokine expression and macrophage infiltration. In addition, IL-18 neutralizing antibodies selectively abated ISO-induced chemokines, proinflammatory cytokines and adhesion molecules but not growth factors. Moreover, blocking IL-18 early after ISO treatment effectively attenuated cardiac inflammation and fibrosis. Conclusion: Inflammasome-dependent activation of IL-18 within the myocardium upon acute β-AR over-activation triggers cytokine cascades, macrophage infiltration and pathological cardiac remodelling. Blocking IL-18 at the early stage of β-AR insult can successfully prevent inflammatory responses and cardiac injuries.
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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.