ArticleJournal of molecular and cellular cardiology2014
Pressure overload induces IL-18 and IL-18R expression, but markedly suppresses IL-18BP expression in a rabbit model. IL-18 potentiates TNF-α-induced cardiomyocyte death.
Article in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 46 citations in OpenAlex.
- Research progress on programmed cell death of cardiomyocytes in pressure-overload hypertrophic cardiomyopathy.Apoptosis : an international journal on programmed cell death · 2025Review
- NLRP3 Inflammasome: A New Target for the Treatment of CVD and Depression Comorbidity.Mediators of inflammation · 2025Review
- New and future heart failure drugs.Nature cardiovascular research · 2024Review
- Regulated Cell Death Pathways in Pathological Cardiac Hypertrophy.Reviews in cardiovascular medicine · 2024Review
- Large animal models of pressure overload-induced cardiac left ventricular hypertrophy to study remodelling of the human heart with aortic stenosis.Cardiovascular research · 2024Review
- Insulin-like growth factor 1 enhances follicle-stimulating hormone-induced phosphorylation of GATA4 in rat granulosa cells.Molecular and cellular endocrinology · 2023Article
- Degenerative changes of the aortic valve during left ventricular assist device support.ESC heart failure · 2022Article
- Cardiac Remodeling in Heart Failure: Role of Pyroptosis and Its Therapeutic Implications.Frontiers in cardiovascular medicine · 2022Review
- Risk assessment model for heart failure in Chinese patients with Takayasu's arteritis.Clinical rheumatology · 2021Article
- In-Depth Analysis of the Plasma Proteome in ME/CFS Exposes Disrupted Ephrin-Eph and Immune System Signaling.Proteomes · 2021Article
- Fontan Circulation Might be Associated with Peripartum Cardiomyopathy: A Review of Mechanistic and Clinical Aspects.Current cardiology reviews · 2021Review
- Mechanobiological Principles Influence the Immune Response in Regeneration: Implications for Bone Healing.Frontiers in bioengineering and biotechnology · 2021Review
- Caspase-1 Abrogates the Salutary Effects of Hypertrophic Preconditioning in Pressure Overload Hearts via IL-1β and IL-18.Frontiers in molecular biosciences · 2021Article
- Comprehensive Mechanism, Novel Markers and Multidisciplinary Treatment of Severe Acute Pancreatitis-Associated Cardiac Injury - A Narrative Review.Journal of inflammation research · 2021Review
- Inflammation in Metabolic Cardiomyopathy.Frontiers in cardiovascular medicine · 2021Review
- Association between C-reactive protein levels at hospital admission and long-term mortality in patients with acute decompensated heart failure.Heart and vessels · 2019Article
- Role of interleukins in heart failure with reduced ejection fraction.Anatolian journal of cardiology · 2019Review
- Regulatory Mechanisms of the NLRP3 Inflammasome, a Novel Immune-Inflammatory Marker in Cardiovascular Diseases.Frontiers in immunology · 2019Review
- Low-level transcutaneous vagus nerve stimulation attenuates cardiac remodelling in a rat model of heart failure with preserved ejection fraction.Experimental physiology · 2019Article
- Inflammation in Right Ventricular Failure: Does It Matter?Frontiers in physiology · 2018Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
Recurrent or sustained inflammation plays a causal role in the development and progression of left ventricular hypertrophy (LVH) and its transition to failure. Interleukin (IL)-18 is a potent pro-hypertrophic inflammatory cytokine. We report that induction of pressure overload in the rabbit, by constriction of the descending thoracic aorta induces compensatory hypertrophy at 4weeks (mass/volume ratio: 1.7±0.11) and ventricular dilatation indicative of heart failure at 6weeks (mass/volume ratio: 0.7±0.04). In concordance with this, fractional shortening was preserved at 4weeks, but markedly attenuated at 6weeks. We cloned rabbit IL-18, IL-18Rα, IL-18Rβ, and IL-18 binding protein (IL-18BP) cDNA, and show that pressure overload, while enhancing IL-18 and IL-18R expression in hypertrophied and failing hearts, markedly attenuated the level of expression of the endogenous IL-18 antagonist IL-18BP. Cyclical mechanical stretch (10% cyclic equibiaxial stretch, 1Hz) induced hypertrophy of primary rabbit cardiomyocytes in vitro and enhanced ANP, IL-18, and IL-18Rα expression. Further, treatment with rhIL-18 induced its own expression and that of IL-18Rα via AP-1 activation, and induced cardiomyocyte hypertrophy in part via PI3K/Akt/GATA4 signaling. In contrast, IL-18 potentiated TNF-α-induced cardiomyocyte death, and by itself induced cardiac endothelial cell death. These results demonstrate that pressure overload is associated with enhanced IL-18 and its receptor expression in hypertrophied and failingrabbit hearts. Since IL-18BP expression is markedly inhibited, our results indicate a positive amplification in IL-18 proinflammatory signaling during pressure overload, and suggest IL-18 as a potential therapeutic target in pathological hypertrophy and cardiac failure.
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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.