ArticleBiochemical pharmacology2017
Ablation of IL-33 gene exacerbate myocardial remodeling in mice with heart failure induced by mechanical stress.
Article in Biochemical pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05335629 (Evaluation of the Effect of Dapagliflozin on Cardiac Remodeling in Post Myocardial Infarction Patients), which is not on this map. Cited by 39 papers.
What it found
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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.
The trial behind it
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.
Evaluation of the Effect of Dapagliflozin on Cardiac Remodeling in Post Myocardial Infarction Patients
Who cites it
39 citing papers in PubMed.
- Using proximity extension proteomics assay to identify biomarkers associated with infarct size and ejection fraction after ST-elevation myocardial infarction.Scientific reports · 2020Trial
- Regulatory T cell attracting therapy accelerates skeletal muscle functional recovery following injury.Scientific reports · 2026Article
- The impact of inflammation, neuromodulation, and gut microbiota on developing cardiac fibrosis and hypertension.Cardiovascular research · 2026Review
- The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment.Journal of the American College of Cardiology · 2025Review
- From Natriuretic Peptides to microRNAs: Multi-Analyte Liquid Biopsy Horizons in Heart Failure.Biomolecules · 2025Review
- Cellular and Molecular Mechanisms Explaining the Link Between Inflammatory Bowel Disease and Heart Failure.Cells · 2025Review
- The immunology of diabetic cardiomyopathy.Frontiers in endocrinology · 2025Review
- Innovation through imitation: IL-33 decoys show promise in pulmonary fibrosis.The Journal of pharmacology and experimental therapeutics · 2025Article
- The Role of Alarmins in the Pathogenesis of Atherosclerosis and Myocardial Infarction.Current issues in molecular biology · 2024Review
- Fentanyl Overdose Causes Prolonged Cardiopulmonary Dysregulation in Male SKH1 Mice.Pharmaceuticals (Basel, Switzerland) · 2024Article
- The Role of Pro-Inflammatory Cytokines in the Pathogenesis of Cardiovascular Disease.International journal of molecular sciences · 2024Review
- Soluble Suppression of Tumorigenicity-2 Predicts Mortality and Right Heart Failure in Patients With a Left Ventricular Assist Device.Journal of the American Heart Association · 2024Observational
- Predictive value of low serum interleukin-33 levels in acute ischemic stroke outcomes.Frontiers in neurology · 2024Article
- Pathophysiological Effects of Various Interleukins on Primary Cell Types in Common Heart Disease.International journal of molecular sciences · 2023Review
- Knowledge mapping of interleukin-33: a bibliometric study.American journal of translational research · 2023Article
- IL-33/Regulatory T-Cell Axis Suppresses Skin Fibrosis.The Journal of investigative dermatology · 2022Article
- Soluble suppression of tumorigenesis-2 is a strong predictor of all-cause, cardiovascular and infection-related mortality risk in haemodialysis patients with diabetes mellitus.Clinical kidney journal · 2022Article
- Sclerostin aggravates cardiac remodeling after myocardial infarction by inhibition of Wnt/β-catenin signaling pathway.Journal of thoracic disease · 2022Article
- Transcriptome sequencing and lncRNA-miRNA-mRNA network construction in cardiac fibrosis and heart failure.Bioengineered · 2022Article
- Soft-Tissue Material Properties and Mechanogenetics during Cardiovascular Development.Journal of cardiovascular development and disease · 2022Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeST2 is one of the interleukin (IL)-1 receptor family members comprising of membrane-bound (ST2L) and soluble (sST2) isoforms. Clinical trials have revealed that serum sST2 levels predict outcome in patient with myocardial infarction or chronic heart failure (HF). Meanwhile, we and others have reported that ablation of ST2 caused exaggerated cardiac remodeling in both ischemic and non-ischemic HF. Here, we tested whether IL-33, the ligand for ST2, protects myocardium against HF induced by mechanical overload using ligand specific knockout (IL-33 METHODS AND
resultsTransverse aortic constriction (TAC)/sham surgery were carried out in both IL-33 and WT-littermates. Echocardiographic measurements were performed at frequent interval during the study period. Heart was harvested for RNA and histological measurements. Following mechanical overload by TAC, myocardial mRNA expressions of Th1 cytokines, such as TNF-α were enhanced in IL-33
conclusionsWe report for the first time that ablation of IL-33 directly and significantly leads to exacerbate cardiac remodeling with impaired cardiac function and survival upon mechanical stress. These data highlight the cardioprotective role of IL-33/ST2 system in the stressed myocardium and reveal a potential therapeutic role for IL-33 in non-ischemic HF.
Indexed as
Identifiers
28450225What Socratic holds
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 Socratic graph.