ArticleCirculation2012
Interleukin-10 treatment attenuates pressure overload-induced hypertrophic remodeling and improves heart function via signal transducers and activators of transcription 3-dependent inhibition of nuclear factor-κB.
Article in Circulation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
112 citing papers in PubMed, 202 citations in OpenAlex.
- SGLT2 inhibitor therapy is associated with IL-10/TGF-α/sVEGFR3 signalling and adipose tissue remodelling in advanced heart failure.Journal of molecular and cellular cardiology plus · 2026Article
- Microfluidic Modeling of Macrophage-Induced Cardiac Inflammation Using NF-κB Reporter Cardiomyocytes.Advanced healthcare materials · 2026Article
- Review
- Pro- and Anti-Inflammatory Cytokines' Implication in Right Heart Disease, Arrhythmogenesis, and Atrial Fibrillation.Biomolecules · 2026Review
- The role of the bidirectional regulatory network between immune cells and stromal cells in cardiac repair and fibrosis following myocardial infarction.Frontiers in immunology · 2026Review
- PHLDA1 is a shared diagnostic and key mediator of inflammatory fibrosis in heart and kidney.Frontiers in immunology · 2026Article
- Unraveling the mechanism of curcumin in coronary slow flow phenomenon through network pharmacology and molecular docking.Scientific reports · 2025Article
- Engineered immune-driven theranostics for clinical cardiology.Military Medical Research · 2025Review
- 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
- CD163Basic research in cardiology · 2025Article
- Unleashing the potential of exercise: conquering cardiovascular disease by targeting inflammasome activation.European journal of medical research · 2025Review
- Molecular Cardiac Changes in Feline Hyperthyroidism and Hypertrophic Cardiomyopathy: Focus on Desmin, Calreticulin, and Interleukin-10 Expression.Animals : an open access journal from MDPI · 2025Article
- Polarized macrophages modulate cardiac structure and contractility under hypoxia in novel immuno-heart on a chip.APL bioengineering · 2025Article
- Small non-coding RNA YF1: A new dawn in heart transplantation.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Hypertrophic heart failure promotes gut dysbiosis and gut leakage in interleukin 10-deficient mice.American journal of physiology. Heart and circulatory physiology · 2025Article
- Global Research Trends and Focus on the Link Between Heart Failure and NLRP3 Inflammasome: A Bibliometric Analysis From 2010 to 2024.Journal of multidisciplinary healthcare · 2025Review
- Inflamed Skin, Burdened Heart: A Multidisciplinary Perspective on Atopic Dermatitis and Cardiovascular Health.Clinical, cosmetic and investigational dermatology · 2025Review
- In Vivo Anti-Inflammatory Activity of D-Limonene in a Rat Model of Monocrotaline-Induced Pulmonary Hypertension: Implications to the Heart Function.Arquivos brasileiros de cardiologia · 2024Article
- Circulating Plasma Proteins in Aortic Stenosis: Associations With Severity, Myocardial Response, and Clinical Outcomes.Journal of the American Heart Association · 2024Article
- Recent advances in understanding the roles of T cells in atrial fibrillation.NPJ cardiovascular health · 2024Article
52 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
backgroundInflammation plays a critical role in adverse cardiac remodeling and heart failure. Therefore, approaches geared toward inhibiting inflammation may provide therapeutic benefits. We tested the hypotheses that genetic deletion of interleukin-10 (IL-10), a potent antiinflammatory cytokine, exacerbates pressure overload-induced adverse cardiac remodeling and hypertrophy and that IL-10 therapy inhibits this pathology. METHODS AND
resultsCardiac hypertrophy was induced in wild-type and IL-10 knockout mice by isoproterenol (ISO) infusion. ISO-induced left ventricular dysfunction and hypertrophic remodeling, including fibrosis and fetal gene expression, were further exaggerated in knockout mice compared with wild-type mice. Systemic recombinant mouse IL-10 administration markedly improved left ventricular function and not only inhibited but also reversed ISO-induced cardiac remodeling. Intriguingly, a very similar cardioprotective response of IL-10 was found in transverse aortic constriction-induced hypertrophy and heart failure models. In neonatal rat ventricular myocytes and H9c2 myoblasts, ISO activated nuclear factor-κB and inhibited signal transducers and activators of transcription 3 (STAT3) phosphorylation. Interestingly, IL-10 suppressed ISO-induced nuclear factor-κB activation and attenuated STAT3 inhibition. Moreover, pharmacological and genetic inhibition of STAT3 reversed the protective effects of IL-10, whereas ectopic expression of constitutively active STAT3 mimicked the IL-10 responses on the ISO effects, confirming that the IL-10-mediated inhibition of nuclear factor-κB is STAT3 dependent.
conclusionTaken together, our results suggest IL-10 treatment as a potential therapeutic approach to limit the progression of pressure overload-induced adverse cardiac remodeling.
Indexed as
Identifiers
What 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.