ArticleScientific reports2019
Dysfunctional EAT thickness may promote maladaptive heart remodeling in CVD patients through the ST2-IL33 system, directly related to EPAC protein expression.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Exploring the impact of metabolic comorbidities on epicardial adipose tissue in heart failure with preserved ejection fraction.Cardiovascular diabetology · 2025Trial
- Review
- Epicardial adipose tissue in cardiovascular diseases: a potential therapeutic target.Frontiers in cardiovascular medicine · 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
- NSTEMI Risk Prediction with the Combination of the Biomarkers Epicardial Adipose Tissue and Soluble Suppression of Tumorigenicity 2.Medical science monitor : international medical journal of experimental and clinical research · 2025Observational
- Exploring the Involvement of New Members of the Interleukin Family in Cardiovascular Disease.Current cardiology reviews · 2025Review
- Unveiling IL-33/ST2 Pathway Unbalance in Cardiac Remodeling Due to Obesity in Zucker Fatty Rats.International journal of molecular sciences · 2023Article
- Risk factors for Keshan disease: a prospective cohort study protocol of gut flora.BMC cardiovascular disorders · 2020Article
- Correlative Study on Impaired Prostaglandin E2 Regulation in Epicardial Adipose Tissue and its Role in Maladaptive Cardiac Remodeling via EPAC2 and ST2 Signaling in Overweight Cardiovascular Disease Subjects.International journal of molecular sciences · 2020Article
- Circulating Soluble ST2 Predicts All-Cause Mortality in Severe Heart Failure Patients with an Implantable Cardioverter Defibrillator.Cardiology research and practice · 2020Article
- PCSK9 Expression in Epicardial Adipose Tissue: Molecular Association with Local Tissue Inflammation.Mediators of inflammation · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysfunctional epicardial adipose tissue (EAT) secretome can influence the heart's stretch response. However, the molecular mechanisms are still poorly understood. The aim of this study was to clarify how dysfunctional EAT promotes maladaptive heart remodeling in cardiovascular disease (CVD) through ST2 production associated with exchange protein directly activated by cAMP (EPAC) proteins. A series of 55 CVD males were enrolled and their EAT thickness, LV mass and volumes were measured by echocardiography. Blood, plasma and EAT biopsies were collected for molecular and proteomic assays. Taking EAT thickness as a continuous variable there was a direct correlation between the ST2 cardiac stretch mediator and EAT thickness (r = 0.54, p < 0.01) and an inverse relation between the ST2 gene and IL-33 expression (r -0.50, p < 0.01). In the CVD population EPAC2 expression directly correlated with the ST2 gene (r = 0.74, p < 0.0001) causing an ST2/IL-33 system local (p < 0.001) and systemic (sST2 = 57.33 ± 3.22 and IL-33 = 0.53 ± 017 pg/mL; p < 0.0001) protein imbalance associated with maladaptive remodeling. This indicated that dysfunctional EAT is a source of both EPAC and ST2 protein and an EPAC2 isoform seems involved in ST2 production in adipose tissue. Both EPAC2 and ST2 expression were directly related to maladaptive heart remodeling indices, suggesting EAT measurements could be useful in the early assessment of CVD complications.
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