ArticleJournal of the American Heart Association2023
Epicardial Adipose Tissue-Derived Leptin Promotes Myocardial Injury in Metabolic Syndrome Rats Through PKC/NADPH Oxidase/ROS Pathway.
Article in Journal of the American Heart Association, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- A new insight on imaging characteristics of pericoronary adipose tissue for cardiovascular risk.Cardiovascular ultrasound · 2026Review
- The Adipokine Axis in Heart Failure: Linking Obesity, Sarcopenia and Cardiac Dysfunction in HFpEF.International journal of molecular sciences · 2026Review
- Oxidative stress and bone marrow adipocytes: Molecular mechanisms and possible implications.Journal of orthopaedic translation · 2026Review
- Epicardial adipose tissue as a metabolically active visceral fat depot: an emerging target in cardiovascular disease.Frontiers in cardiovascular medicine · 2026Review
- Selective Mid-Wall Cardiac Dysfunction in Obesity: The Role of Muscle-to-Fat Balance.Biomedicines · 2025Article
- Desloratadine as the selective 5HTJournal of neuroinflammation · 2025Article
- Heart-guarding or heart-harming? The dual role of epicardial adipose tissue in cardiovascular health and disease.International journal of obesity (2005) · 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
- Beyond Traditional Risk Factors: Integrating Epicardial Adipose Tissue into the Comorbidity Landscape of HFpEF.Journal of clinical medicine · 2025Review
- Methods to model epicardial adipose tissue-mediated atrial fibrillation.NPJ cardiovascular health · 2025Review
- Understanding the Role of Adipokines in Cardiometabolic Dysfunction: A Review of Current Knowledge.Biomolecules · 2025Review
- Correlation analysis between epicardial adipose tissue and acute coronary syndrome.Scientific reports · 2025Article
- Linking serum leptin and TSH among metabolic syndrome patients with and without hypothyroidism.Bioinformation · 2025Article
- New Mechanisms to Prevent Heart Failure with Preserved Ejection Fraction Using Glucagon-like Peptide-1 Receptor Agonism (GLP-1 RA) in Metabolic Syndrome and in Type 2 Diabetes: A Review.International journal of molecular sciences · 2024Review
- The Role of Epicardial Adipose Tissue in Acute Coronary Syndromes, Post-Infarct Remodeling and Cardiac Regeneration.International journal of molecular sciences · 2024Review
- Assessing the Relationship between Indexed Epicardial Adipose Tissue Thickness, Oxidative Stress in Adipocytes, and Coronary Artery Disease Complexity in Open-Heart Surgery Patients.Medicina (Kaunas, Lithuania) · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background The epicardial adipose tissue (EAT) of metabolic syndrome (MetS) is abnormally accumulated with dysfunctional secretion of adipokines, closely relating to cardiac dysfunction. The current study was designed to identify the effects of EAT-derived leptin on the myocardium of MetS rats and explore the potential molecular mechanisms. Methods and Results A MetS rat model was established in 8-week-old Wistar rats by a 12-week high-fat diet. MetS rats exhibited increased leptin secretion from EAT, cardiac hypertrophy, and diastolic dysfunction with preserved systolic function. The myocardium of MetS rats had abnormal structure, increased oxidative stress injury, and higher inflammatory factor levels, especially the subepicardial myocardium, which was correlated with the EAT-derived leptin level but not the serum leptin. The EAT was separated from each group of rats to prepare EAT-conditioned medium. H9C2 rat cardiomyoblasts were treated with EAT-conditioned medium or leptin, plus various inhibitors. EAT-derived leptin from MetS rats promoted mitochondrial oxidative stress and dysfunction, induced mitochondrial pathway apoptosis, and inhibited cell viability in H9C2 cardiomyoblasts via the protein kinase C/reduced nicotinamide adenine dinucleotide phosphate oxidase/reactive oxygen species (PKC/NADPH oxidase/ROS) pathway. EAT-derived leptin from MetS rats stimulated inflammation in H9C2 cardiomyocytes by promoting activator protein 1 nuclear translocation via the PKC/NADPH oxidase/ROS pathway. Leptin promoted the interaction between p-p47
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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 Socratic graph.