ArticleScientific reports2017
Very-Low-Density Lipoprotein of Metabolic Syndrome Modulates Gap Junctions and Slows Cardiac Conduction.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Patients' experiences across the trajectory of atrial fibrillation: A qualitative systematic review.Health expectations : an international journal of public participation in health care and health policy · 2022Pooled it
- The role of postprandial very-low-density lipoprotein in the development of atrial remodeling in metabolic syndrome.Lipids in health and disease · 2020Trial
- Very low-density lipoprotein and the human health.World journal of experimental medicine · 2026Review
- Phenotypic Analysis of P-Wave Morphology as a Key Determinant of Late Recurrence Post-Ablation in Paroxysmal Atrial Fibrillation.Journal of arrhythmia · 2026Article
- Cellular basis of HFpEF: contributions of abnormal lipids.Frontiers in cardiovascular medicine · 2026Review
- Mechanism of the cardioprotective effect of empagliflozin on diabetic nephropathy mice based on the basis of proteomics.Proteome science · 2024Article
- Aging-associated atrial fibrillation: A comprehensive review focusing on the potential mechanisms.Aging cell · 2024Review
- Association of lipid composition and unsaturated fatty acids of VLDL with atrial remodeling in metabolic syndrome.Scientific reports · 2023Article
- The roles of connexins and gap junctions in the progression of cancer.Cell communication and signaling : CCS · 2023Review
- Connexins and Glucose Metabolism in Cancer.International journal of molecular sciences · 2022Review
- Emerging Evidence of Pathological Roles of Very-Low-Density Lipoprotein (VLDL).International journal of molecular sciences · 2022Review
- Article
- Research Progress of Myocardial Fibrosis and Atrial Fibrillation.Frontiers in cardiovascular medicine · 2022Review
- Characteristics of Ventricular Electrophysiological Substrates in Metabolic Mice Treated with Empagliflozin.International journal of molecular sciences · 2021Article
- The Pathogenic Role of Very Low Density Lipoprotein on Atrial Remodeling in the Metabolic Syndrome.International journal of molecular sciences · 2020Review
- Shensong Yangxin Protects Against Metabolic Syndrome-Induced Ventricular Arrhythmias by Inhibiting Electrical Remodeling.Frontiers in pharmacology · 2020Article
- Very Low-Density Lipoproteins of Metabolic Syndrome Modulates STIM1, Suppresses Store-Operated Calcium Entry, and Deranges Myofilament Proteins in Atrial Myocytes.Journal of clinical medicine · 2019Article
- Therapeutic Potential of Oxytocin in Atherosclerotic Cardiovascular Disease: Mechanisms and Signaling Pathways.Frontiers in neuroscience · 2019Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Very-low-density lipoproteins (VLDL) is a hallmark of metabolic syndrome (MetS) and each manifestation of MetS is related to atrial fibrillation (AF) risks. Slowed atrial conduction is a mechanism of AF in MetS. We hypothesized that VLDL can modulate and reduce atrial gap junctions. VLDLs were separated from normal (Normal-VLDL) and MetS (MetS-VLDL) individuals. VLDLs (15 µg/g) and equivalent volumes of saline (CTL) were injected respectively to C57BL/6 mice for 6 weeks. Electrocardiograms demonstrated that MetS-VLDL induced prolongation of P wave (P = 0.041), PR intervals (P = 0.014), QRS duration and QTc interval (both P = 0.003), but Normal-VLDL did not. Optical mapping of perfused hearts confirmed slowed conduction on atria and ventricles of MetS-VLDL mice. Slowed cardiac conduction was associated with significant atrial and ventricular remodeling, along with systolic dysfunction and comparable intra-cardiac fibrosis. MetS-VLDL induced downregulation of Cx40 and Cx43 at transcriptional, translational and tissue levels, and it also enhanced O-GlcNAcylation of Cx40 and Cx43. Protein structure analyses predicted O-GlcNAcylation at serine 18 of Cx40 and Cx43 which may impair stability of gap junctions. In conclusion, MetS-VLDL modulates gap junctions and delays both atrial and ventricular conduction. VLDL may contribute to the pathophysiology of atrial fibrillation and ventricular arrhythmias in MetS.
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Registered trials
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