ArticleInternational journal of molecular sciences2018
High-Fat-Diet-Induced Obesity Produces Spontaneous Ventricular Arrhythmias and Increases the Activity of Ryanodine Receptors in Mice.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Hydroxytyrosol attenuates obesity-induced myocardial fibrosis by inhibiting NLRP3/CYLD/NOX4 mediated oxidative stress.NPJ science of food · 2026Article
- Article
- Oxidative Modifications in Cardiac Mitochondrial and CaHandbook of experimental pharmacology · 2026Review
- Effects of switching from a high-fat diet to a ketogenic diet on oxidative stress, nitrosative damage, and protein glycation in rat skin.Frontiers in immunology · 2026Article
- Brown adipose tissue: a potential therapeutic target for preventing cardiovascular disease in metabolic disorders.Diabetology & metabolic syndrome · 2025Article
- Impact of Obesity Caused by a High-Fat Diet on the Heart's Redox Balance.Antioxidants (Basel, Switzerland) · 2025Article
- Mechanistic Relevance of Ventricular Arrhythmias in Heart Failure with Preserved Ejection Fraction.International journal of molecular sciences · 2024Review
- Impact of high-fat diet on cognitive behavior and central and systemic inflammation with aging and sex differences in mice.Brain, behavior, and immunity · 2024Article
- Emerging Therapy for Diabetic Cardiomyopathy: From Molecular Mechanism to Clinical Practice.Biomedicines · 2023Review
- Adrenomedullin Improves Cardiac Remodeling and Function in Obese Rats with Hypertension.Pharmaceuticals (Basel, Switzerland) · 2022Article
- The role of metabolic syndrome in sudden cardiac death risk: Recent evidence and future directions.European journal of clinical investigation · 2022Review
- CaPflugers Archiv : European journal of physiology · 2022Review
- Tale of two kinases: Protein kinase A and CaWorld journal of diabetes · 2021Review
- Classic and Novel Sex Hormone Binding Globulin Effects on the Cardiovascular System in Men.International journal of endocrinology · 2021Review
- Preserved CaDiabetologia · 2020Article
- Mechanisms of Chronic Metabolic Stress in Arrhythmias.Antioxidants (Basel, Switzerland) · 2020Review
- Apocynin Treatment Prevents Cardiac Connexin 43 Hemichannels Hyperactivity by Reducing Nitroso-Redox Stress in Mdx Mice.International journal of molecular sciences · 2020Article
- Short high-fat diet interferes with the physiological maturation of the late adolescent mouse heart.Physiological reports · 2020Article
- Murine model of left ventricular diastolic dysfunction and electro-mechanical uncoupling following high-fat diet.International journal of obesity (2005) · 2020Article
- Calcium Homeostasis in Ventricular Myocytes of Diabetic Cardiomyopathy.Journal of diabetes research · 2020Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ventricular arrhythmias are a common cause of sudden cardiac death, and their occurrence is higher in obese subjects. Abnormal gating of ryanodine receptors (RyR2), the calcium release channels of the sarcoplasmic reticulum, can produce ventricular arrhythmias. Since obesity promotes oxidative stress and RyR2 are redox-sensitive channels, we investigated whether the RyR2 activity was altered in obese mice. Mice fed a high fat diet (HFD) became obese after eight weeks and exhibited a significant increase in the occurrence of ventricular arrhythmias. Single RyR2 channels isolated from the hearts of obese mice were more active in planar bilayers than those isolated from the hearts of the control mice. At the molecular level, RyR2 channels from HFD-fed mice had substantially fewer free thiol residues, suggesting that redox modifications were responsible for the higher activity. Apocynin, provided in the drinking water, completely prevented the appearance of ventricular arrhythmias in HFD-fed mice, and normalized the activity and content of the free thiol residues of the protein. HFD increased the expression of NOX4, an isoform of NADPH oxidase, in the heart. Our results suggest that HFD increases the activity of RyR2 channels via a redox-dependent mechanism, favoring the appearance of ventricular arrhythmias.
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