ArticleAging cell2022
Advanced glycation end products induce senescence of atrial myocytes and increase susceptibility of atrial fibrillation in diabetic mice.
Article in Aging cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- Association of the chemerin-CMKLR1 with atrial potassium current dysregulation and atrial fibrillation in obese mice.Channels (Austin, Tex.) · 2026Article
- CaClinical and experimental pharmacology & physiology · 2026Article
- Multicellular senescence programs in the aged heart.Journal of molecular and cellular cardiology plus · 2026Review
- Racial and ethnic disparities in the management of risk factors in individuals with atrial fibrillation: A narrative review.American journal of preventive cardiology · 2026Review
- Sympathetic-like-integrated engineered heart tissue models AGEs-induced adverse remodeling.Cardiovascular diabetology · 2026Article
- Integrated Bioinformatic and Experimental Identification of DHCR24 and NRG1 as Key Cellular Aging Genes in Diabetic Cardiomyopathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Pathogenesis of Oxidative Stress Biomarkers in Atrial Fibrillation: A Narrative Review.The Journal of innovations in cardiac rhythm management · 2026Review
- Complex interrelationship and therapeutic advances in diabetic patients with atrial fibrillation.World journal of cardiology · 2025Review
- Cancer gene therapy: historical perspectives, current applications, and future directions.Functional & integrative genomics · 2025Review
- Multi-omics reveals mechanism of Qi-Po-Sheng-Mai granule in reducing atrial fibrillation susceptibility in aged rats.Chinese medicine · 2025Article
- Decreased PLK2 promotes atrial fibrillation in diabetic mice through Nrf2/HO-1 pathway.Acta diabetologica · 2025Article
- Cisd2 delays atrial aging via a modulation of calcium homeostasis that mitigates atrial myopathy.Cell communication and signaling : CCS · 2025Article
- Fructose-Induced Glycation End Products Promote Skin-Aging Phenotypes and Senescence Marker Expression in Human Dermal Fibroblasts.International journal of molecular sciences · 2025Article
- Dihydromyricetin May Attenuate Skin Aging as a RAGE Inhibitor.Nutrients · 2025Article
- The Advanced Glycation End-Products (AGE)-Receptor for AGE System (RAGE): An Inflammatory Pathway Linking Obesity and Cardiovascular Diseases.International journal of molecular sciences · 2025Review
- Ferroptosis: mechanism and role in diabetes-related cardiovascular diseases.Cardiovascular diabetology · 2025Review
- The Remodeling of Mitochondrial-Endoplasmic Reticulum Contacts by Omega-3 Fatty Acids Mitigates Dietary Advanced Glycation End Product-Driven Sertoli Cell Senescence and Oligoasthenozoospermia.International journal of biological sciences · 2025Article
- Distinct patterns of association between the hemoglobin glycation index, the stress-hyperglycemia ratio, and the risk of new-onset atrial fibrillation in critically ill patients.Frontiers in endocrinology · 2025Article
- Atrial myocyte senescence as a driver of atrial fibrillation: mechanisms and therapeutic implications.Frontiers in cell and developmental biology · 2025Review
- Glucose metabolic dysregulation of diabetes and Its role in atrial fibrillation pathogenesis.Frontiers in cardiovascular medicine · 2025Review
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Diabetes mellitus (DM) is a common chronic metabolic disease caused by significant accumulation of advanced glycation end products (AGEs). Atrial fibrillation (AF) is a common cardiovascular complication of DM. Here, we aim to clarify the role and mechanism of atrial myocyte senescence in the susceptibility of AF in diabetes. Rapid transesophageal atrial pacing was used to monitor the susceptibility of mice to AF. Whole-cell patch-clamp was employed to record the action potential (AP) and ion channels in single HL-1 cell and mouse atrial myocytes. More importantly, anti-RAGE antibody and RAGE-siRNA AAV9 were used to investigate the relationship among diabetes, aging, and AF. The results showed that elevated levels of p16 and retinoblastoma (Rb) protein in the atrium were associated with increased susceptibility to AF in diabetic mice. Mechanistically, AGEs increased p16/Rb protein expression and the number of SA-β-gal-positive cells, prolonged the action potential duration (APD), reduced protein levels of Cav1.2, Kv1.5, and current density of I
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