ArticleJournal of cardiovascular translational research2020
Role of NLRP3-Inflammasome/Caspase-1/Galectin-3 Pathway on Atrial Remodeling in Diabetic Rabbits.
Article in Journal of cardiovascular translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
- The clinical pathophysiology of atrial fibrillation: outstanding questions from bedside to bench and back.Physiological reviews · 2026Review
- Expression, Localization and Actions of Galectin-3: Implications in the Pathophysiology and Therapy of Cardiovascular Disease.International journal of molecular sciences · 2026Review
- Complex interrelationship and therapeutic advances in diabetic patients with atrial fibrillation.World journal of cardiology · 2025Review
- Atrial Fibrillation in Diabetes: Pathogenesis and Targeted Rhythm Control Strategies.Current issues in molecular biology · 2025Review
- Concomitant Diabetes and Atrial Fibrillation: Epicardial Fat and Macrophage-Related Mechanisms.Diabetes/metabolism research and reviews · 2025Review
- Inflammasome Signaling in Cardiac Arrhythmias: Linking Inflammation, Fibrosis, and Electrical Remodeling.International journal of molecular sciences · 2025Review
- Efficacy of Colchicine in Reducing NT-proBNP, Caspase-1, TGF-β, and Galectin-3 Expression and Improving Echocardiography Parameters in Acute Myocardial Infarction: A Multi-Center, Randomized, Placebo-Controlled, Double-Blinded Clinical Trial.Journal of clinical medicine · 2025Article
- Interactions between atrial fibrosis and inflammation in atrial fibrillation.Frontiers in cardiovascular medicine · 2025Review
- Article
- Conventional and Novel Inflammatory Biomarkers in Chronic Heart Failure Patients with Atrial Fibrillation.Medicina (Kaunas, Lithuania) · 2024Article
- The Possible Effects of Galectin-3 on Mechanisms of Renal and Hepatocellular Injury Induced by Intravascular Hemolysis.International journal of molecular sciences · 2024Review
- LNK/SH2B3 loss of function increases susceptibility to murine and human atrial fibrillation.Cardiovascular research · 2024Article
- Pathophysiology and clinical relevance of atrial myopathy.Basic research in cardiology · 2024Review
- Atrial Fibrillation and Diabetes Mellitus: Dangerous Liaisons or Innocent Bystanders?Journal of clinical medicine · 2023Review
- Potential clinical biomarkers and perspectives in diabetic cardiomyopathy.Diabetology & metabolic syndrome · 2023Review
- Inflammatory signalling in atrial cardiomyocytes: a novel unifying principle in atrial fibrillation pathophysiology.Nature reviews. Cardiology · 2023Review
- Insights into the Role of Galectin-3 as a Diagnostic and Prognostic Biomarker of Atrial Fibrillation.Disease markers · 2023Review
- Effects of Inflammatory Cell Death Caused by Catheter Ablation on Atrial Fibrillation.Journal of inflammation research · 2023Review
- The relationship between atrial fibrillation and NLRP3 inflammasome: a gut microbiota perspective.Frontiers in immunology · 2023Review
- Silencing of TLR4 Inhibits Atrial Fibrosis and Susceptibility to Atrial Fibrillation via Downregulation of NLRP3-TGF-Disease markers · 2022Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both diabetes mellitus (DM) and atrial fibrillation (AF) are usually associated with enhanced inflammatory response. The effect of the "NACHT, LRR and PYD domain containing protein 3" (NLRP3)-inflammasome/caspase-1/galectin-3 pathway and the potential benefits of NLRP3-inflammasome inhibitor glibenclamide (GLB) on atrial remodeling in the DM state are still unknown. Here, we demonstrated that higher AF inducibility and conduction inhomogeneity, slower epicardial conduction velocity, and increased amount of fibrosis in diabetic rabbits as against normal ones were markedly reduced by GLB. Atrial caspase-1 activity as well as serum IL-1β and IL-18 levels were elevated in diabetic animals but suppressed by GLB. Moreover, GLB decreased the DM-induced protein expression enhancement of NLRP3, Gal-3, TGF-β1, and CaV1.2 according to western blot analysis. Summarily, our findings indicate that the NLRP3-inflammasome/caspase-1/Gal-3 signaling pathway is related to the pathogenesis of AF in the diabetic state. NLRP3-inflammasome inhibitor GLB prevents AF inducibility and moderates atrial structural remodeling in DM.
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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 OpenQuestion graph.