ArticleHeart rhythm2016
Relaxin suppresses atrial fibrillation in aged rats by reversing fibrosis and upregulating Na+ channels.
Article in Heart rhythm, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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Who cites it
33 citing papers in PubMed, 68 citations in OpenAlex.
- Relaxin-2: Shaping the Proteomic Landscape of Skeletal Muscle Physiology, Glucose Trafficking, and Mitochondrial Function in Rat.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Therapeutic potential of Relaxin-2 in Heart Failure with preserved Ejection Fraction (HFpEF).bioRxiv : the preprint server for biology · 2026Article
- Relevance of Targeting Oxidative Stress, Inflammatory, and Pro-Resolution Mechanisms in the Prevention and Management of Postoperative Atrial Fibrillation.Antioxidants (Basel, Switzerland) · 2025Review
- Relaxin-2 Exhibits a Beneficial Role in Energy Metabolism to Alleviate Atrial Fibrillation Susceptibility.ACS pharmacology & translational science · 2025Article
- Cardiac and Renal Fibrosis, the Silent Killer in the Cardiovascular Continuum: An Up-to-Date.Journal of cardiovascular development and disease · 2024Review
- Article
- Involvement of plasminogen activator inhibitor-1 in p300/p53-mediated age-related atrial fibrosis.PeerJ · 2023Article
- Relaxin-2 as a Potential Biomarker in Cardiovascular Diseases.Journal of personalized medicine · 2022Review
- Chronic treatment with serelaxin mitigates adverse remodeling in a murine model of ischemic heart failure and modulates bioactive sphingolipid signaling.Scientific reports · 2022Article
- Evidence of Failed Resolution Mechanisms in Arrhythmogenic Inflammation, Fibrosis and Right Heart Disease.Biomolecules · 2022Review
- Cardiac Gene Therapy With Relaxin Receptor 1 Overexpression Protects Against Acute Myocardial Infarction.JACC. Basic to translational science · 2022Article
- Molecular Insights in Atrial Fibrillation Pathogenesis and Therapeutics: A Narrative Review.Diagnostics (Basel, Switzerland) · 2021Review
- Fibrosis after Myocardial Infarction: An Overview on Cellular Processes, Molecular Pathways, Clinical Evaluation and Prognostic Value.Medical sciences (Basel, Switzerland) · 2021Review
- Relaxin Inhibits Ventricular Arrhythmia and Asystole in Rats With Pulmonary Arterial Hypertension.Frontiers in cardiovascular medicine · 2021Article
- Myocardial Fibrosis in Heart Failure: Anti-Fibrotic Therapies and the Role of Cardiovascular Magnetic Resonance in Drug Trials.Cardiology and therapy · 2020Review
- The relaxin family peptide receptor 1 (RXFP1): An emerging player in human health and disease.Molecular genetics & genomic medicine · 2020Review
- Apelin Inhibits Angiotensin II-Induced Atrial Fibrosis and Atrial Fibrillation via TGF-β1/Smad2/α-SMA Pathway.Frontiers in physiology · 2020Article
- Relaxin reverses maladaptive remodeling of the aged heart through Wnt-signaling.Scientific reports · 2019Article
- Serum relaxin level predicts recurrence of atrial fibrillation after radiofrequency catheter ablation.Heart and vessels · 2019Observational
- Role of SCN5A coding and non-coding sequences in Brugada syndrome onset: What's behind the scenes?Biomedical journal · 2019Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAtrial fibrillation (AF) contributes significantly to morbidity and mortality in elderly patients and has been correlated with enhanced age-dependent atrial fibrosis. Reversal of atrial fibrosis has been proposed as therapeutic strategy to suppress AF.
objectiveTo test the ability of relaxin to reverse age-dependent atrial fibrosis and suppress AF.
methodsAged F-344 rats (24 months old) were treated with subcutaneous infusion of vehicle or relaxin (0.4 mg/kg/day) for 2 weeks. Rat hearts were excised, perfused on a Langendorff apparatus, and stained with voltage and Ca(2+) indicator dyes. Optical mapping and programmed electrical stimulation was used to test arrhythmia vulnerability and changes in electrophysiological characteristics. Changes in protein expression and Na(+) current density (INa) were measured by tissue immunofluorescence and whole-cell patch clamp technique.
resultsIn aged rats, sustained AF was readily induced with a premature pulse (n = 7/8) and relaxin treatment suppressed sustained AF by a premature impulse or burst pacing (n = 1/6) (P < .01). Relaxin significantly increased atrial action potential conduction velocity and decreased atrial fibrosis. Relaxin treatment increased Nav1.5 expression (n = 6; 36% ± 10%) and decreased total collagen and collagen I (n = 5-6; 55%-66% ± 15%) in aged atria (P < .05) and decreased collagen I and III and TGF-β1 mRNA (P < .05). Voltage-clamp experiments demonstrated that relaxin treatment (100 nM for 2 days) increased atrial INa by 46% ± 4% (n = 12-13/group, P < .02).
conclusionRelaxin suppresses AF through an increase in atrial conduction velocity by decreasing atrial fibrosis and increasing INa. These data provide compelling evidence that relaxin may serve as an effective therapy to manage AF in geriatric patients by reversing fibrosis and modulating cardiac ionic currents.
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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 OpenQuestion graph.