ArticleThe Journal of physiology2015
Impaired sinoatrial node function and increased susceptibility to atrial fibrillation in mice lacking natriuretic peptide receptor C.
Article in The Journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 69 citations in OpenAlex.
- HIV-Associated Pulmonary Arterial Hypertension in Resource-Limited Settings: A "Forgotten" Diagnosis, a Great Imitator, and a Multi-Hit Pulmonary Vasculopathy.Pulmonary circulation · 2026Review
- Aging and sinus node dysfunction: mechanisms and future directions.Clinical science (London, England : 1979) · 2025Review
- Dim light at night unmasks sex-specific differences in circadian and autonomic regulation of cardiovascular physiology.Communications biology · 2024Article
- Feeding behavior modifies the circadian variation in RR and QT intervals by distinct mechanisms in mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2024Article
- Review
- Cardiac conduction diseases: understanding the molecular mechanisms to uncover targets for future treatments.Expert opinion on therapeutic targets · 2024Review
- NPRC deletion attenuates cardiac fibrosis in diabetic mice by activating PKA/PKG and inhibiting TGF-β1/Smad pathways.Science advances · 2023Article
- Emerging Signaling Regulation of Sinoatrial Node Dysfunction.Current cardiology reports · 2023Review
- The role of P21-activated kinase (Pak1) in sinus node function.Journal of molecular and cellular cardiology · 2023Article
- Overview of programmed electrical stimulation to assess atrial fibrillation susceptibility in mice.Frontiers in physiology · 2023Review
- Guidelines for assessment of cardiac electrophysiology and arrhythmias in small animals.American journal of physiology. Heart and circulatory physiology · 2022Review
- Role of Cardiac Natriuretic Peptides in Heart Structure and Function.International journal of molecular sciences · 2022Review
- Natriuretic peptide receptor B maintains heart rate and sinoatrial node function via cyclic GMP-mediated signalling.Cardiovascular research · 2022Article
- Loss of Natriuretic Peptide Receptor C Enhances Sinoatrial Node Dysfunction in Aging and Frail Mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022Article
- A Series of Substituted Bis-Aminotriazines Are Activators of the Natriuretic Peptide Receptor C.Journal of medicinal chemistry · 2022Article
- Regional and temporal progression of atrial remodeling in angiotensin II mediated atrial fibrillation.Frontiers in physiology · 2022Article
- Optimizing transesophageal atrial pacing in mice to detect atrial fibrillation.American journal of physiology. Heart and circulatory physiology · 2022Article
- Distinct Effects of Ibrutinib and Acalabrutinib on Mouse Atrial and Sinoatrial Node Electrophysiology and Arrhythmogenesis.Journal of the American Heart Association · 2021Article
- Attenuating persistent sodium current-induced atrial myopathy and fibrillation by preventing mitochondrial oxidative stress.JCI insight · 2021Article
- New aspects of endocrine control of atrial fibrillation and possibilities for clinical translation.Cardiovascular research · 2021Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Natriuretic peptides (NPs) are critical regulators of the cardiovascular system that are currently viewed as possible therapeutic targets for the treatment of heart disease. Recent work demonstrates potent NP effects on cardiac electrophysiology, including in the sinoatrial node (SAN) and atria. NPs elicit their effects via three NP receptors (NPR-A, NPR-B and NPR-C). Among these receptors, NPR-C is poorly understood. Accordingly, the goal of this study was to determine the effects of NPR-C ablation on cardiac structure and arrhythmogenesis. Cardiac structure and function were assessed in wild-type (NPR-C(+/+)) and NPR-C knockout (NPR-C(-/-)) mice using echocardiography, intracardiac programmed stimulation, patch clamping, high-resolution optical mapping, quantitative polymerase chain reaction and histology. These studies demonstrate that NPR-C(-/-) mice display SAN dysfunction, as indicated by a prolongation (30%) of corrected SAN recovery time, as well as an increased susceptibility to atrial fibrillation (6% in NPR-C(+/+) vs. 47% in NPR-C(-/-)). There were no differences in SAN or atrial action potential morphology in NPR-C(-/-) mice; however, increased atrial arrhythmogenesis in NPR-C(-/-) mice was associated with reductions in SAN (20%) and atrial (15%) conduction velocity, as well as increases in expression and deposition of collagen in the atrial myocardium. No differences were seen in ventricular arrhythmogenesis or fibrosis in NPR-C(-/-) mice. This study demonstrates that loss of NPR-C results in SAN dysfunction and increased susceptibility to atrial arrhythmias in association with structural remodelling and fibrosis in the atrial myocardium. These findings indicate a critical protective role for NPR-C in the heart.
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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.