ArticleiScience2024
CCRR regulate MYZAP-PKP2-Nav1.5 signaling pathway in atrial fibrillation following myocardial infarction.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed.
- Article
- Case Report: A rare stop-gainedFrontiers in cardiovascular medicine · 2026Article
- Ventricular ion channels and arrhythmias: an overview of physiology, pathophysiology and pharmacology.Medical review (2021) · 2025Review
- Layer-specific proteomic analysis of human hearts in patients with sudden cardiac death.PloS one · 2025Article
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atrial fibrillation (AF) is the most common sustained arrhythmia which brings a heavy burden to the lives and health of patients worldwide. Our earlier research documented cardiac conduction regulatory RNA (CCRR) as an antiarrhythmic lncRNA in heart failure. Here, we report that CCRR was decreased in atrial tissue after MI, MYZAP, and Nav1.5 were increased in the atrium in cardiac-specific transgenic CCRR overexpression mice. Overexpression of CCRR carried by AAV-9 reversed the incidence and duration of AF and atrial conduction velocity in MI mice. MYZAP overexpression reversed the decreasing levels of PKP2, Nav1.5, and AF incidence after MI in addition to downregulating the expression levels of TLR2, TLR4, and inflammation-related factors following MI. Our work revealed that CCRR can improve the occurrence and development of AF after MI through the MYZAP-PKP2 pathway and inhibit Nav1.5 and TLR signaling pathways associated with inflammation, thus serving as a therapeutic target for AF.
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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 Socratic graph.