ArticleInternational journal of cardiology2017
Abnormal sodium channel mRNA splicing in hypertrophic cardiomyopathy.
Article in International journal of cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- Cardiac Sodium Channel Regulation: A Potential New Therapeutic Target in Cardiomyopathy.Circulation research · 2026Article
- The many faces of SCN5A pathogenic variants: from channelopathy to cardiomyopathy.Heart failure reviews · 2025Review
- RBM25 regulates hypoxic cardiomyocyte apoptosis through CHOP-associated endoplasmic reticulum stress.Cell stress & chaperones · 2023Article
- SLM2 Is A Novel Cardiac Splicing Factor Involved in Heart Failure due to Dilated Cardiomyopathy.Genomics, proteomics & bioinformatics · 2022Article
- Proteomic and functional mapping of cardiac NaV1.5 channel phosphorylation sites.The Journal of general physiology · 2021Article
- A Heart Failure-AssociatedFrontiers in physiology · 2021Article
- Further Considerations in Childhood-Onset Hypertrophic Cardiomyopathy Genetic Testing.Frontiers in cardiovascular medicine · 2021Article
- Genetic basis and molecular biology of cardiac arrhythmias in cardiomyopathies.Cardiovascular research · 2020Review
- Life Cycle of the Cardiac Voltage-Gated Sodium Channel NaFrontiers in physiology · 2020Review
- Hypertrophic Cardiomyopathy: An Overview of Genetics and Management.Biomolecules · 2019Review
- Angiotensin II Influences Pre-mRNA Splicing Regulation by EnhancingInternational journal of molecular sciences · 2019Article
- CRISPR -Mediated Expression of the Fetal Scn5a Isoform in Adult Mice Causes Conduction Defects and Arrhythmias.Journal of the American Heart Association · 2018Article
- Alternative splicing in cardiomyopathy.Biophysical reviews · 2018Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundOur previous studies showed that in ischemic and nonischemic heart failure (HF), the voltage-gated cardiac Na MATERIAL AND
methodsHuman heart tissue was obtained from HCM patients. The changes in relative abundances of SCN5A, its variants, splicing factors RBM25 and LUC7A, and PERK, a major effector of the UPR, were analyzed by real time RT-PCR and the expression changes were confirmed by Western Blot.
resultsWe found reduced full-length transcript, increased SCN5A truncation variants and activation of UPR in HCM when compared to control hearts. In these patients, real time RT-PCR revealed that HCM patients had decreased SCN5A mRNA to 27.8±4.07% of control (P<0.01) and an increased abundance of E28C and E28D (3.4±0.3 and 2.8±0.3-fold, respectively, P<0.05). PERK mRNA increased 8.2±3.1 fold (P<0.01) in HCM patients. Western blot confirmed a significant increase of PERK.
conclusionsThese data suggested that the full-length SCN5A was reduced in patients with HCM. This reduction was accompanied by abnormal SCN5A pre-mRNA splicing and UPR activation. These changes may contribute to the arrhythmic risk in HCM.
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