ArticleClinical and translational medicine2023
Novel insights in the pathomechanism of Brugada syndrome and fever-related type 1 ECG changes in a preclinical study using human-induced pluripotent stem cell-derived cardiomyocytes.
Article in Clinical and translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Type 1 Brugada Pattern Triggered by Low-Grade Fever: Implications for Diagnosis and Risk Stratification.International journal of molecular sciences · 2026Article
- Roles of Catecholamines and Inflammation in Endothelial Dysfunction: a Study Using Takotsubo Syndrome Patient-specific hiPSC-ECs.Stem cell reviews and reports · 2026Article
- Phenotypes in Brugada syndrome with different genotypes triggered by fever or inflammation using gene-edited iPSCs.Stem cell research & therapy · 2025Article
- The Role of Human-Induced Pluripotent Stem Cells in Studying Cardiac Channelopathies.International journal of molecular sciences · 2024Review
- Ion Channel Diseases as a Cause of Sudden Cardiac Death in Young People: Aspects of Their Diagnosis, Treatment, and Pathogenesis.Deutsches Arzteblatt international · 2024Review
- Can Hyperthermia Unveil Brugada Pattern?Journal of medical cases · 2024Article
- Biophysical mechanisms of myocardium sodium channelopathies.Pflugers Archiv : European journal of physiology · 2024Review
- Stem cell models of inherited arrhythmias.Nature cardiovascular research · 2024Review
- Review
- Novel insights in the pathomechanism of Brugada syndrome and fever-related type 1 ECG changes in a preclinical study using human-induced pluripotent stem cell-derived cardiomyocytes.Clinical and translational medicine · 2023Article
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Authors and funding
24 authors at 5 institutions in 4 countries.
Funding
Abstract
backgroundBrugada syndrome (BrS) is causing sudden cardiac death (SCD) mainly at young age. Studying the underlying mechanisms associated with BrS type I electrocardiogram (ECG) changes in the presence of fever and roles of autophagy for BrS remains lacking.
objectivesWe sought to study the pathogenic role of an SCN5A gene variant for BrS with fever-induced type 1 ECG phenotype. In addition, we studied the role of inflammation and autophagy in the pathomechanism of BrS.
methodsHuman-induced pluripotent stem cell (hiPSC) lines from a BrS patient harboring a pathogenic variant (c.3148G>A/p. Ala1050Thr) in SCN5A and two healthy donors (non-BrS) and a CRISPR/Cas9 site-corrected cell line (BrS-corr) were differentiated into cardiomyocytes (hiPSC-CMs) for the study.
resultsReductions of Na
conclusionsThe study demonstrated that the SCN5A variant (c.3148G>A/p.Ala1050Thr) caused loss-of-function of sodium channels and increased the channel sensitivity to high temperature and LPS challenge in hiPSC-CMs from a BrS cell line with this variant but not in two non-BrS hiPSC-CM lines. The results suggest that LPS may exacerbate BrS phenotype via enhancing autophagy, whereas fever may exacerbate BrS phenotype via inhibiting PKA-signalling in BrS cardiomyocytes with but probably not limited to this variant.
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