ArticleStem cell reports2020
Isogenic Sets of hiPSC-CMs Harboring Distinct KCNH2 Mutations Differ Functionally and in Susceptibility to Drug-Induced Arrhythmias.
Article in Stem cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 38 citations in OpenAlex.
- Induced pluripotent stem cells from discovery to translation.Nature medicine · 2026Review
- A simplified co-culture reveals altered cardiotoxic responses to doxorubicin in hPSC-derived cardiomyocytes in the presence of endothelial cells.Stem cell reports · 2026Article
- Personalized in vitro models reveal functional impact of aHeart rhythm O2 · 2026Article
- STRAIGHT-IN Dual: a platform for dual, single-copy integrations of DNA payloads and gene circuits into human induced pluripotent stem cell.bioRxiv : the preprint server for biology · 2025Article
- Biomaterial-assisted organoid technology for disease modeling and drug screening.Materials today. Bio · 2025Review
- Ion channel traffic jams: the significance of trafficking deficiency in long QT syndrome.Cell discovery · 2025Review
- Pathogenic KCNH2-G53S variant in the PAS domain influences the electrophysiological phenotype in long QT syndrome type 2.Frontiers in cardiovascular medicine · 2025Article
- Toward the latest advancements in cardiac regeneration using induced pluripotent stem cells (iPSCs) technology: approaches and challenges.Journal of translational medicine · 2024Review
- Using induced pluripotent stem cells for drug discovery in arrhythmias.Expert opinion on drug discovery · 2024Review
- Population-specific variations inAntimicrobial agents and chemotherapy · 2024Article
- Modeling mutation-specific arrhythmogenic phenotypes in isogenic human iPSC-derived cardiac tissues.Scientific reports · 2024Article
- Decellularized heart extracellular matrix alleviates activation of hiPSC-derived cardiac fibroblasts.Bioactive materials · 2024Article
- Organoids are not organs: Sources of variation and misinformation in organoid biology.Stem cell reports · 2023Review
- Injection of IFrontiers in physiology · 2023Article
- Modeling long QT syndrome type 2 on-a-chip via in-depth assessment of isogenic gene-edited 3D cardiac tissues.Science advances · 2022Article
- Genetics of congenital arrhythmia syndromes: the challenge of variant interpretation.Current opinion in genetics & development · 2022Review
- STRAIGHT-IN enables high-throughput targeting of large DNA payloads in human pluripotent stem cells.Cell reports methods · 2022Article
- Optogenetic Reporters Delivered as mRNA Facilitate Repeatable Action Potential and Calcium Handling Assessment in Human iPSC-Derived Cardiomyocytes.Stem cells (Dayton, Ohio) · 2022Article
- What Is the Potential for Lumacaftor as a Chemical Chaperone in Promoting hERG Trafficking?Frontiers in cardiovascular medicine · 2022Article
- Deciphering Common Long QT Syndrome Using CRISPR/Cas9 in Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in KCNH2 can lead to long QT syndrome type 2. Variable disease manifestation observed with this channelopathy is associated with the location and type of mutation within the protein, complicating efforts to predict patient risk. Here, we demonstrated phenotypic differences in cardiomyocytes derived from isogenic human induced pluripotent stem cells (hiPSC-CMs) genetically edited to harbor mutations either within the pore or tail region of the ion channel. Electrophysiological analysis confirmed that the mutations prolonged repolarization of the hiPSC-CMs, with differences between the mutations evident in monolayer cultures. Blocking the hERG channel revealed that the pore-loop mutation conferred greater susceptibility to arrhythmic events. These findings showed that subtle phenotypic differences related to KCNH2 mutations could be captured by hiPSC-CMs under genetically matched conditions. Moreover, the results support hiPSC-CMs as strong candidates for evaluating the underlying severity of individual KCNH2 mutations in humans, which could facilitate patient risk stratification.
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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.