ReviewFrontiers in cardiovascular medicine2022
Deciphering Common Long QT Syndrome Using CRISPR/Cas9 in Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes.
Review in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Modeling ventricular tachycardia in genetic long QT syndrome using engineered cardiac tissues.Bioactive materials · 2026Article
- Biomimetic electrospun scaffolds for engineered heart tissue: from design parameters to drug testing platforms.Frontiers in bioengineering and biotechnology · 2026Review
- Arrhythmogenic Risk in iPSC-Derived Cardiomyocytes: Current Limitations and Therapeutic Perspectives.Medicina (Kaunas, Lithuania) · 2025Review
- Review
- Off-target interactions in the CRISPR-Cas9 Machinery: mechanisms and outcomes.Biochemistry and biophysics reports · 2025Review
- Cardiac Channelopathies: Clinical Diagnosis and Promising Therapeutics.Journal of the American Heart Association · 2025Review
- Review
- WhenFrontiers in pharmacology · 2025Article
- Review
- The Current State of Realistic Heart Models for Disease Modelling and Cardiotoxicity.International journal of molecular sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
From carrying potentially pathogenic genes to severe clinical phenotypes, the basic research in the inherited cardiac ion channel disease such as long QT syndrome (LQTS) has been a significant challenge in explaining gene-phenotype heterogeneity. These have opened up new pathways following the parallel development and successful application of stem cell and genome editing technologies. Stem cell-derived cardiomyocytes and subsequent genome editing have allowed researchers to introduce desired genes into cells in a dish to replicate the disease features of LQTS or replace causative genes to normalize the cellular phenotype. Importantly, this has made it possible to elucidate potential genetic modifiers contributing to clinical heterogeneity and hierarchically manage newly identified variants of uncertain significance (VUS) and more therapeutic options to be tested
Indexed as
Identifiers
What Socratic holds
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.