Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Identifying Features of Cardiac Disease Phenotypes Based on Mechanical Function in a Catecholaminergic Polymorphic Ventricular Tachycardia Model

10 May 2022

Abstract excerpt

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is characterized by an arrhythmogenic mechanism involving disruption of calcium handling. This genetic disease can lead to sudden death in children and young adults during physical or emotional stress. Prior CPVT studies have focused on calcium handling, but mechanical functionality has rarely been investigated in vitro. In this research we combine stem...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cardiac electrophysiology and arrhythmias
Share to Cardiomyopathy and Myosin Studies
Share to Neurological disorders and treatments

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 35620470
DOI: 10.3389/fbioe.2022.873531

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Identifying Features of Cardiac Disease Phenotypes Based on Mechanical Function in a Catecholaminergic Polymorphic Ventricular Tachycardia ModelPMID 35620470Read ↗

Insights Into the Pathogenesis of Catecholaminergic Polymorphic Ventricular Tachycardia From Engineered Human Heart TissueSemantic proximity Read ↗

Functional abnormalities in iPSC-derived cardiomyocytes generated from CPVT1 and CPVT2 patients carrying ryanodine or calsequestrin mutations.Semantic proximity Read ↗

Mutation-specific differences in arrhythmias and drug responses in CPVT patients: simultaneous patch clamp and video imaging of iPSC derived cardiomyocytes.Semantic proximity Read ↗

Human engineered cardiac tissue model of hypertrophic cardiomyopathy recapitulates key hallmarks of the disease and the effect of chronic mavacamten treatmentSemantic proximity Read ↗

Patient-Specific Human Induced Pluripotent Stem Cell Model Assessed with Electrical Pacing Validates S107 as a Potential Therapeutic Agent for Catecholaminergic Polymorphic Ventricular TachycardiaSemantic proximity Read ↗

In vitro modeling of ryanodine receptor 2 dysfunction using human induced pluripotent stem cells.Semantic proximity Read ↗

Molecular and tissue mechanisms of catecholaminergic polymorphic ventricular tachycardia.Semantic proximity Read ↗

Modelling sarcomeric cardiomyopathies with human cardiomyocytes derived from induced pluripotent stem cellsSemantic proximity Read ↗

A Novel Mice Model of Catecholaminergic Polymorphic Ventricular Tachycardia Generated by CRISPR/Cas9Semantic proximity Read ↗

Catecholaminergic Polymorphic Ventricular Tachycardia.Semantic proximity Read ↗

A human pluripotent stem cell model of catecholaminergic polymorphic ventricular tachycardia recapitulates patient-specific drug responsesSemantic proximity Read ↗

The novel SCN5A-P1891A mutation is associated with left ventricular hypertrabeculation and links Na <sub>v</sub> 1.5 to cardiomyocyte proliferation and disrupted 3D cardiac tissue formationSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.