ArticlePhysiological reports2022
An iPS-derived in vitro model of human atrial conduction.
Article in Physiological reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 5 citations in OpenAlex.
- Review: Human stem cell-based 3D in vitro angiogenesis models for preclinical drug screening applications.Molecular biology reports · 2024Review
- In Vitro Models for Improved Therapeutic Interventions in Atrial Fibrillation.Journal of personalized medicine · 2023Review
- Mitigating neutrophil trafficking and cardiotoxicity with DS-IkL in a microphysiological system of a cytokine storm.Lab on a chip · 2023Article
- An iPS-derived in vitro model of human atrial conduction.Physiological reports · 2022Article
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Atrial fibrillation (AF) is the most common arrhythmia in the United States, affecting approximately 1 in 10 adults, and its prevalence is expected to rise as the population ages. Treatment options for AF are limited; moreover, the development of new treatments is hindered by limited (1) knowledge regarding human atrial electrophysiological endpoints (e.g., conduction velocity [CV]) and (2) accurate experimental models. Here, we measured the CV and refractory period, and subsequently calculated the conduction wavelength, in vivo (four subjects with AF and four controls), and ex vivo (atrial slices from human hearts). Then, we created an in vitro model of human atrial conduction using induced pluripotent stem (iPS) cells. This model consisted of iPS-derived human atrial cardiomyocytes plated onto a micropatterned linear 1D spiral design of Matrigel. The CV (34-41 cm/s) of the in vitro model was nearly five times faster than 2D controls (7-9 cm/s) and similar to in vivo (40-64 cm/s) and ex vivo (28-51 cm/s) measurements. Our iPS-derived in vitro model recapitulates key features of in vivo atrial conduction and may be a useful methodology to enhance our understanding of AF and model patient-specific disease.
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