Mark C Daley, Peter Bronk, Tae Yun Kim, Arvin H Soepriatna, Cao T Tran, Ulrike Mende, Kareen L K Coulombe, Bum-Rak Choi
{"title":"使用来自人类ipsc衍生心肌细胞的3D工程心脏微组织进行心律失常前心脏毒性评估的计算通知出发点评估。","authors":"Mark C Daley, Peter Bronk, Tae Yun Kim, Arvin H Soepriatna, Cao T Tran, Ulrike Mende, Kareen L K Coulombe, Bum-Rak Choi","doi":"10.1093/toxsci/kfaf094","DOIUrl":null,"url":null,"abstract":"<p><p>Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) are a promising new approach for in vitro proarrhythmic cardiotoxicity assessment. However, variation due to differentiation batch, individual sample variation, and non-linear responses to test drugs complicate the prediction of proarrhythmic drug concentrations. This study combines a computational human action potential (AP) model of hERG channel block with experimental data from three-dimensional hiPSC-CM engineered microtissues to optimize point of departure (POD) estimation of drug-induced prolongation of AP duration (APD). Computer simulations predicted that APD prolongation from hERG block follows a logistic curve and that >81% hERG block induced early afterdepolarizations (EADs), which significantly shifted the APD response curve. Curve fitting of APD response by logistic, bilinear breakpoint, and maximal curvature was more accurate prior to EAD onset. Goodness-of-fit testing indicated that logistic regression with ≥6 test concentrations was sufficient to accurately estimate PODs. Power analysis, based on experimental variations between batches (n = 14), molds (n = 57), and microtissues (n = 1701), predicted that PODs from 2 ∼ 3 batches with 10 microtissues per mold using a 5% threshold for APD prolongation detected proarrhythmic cardiotoxicity with a negligible false positive rate. We then applied this POD analysis to hiPSC-CM microtissue data after treatment with well-characterized drugs (i.e. cisapride, ranolazine, quinidine, and verapamil). Using bootstrapping, we estimated PODs and confidence intervals that matched concentrations known to cause proarrhythmic effects in patients. This study identified a robust method for calculating PODs for proarrhythmic cardiotoxicity risk in vitro and developed a framework for experimental design in this and other in vitro platforms.</p>","PeriodicalId":23178,"journal":{"name":"Toxicological Sciences","volume":" ","pages":"221-237"},"PeriodicalIF":4.1000,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12448244/pdf/","citationCount":"0","resultStr":"{\"title\":\"Computationally informed point of departure evaluation for proarrhythmic cardiotoxicity assessment using 3D engineered cardiac microtissues from human iPSC-derived cardiomyocytes.\",\"authors\":\"Mark C Daley, Peter Bronk, Tae Yun Kim, Arvin H Soepriatna, Cao T Tran, Ulrike Mende, Kareen L K Coulombe, Bum-Rak Choi\",\"doi\":\"10.1093/toxsci/kfaf094\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) are a promising new approach for in vitro proarrhythmic cardiotoxicity assessment. However, variation due to differentiation batch, individual sample variation, and non-linear responses to test drugs complicate the prediction of proarrhythmic drug concentrations. This study combines a computational human action potential (AP) model of hERG channel block with experimental data from three-dimensional hiPSC-CM engineered microtissues to optimize point of departure (POD) estimation of drug-induced prolongation of AP duration (APD). Computer simulations predicted that APD prolongation from hERG block follows a logistic curve and that >81% hERG block induced early afterdepolarizations (EADs), which significantly shifted the APD response curve. Curve fitting of APD response by logistic, bilinear breakpoint, and maximal curvature was more accurate prior to EAD onset. Goodness-of-fit testing indicated that logistic regression with ≥6 test concentrations was sufficient to accurately estimate PODs. Power analysis, based on experimental variations between batches (n = 14), molds (n = 57), and microtissues (n = 1701), predicted that PODs from 2 ∼ 3 batches with 10 microtissues per mold using a 5% threshold for APD prolongation detected proarrhythmic cardiotoxicity with a negligible false positive rate. We then applied this POD analysis to hiPSC-CM microtissue data after treatment with well-characterized drugs (i.e. cisapride, ranolazine, quinidine, and verapamil). Using bootstrapping, we estimated PODs and confidence intervals that matched concentrations known to cause proarrhythmic effects in patients. This study identified a robust method for calculating PODs for proarrhythmic cardiotoxicity risk in vitro and developed a framework for experimental design in this and other in vitro platforms.</p>\",\"PeriodicalId\":23178,\"journal\":{\"name\":\"Toxicological Sciences\",\"volume\":\" \",\"pages\":\"221-237\"},\"PeriodicalIF\":4.1000,\"publicationDate\":\"2025-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12448244/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Toxicological Sciences\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1093/toxsci/kfaf094\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"TOXICOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicological Sciences","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/toxsci/kfaf094","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"TOXICOLOGY","Score":null,"Total":0}
Computationally informed point of departure evaluation for proarrhythmic cardiotoxicity assessment using 3D engineered cardiac microtissues from human iPSC-derived cardiomyocytes.
Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) are a promising new approach for in vitro proarrhythmic cardiotoxicity assessment. However, variation due to differentiation batch, individual sample variation, and non-linear responses to test drugs complicate the prediction of proarrhythmic drug concentrations. This study combines a computational human action potential (AP) model of hERG channel block with experimental data from three-dimensional hiPSC-CM engineered microtissues to optimize point of departure (POD) estimation of drug-induced prolongation of AP duration (APD). Computer simulations predicted that APD prolongation from hERG block follows a logistic curve and that >81% hERG block induced early afterdepolarizations (EADs), which significantly shifted the APD response curve. Curve fitting of APD response by logistic, bilinear breakpoint, and maximal curvature was more accurate prior to EAD onset. Goodness-of-fit testing indicated that logistic regression with ≥6 test concentrations was sufficient to accurately estimate PODs. Power analysis, based on experimental variations between batches (n = 14), molds (n = 57), and microtissues (n = 1701), predicted that PODs from 2 ∼ 3 batches with 10 microtissues per mold using a 5% threshold for APD prolongation detected proarrhythmic cardiotoxicity with a negligible false positive rate. We then applied this POD analysis to hiPSC-CM microtissue data after treatment with well-characterized drugs (i.e. cisapride, ranolazine, quinidine, and verapamil). Using bootstrapping, we estimated PODs and confidence intervals that matched concentrations known to cause proarrhythmic effects in patients. This study identified a robust method for calculating PODs for proarrhythmic cardiotoxicity risk in vitro and developed a framework for experimental design in this and other in vitro platforms.
期刊介绍:
The mission of Toxicological Sciences, the official journal of the Society of Toxicology, is to publish a broad spectrum of impactful research in the field of toxicology.
The primary focus of Toxicological Sciences is on original research articles. The journal also provides expert insight via contemporary and systematic reviews, as well as forum articles and editorial content that addresses important topics in the field.
The scope of Toxicological Sciences is focused on a broad spectrum of impactful toxicological research that will advance the multidisciplinary field of toxicology ranging from basic research to model development and application, and decision making. Submissions will include diverse technologies and approaches including, but not limited to: bioinformatics and computational biology, biochemistry, exposure science, histopathology, mass spectrometry, molecular biology, population-based sciences, tissue and cell-based systems, and whole-animal studies. Integrative approaches that combine realistic exposure scenarios with impactful analyses that move the field forward are encouraged.