Drug-induced transcriptome variation in PSC-derived cardiomyocytes

This dataset provides a curated summary of drug-induced transcriptomic variation in serum-free human pluripotent stem cell-derived cardiomyocytes (WA09/H9). The dataset aggregates differential expression outputs across multiple pharmacological perturbations relevant to cardiometabolic aging and geroprotection, including mTOR inhibition, AMPK modulation, senolytic interventions, and hormonal signaling regulators. The experimental model consists of serum-free PSC-derived cardiomyocytes with a senescent reference state. Differential expression was computed using DESeq2, and the dataset compiles gene-level log2 fold changes and adjusted p-values across all compound–dose contrasts relative to senescent cardiomyocyte controls. The primary data product is a long-format gene-level table containing differential expression metrics across all perturbations. A companion summary table provides compound-level DEG counts and reversal metrics to facilitate comparative pharmacotranscriptomic analyses. This dataset is suitable for:- pharmacotranscriptomic benchmarking- senescence reversal studies- geroprotector screening- integration with epigenetic or multi-omics datasets Analysis was performed using standardized RNA-seq pipelines with DESeq2-based differential expression. Significance thresholds applied in summaries were adjusted p-value < 0.05 and |log2 fold change| ≥ 1. This release represents version 1.0 of the dataset. This dataset is associated with a previously published Data Management Plan (DMP) describing data governance, storage, and sharing strategies for the project: Megnis, K. (2025). Therapy-induced transcriptome variations to promote heart cell senescence reversal (Version 1). Zenodo. https://doi.org/10.5281/zenodo.16309877 The DMP defines the FAIR data framework under which this dataset was generated and released. This research was supported within the framework of the European Union’s Recovery and Resilience Mechanism project No.5.2.1.1.i.0/2/24/I/CFLA/001 "Consolidation of the Latvian Institute of Organic Synthesis and the Latvian Biomedical Research and Study Centre" (ANM_K_PG_17).本数据集经系统整理，汇总了无血清培养人多能干细胞衍生心肌细胞（WA09/H9）中药物诱导的转录组变异特征。数据集整合了多项与心脏代谢衰老及抗衰老防护相关的药理学扰动的差异表达分析结果，涵盖雷帕霉素靶蛋白（mTOR）抑制、腺苷酸活化蛋白激酶（AMPK）调控、衰老清除干预以及激素信号通路调节剂等干预手段。 本实验模型采用处于衰老参考状态的无血清培养多能干细胞衍生心肌细胞。差异表达分析采用DESeq2工具完成，数据集汇总了所有化合物-剂量梯度对比组相较于衰老心肌细胞对照组的基因水平log₂倍变化值及校正后P值。 核心数据产物为长格式基因水平表格，包含所有扰动条件下的差异表达分析指标；配套汇总表格则提供了化合物水平的差异表达基因（Differentially Expressed Gene，DEG）计数及逆转相关指标，以支持比较转录组药理学分析。 本数据集适用场景包括： - 转录组药理学基准测试 - 细胞衰老逆转研究 - 抗衰老药物筛选 - 与表观基因组或多组学数据集的整合分析 本分析采用标准化RNA测序流程及基于DESeq2的差异表达分析方法，汇总时采用的显著性阈值为校正后P值<0.05且|log₂倍变化值|≥1。 本数据集为1.0版本。 本数据集关联已发表的数据集管理计划（Data Management Plan，DMP），该计划阐述了本项目的数据治理、存储及共享策略：Megnis, K. (2025). 治疗诱导的心肌细胞衰老逆转相关转录组变异（版本1）. Zenodo. https://doi.org/10.5281/zenodo.16309877。本数据集正是在该计划定义的FAIR数据框架下生成并发布的。 本研究依托欧盟复苏与韧性机制项目No.5.2.1.1.i.0/2/24/I/CFLA/001“拉脱维亚有机合成研究所与拉脱维亚生物医学研究与中心整合”（ANM_K_PG_17）框架开展。