ArticleNPJ systems biology and applications2025
Temporal analysis of doxorubicin-induced cardiac toxicity and hypertrophy.
Article in NPJ systems biology and applications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed.
- Doxorubicin exposure leads to cardiac fibroblast dysregulation and worsens fibrotic remodeling in the pathological heart.Journal of molecular and cellular cardiology plus · 2026Article
- Multicellular senescence programs in the aged heart.Journal of molecular and cellular cardiology plus · 2026Review
- Molecular profiling of glioblastoma-derived extracellular vesicles identifies small nucleolar RNAs as candidate liquid biomarkers for radiation- induced senescence.bioRxiv : the preprint server for biology · 2026Article
- Enhancing human-induced pluripotent stem cell proliferation and cardiac differentiation through 810-nm photobiomodulation.Lasers in medical science · 2026Article
- Integrated multi-omics reveals acylcarnitine accumulation as an early driver of doxorubicin-induced cardiotoxicity targeted by chlorogenic acid.Frontiers in pharmacology · 2026Article
- Disulfidptosis in heart failure: an emerging mechanism awaiting exploration.Frontiers in cardiovascular medicine · 2026Review
- Decoding cardiac metabolic reprogramming through single-cell multi-omics: from mechanisms to therapeutic applications.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Doxorubicin (DOX), although effective in treating cancer, has significant cardiac side effects, which limit its clinical utility. In this study, we collected time-course transcriptomics and metabolomics data from the human cardiomyocyte cell line AC16, which we analyzed along with curated public transcriptomics data on DOX-induced toxicity. We developed a multiomics analysis workflow and a computational toolbox, pipeGEM, to integrate RNA-seq data with metabolic models, enabling the simulation of DOX-induced metabolic perturbations at a sample-specific level. Our results revealed that DOX affected mitochondrial damage and mitochondria-to-nucleus retrograde signaling, potentially contributing to the observed cellular enlargement, senescence and metabolic shift. Cardiac cells that survived DOX treatment presented elevated glycolysis, increased pentose phosphate pathway activity, an altered TCA cycle, and modified glutathione and fatty acid metabolism. These findings provide a comprehensive understanding of DOX-induced toxicity and its implications for cardiac hypertrophy, suggesting potential strategies to mitigate side effects while retaining the anticancer efficacy of DOX.
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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 OpenQuestion graph.