ArticleNPJ Regenerative medicine2026
Priming of human iPSCs with doxorubicin causes genome-wide transcriptional reprogramming and functional impairments in iPSC-derived cardiomyocytes.
Article in NPJ Regenerative medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
How Doxorubicin (Dox) mediated damage to stem cells or cardiomyocytes contributes to cardiotoxicity and cardiac regeneration is unclear. Using a human iPSC-based model together with corresponding iPSC-derived cardiomyocytes (iCMs) revealed that iPSCs are much more sensitive against single short pulse-treatments with Dox than iCMs. Major mitochondrial impairments such as increased mitochondrial fragmentation, loss of mitochondrial membrane potential, reduced ATP levels, and altered mitochondrial DNA (mtDNA) organization, yet neither increased ROS formation, nuclear DNA damage response, nor apoptosis were detected in Dox-treated iPSCs. Whole genome transcriptome profiling revealed major differences in the transcriptional response to Dox including downregulation of genes regulating cellular homeostasis and energy metabolism. Dox exposure at the iPSC stage, termed priming here, shifts the global transcriptional landscape of iCMs towards reduced cardiac muscle regeneration, energy metabolism, muscle contraction, and increased fibrosis. Functionally, priming caused iCMs to 'memorize' this early Dox treatment resulting in reduced ATP levels, altered mtDNA organization, and in impaired contractility and oscillating Ca
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