GEO series
Endothelial transcription factor EB protects against doxorubicin-induced endothelial toxicity and cardiac dysfunction
GSE237200
Homo sapiens
Expression profiling by high throughput sequencing
20 samples
2025/12/18
GPL21697
Summary
Doxorubicin (DOX), an effective chemotherapeutic drug for various cancers, has been demonstrated to induce cardiovascular toxicity in cancer survivors. Endothelial cell (EC) dysfunction is recognized to play a critical role in the onset and severity of cardiotoxicity associated with DOX. Transcription factor EB (TFEB), a master autophagy regulator, regulates cardiovascular homeostasis. In the present study, we aimed to test whether endothelial TFEB protects against EC damage after DOX treatment.
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Paper (PMID 41410033) ↗
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