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Endothelial transcription factor EB protects against doxorubicin-induced endothelial toxicity and cardiac dysfunction

ABSTRACT: Doxorubicin (DOX) has been demonstrated to induce cardiovascular toxicity in cancer survivors. Endothelial cell dysfunction is recoginized to play a critical role in the onset and severity of cardiotoxicity associated with DOX. Endothelial TFEB protects against EC damage and cardiac dysfunction. Cardiac single cells isolated from vehicle and doxorubicin treated wild type and EC-Tfeb Tg mice were collected for scRNA-seq analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE285475 | GEO | 2025/12/18

REPOSITORIES: GEO

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Endothelial transcription factor EB protects against doxorubicin-induced endothelial toxicity and cardiac dysfunction

Project description: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.

2025-12-18 | GSE237200 | GEO

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Endothelial transcription factor EB protects against doxorubicin-induced endothelial toxicity and cardiac dysfunction

Project description:Endothelial transcription factor EB protects against doxorubicin-induced endothelial toxicity and cardiac dysfunction

| PRJNA1203896 | ENA

Endothelial transcription factor EB protects against doxorubicin-induced endothelial toxicity and cardiac dysfunction

Project description:Endothelial transcription factor EB protects against doxorubicin-induced endothelial toxicity and cardiac dysfunction

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Ubiquitome profiling uncovers disturbed mitochondrial remodeling as an outcome of doxorubicin-induced cardiotoxicity in old mice

Project description:The urgent need to understand the molecular modulation associated with chronic cardiotoxicity of doxorubicin (DOX) has prompted us to investigate the ubiquitome profile of aged cardiac muscle. Using old CD-1 male mice administered with a DOX dosage established to induce cardiotoxicity, we performed a comprehensive analysis of the proteomic profile of the enriched pool of poly-ubiquitinated proteins obtained from cardiac muscle using tandem ubiquitin-binding entities (TUBEs). GeLC-MS/MS and subsequent bioinformatic analysis revealed several proteins with the poly-ubiquitination modification involved in DOX-induced cardiotoxicity. Increased poly-ubiquitination levels were found for sarcomeric proteins including alpha-actinin-2 and desmin as well as mitochondrial proteins such as ATP synthase subunit beta and cytochrome b-c1 complex subunit 1. Thus, impaired protein ubiquitination emerges as an enduring consequence of DOX-induced cardiotoxicity. The present exploratory analysis could be considered an important starting point for further studies targeting molecular pathways under the side effects of the widely used anticancer drug DOX.

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