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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE237200 | 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) 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.

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Phosphodiesterase 10A inactivation protects against doxorubicin-induced cardiotoxicity and concomitantly inhibits tumor growth

Project description:Phosphodiesterase 10A (PDE10A), by degrading cAMP/cGMP, play critical roles in cardiovascular biology/disease. Cardiotoxicity is a clinical complication of chemotherapy. We aim to determine the role of PDE10A in cancer growth and cardiotoxicity induced by doxorubicin (DOX), a chemotherapy drug. We found that PDE10A deficiency/inhibition alleviated DOX-induced cardiotoxicity in C57Bl/6J mice, including myocardial atrophy, apoptosis, and dysfunction. RNAseq study revealed several PDE10A-regulated signaling associated with DOX-induced cardiotoxicity. In cancer cells, PDE10A inhibition increased the death, decreased the proliferation, and potentiated the effect of DOX in various cancer-cell lines. Importantly, in nude mice with implanted ovarian cancer xenografts, PDE10A inhibition attenuated tumor growth while protected against DOX-induced cardiotoxicity. In isolated cardiomyocytes (CMs), PDE10A contributed to DOX-induced CM death via promoting mitochondrial dysfunction, and to CM atrophy via potentiating foxo3 signaling. Collectively, our study elucidates a novel role for PDE10A in cardiotoxicity and cancer growth in vitro and in vivo, and suggest that PDE10A inhibition may represent a novel strategy in cancer therapy.

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Effect of doxorubicin and SPEDOX-6 on human iPSC-derived cardiac spheroids comprised of cardiomyocytes, endothelial cells, and fibroblasts.

Project description:The chemotherapeutic doxorubicin (DOX) detrimentally impacts the heart during cancer treatment. This necessitates development of non-cardiotoxic delivery systems that retain DOX anticancer efficacy. We utilized human induced pluripotent stem cell-derived multi-lineage cardiac spheroids (hiPSC-CSs) to compare the anticancer efficacy and reduced cardiotoxicity of single protein encapsulated doxorubicin (SPEDOX-6), to standard unformulated (UF) DOX using RNA-sequencing. The cardiac spheroids are comprised of hiPSC-derived cardiomyocytes (hiPSC-CMs), hiPSC-derived endothelial cells (ECs), and hiPSC-derived cardiac fibroblasts (CFs) at an 8:1:1 ratio.

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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

| PRJNA994158 | 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

| PRJNA1203896 | ENA

Endothelial TFEB improves glucose intolerance via upregulation of IRS1 and IRS2

Project description:To determine whether endothelial TFEB is critical for glucose metabolism in vivo, we utilized EC-selective TFEB knockout mice and EC selective TFEB transgenic mice fed a high fat diet (HFD). EC-TFEB knockout mice exhibited significantly impaired glucose tolerance compared with control mice. Consistently, EC-TFEB transgenic mice showed improved glucose intolerance. In primary human ECs, small interfering RNA-mediated TFEB knockdown blunts the Akt signaling. adenovirus-mediated overexpression of TFEB consistently activates Akt signaling and significantly increases glucose uptake in ECs. Mechanically, TFEB upregulates insulin receptor substrate 1 and 2 (IRS1 and IRS2). TFEB increases IRS2 transcription measured by reporter gene and chromatin immunoprecipitation assays. Furthermore, we found that TFEB increases IRS1 protein via downregulation of microRNAs (miR-335, miR-495 and miR548o). In vivo, Akt signaling in the skeletal muscle and adipose tissue was significantly impaired in EC-TFEB knockout mice and consistently improved in EC-TFEB transgenic mice on HFD

2021-03-01 | GSE148026 | GEO

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2025-06-25 | PXD065109 | Pride

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.

2025-06-30 | PXD048078 | Pride

Imatinib-induced changes in expression profile of microRNA in plasma of mice - comparison with doxorubicin

Project description:Cardiotoxicity is serious adverse reaction of cancer chemotherapy and may lead to critical heart damage. Imatinib mesylate (IMB), a selective tyrosine kinase inhibitor, is sometimes accompanied by severe cardiovascular complications. To minimize the risk, early biomarkers of such complications are of utmost importance. MicroRNAs (miRNAs) are, nowadays intensively studied as potential biomarkers of many pathological processes. Many miRNAs appear to be specific in some tissues, including heart. Here, we have explored the potential of specific miRNAs to be early markers of IMB-induced cardiotoxicity. Doxorubicin (DOX), an anthracycline with well-known cardiotoxicity, was used for comparison. NMRI mice were treated with IMB or DOX for nine days in doses corresponding to the highest recommended doses in oncological patients. Then, plasmatic levels of miRNAs were analyzed by miRNA microarrays and selected cardio-specific miRNAs were quantified using qPCR. The plasmatic level of miR-1a, miR-133a, miR-133b, miR-339, miR-7058, miR-6236 and miR-6240 were the most different between IMB-treated and control mice. Interestingly, most of the miRNAs affected by DOX were also affected by IMB with the same trends. Concerning selected microRNAs in hearts of individual mice, only miR-34a was significantly increased after DOX treatment and only miR-205 was significantly decreased after IMB and DOX treatment. However, changes in any miRNA expression did not correlate with level of troponin T, classical marker of heart injury.

2020-01-01 | GSE121275 | GEO

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