ArticleJournal of the American Heart Association2025
Diacylglycerol Kinase ζ Attenuates Doxorubicin-Induced Cardiotoxicity Through p53 Degradation.
Article in Journal of the American Heart Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- A novel mouse model of adenine-supplemented high-fat diet induced cardiovascular-kidney-metabolic syndrome.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Article
- Hspa1b attenuates hypoxia/reoxygenation-induced cardiomyocyte injury through dual suppression of P53-driven apoptotic and ferroptotic pathways.Cell stress & chaperones · 2026Article
- Lymphatic Endothelial C-C Motif Chemokine Ligand 2 Enhances Lymphangiogenesis and Lymphatic Clearance of Macrophages Following Myocardial Infarction.Journal of the American Heart Association · 2026Article
- Special topics: heart failure-related cardiogenic shock, valvular heart disease and end-stage renal disease. Part 4 of the International Expert Opinion Series on Acute Heart Failure Management.Heart failure reviews · 2025Review
- DGKs in lipid signaling and disease intervention: structural basis, pathological mechanisms, and emerging therapeutic strategies.Cellular & molecular biology letters · 2025Review
- Ubiquitin E3 Ligases and p53 in Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2025Review
- Comprehensive bioinformatic analysis identifies potential therapeutic drugs for CryAB (R120G)-related cardiomyopathy.BMC cardiovascular disorders · 2025Article
- AIG1 protects against doxorubicin-induced cardiomyocyte ferroptosis and cardiotoxicity by promoting ubiquitination-mediated p53 degradation.Theranostics · 2025Article
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDoxorubicin-induced cardiotoxicity is still an important medical problem associated with a high mortality rate in cancer survivors. p53 plays a key role in doxorubicin-induced cardiotoxicity. Diacylglycerol kinase ζ (Dgkζ), a 130-kDa enzyme abundant in cardiomyocytes, regulates the p53 protein expression level in neurons. To elucidate the mechanism of doxorubicin-induced cardiotoxicity, we focused on the functional role of Dgkζ and its interaction with heat shock protein 70 (Hsp70)-related ubiquitin E3 ligases such as E6-associated protein (E6ap) and C-terminus of Hsp70-interacting protein. METHODS AND
resultsProtein interactions of Dgkζ with Hsp70 and E6ap were confirmed by immunoprecipitation, but not C-terminus of Hsp70-interacting protein. We administered doxorubicin in cardiac-specific overexpression of Dgkζ transgenic (Dgkζ-Tg) mice and wild-type littermates. Dgkζ-Tg mice showed lower p53 protein expression levels, preserved cardiac function, and improved survival rates compared with wild-type littermates after doxorubicin administration. RNA sequence analysis of myocardial tissues from Dgkζ-Tg after doxorubicin stimulation identified
conclusionsWe demonstrated for the first time that Dgkζ augments p53 ubiquitin-proteasome degradation and ameliorates doxorubicin-induced cardiotoxicity by interacting with Hsp70 and E3 ligases such as E6ap and C-terminus of Hsp70-interacting protein.
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