ArticleFrontiers in cell and developmental biology2020
Histone Demethylase JMJD3 Mediated Doxorubicin-Induced Cardiomyopathy by Suppressing SESN2 Expression.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Sustained alternate-day fasting potentiates doxorubicin cardiotoxicity.Cell metabolism · 2023Trial
- Nutritional Prevention of Oxidative Stress-Induced Cardiotoxicity in Pediatric Cardio-Oncology: Molecular Mechanisms and Translational Perspectives-A Narrative Review.International journal of molecular sciences · 2026Review
- Methylation-centric epigenetic regulation in dilated cardiomyopathy: mechanisms, metabolic interplay, and translational potential.Frontiers in cardiovascular medicine · 2026Review
- Identification of potential hub genes related to ferroptosis and hypoxia in dilated cardiomyopathy: a bioinformatic analysis with preliminary experimental validation.Experimental biology and medicine (Maywood, N.J.) · 2026Article
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- Doxorubicin-Induced Cardiotoxicity: A Comprehensive Update.Journal of cardiovascular development and disease · 2025Review
- The role and mechanism of epigenetics in anticancer drug-induced cardiotoxicity.Basic research in cardiology · 2025Review
- Methylations in dilated cardiomyopathy and heart failure.Frontiers in cardiovascular medicine · 2025Review
- Emerging role of Jumonji domain-containing protein D3 in inflammatory diseases.Journal of pharmaceutical analysis · 2024Review
- The Essential Strategies to Mitigate Cardiotoxicity Caused by Doxorubicin.Life (Basel, Switzerland) · 2023Review
- JMJD6 protects against isoproterenol-induced cardiac hypertrophy via inhibition of NF-κB activation by demethylating R149 of the p65 subunit.Acta pharmacologica Sinica · 2023Article
- Muscular Sestrins: Roles in Exercise Physiology and Stress Resistance.Biomolecules · 2023Review
- Apolipoprotein M Attenuates Anthracycline Cardiotoxicity and Lysosomal Injury.JACC. Basic to translational science · 2023Article
- Cardiac SIRT1 ameliorates doxorubicin-induced cardiotoxicity by targeting sestrin 2.Redox biology · 2022Article
- JMJD5 attenuates oxygen-glucose deprivation and reperfusion-induced injury in cardiomyocytes through regulation of HIF-1α-BNIP3.The Kaohsiung journal of medical sciences · 2022Article
- Identification of novel biomarkers involved in doxorubicin-induced acute and chronic cardiotoxicity, respectively, by integrated bioinformatics.Frontiers in cardiovascular medicine · 2022Article
- GSK-J4, a Specific Histone Lysine Demethylase 6A Inhibitor, Ameliorates Lipotoxicity to CardiomyocytesFrontiers in cardiovascular medicine · 2022Article
- JMJD3: a critical epigenetic regulator in stem cell fate.Cell communication and signaling : CCS · 2021Review
- Histone Methylation Related Therapeutic Challenge in Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2021Review
- Advances in Cardiotoxicity Induced by Altered Mitochondrial Dynamics and Mitophagy.Frontiers in cardiovascular medicine · 2021Review
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Jumonji domain-containing 3 (JMJD3) protein, a histone demethylase protein, specifically catalyzes the demethylation of H3K27 (H3K27me3) and regulates gene expression. Sestrin2 (SESN2), a stress-inducible protein, protected against doxorubicin (DOX)-induced cardiomyopathy by regulating mitophagy and mitochondrial function. Here, the expression of JMJD3 was increased and that of SESN2 was decreased in both the heart samples from patients with dilated cardiomyopathy and chronic DOX-stimulation induced cardiomyopathy. Inhibition or knockdown of JMJD3 attenuated DOX-induced cardiomyocytes apoptosis, mitochondrial injury and cardiac dysfunction. However, JMJD3 overexpression aggravated DOX-induced cardiomyopathy, which were relieved by SESN2 overexpression. JMJD3 inhibited the transcription of SESN2 by reducing tri-methylation of H3K27 in the promoter region of SESN2. In conclusion, JMJD3 negatively regulated SESN2 via decreasing H3K27me3 enrichment in the promoter region of SESN2, subsequently inducing mitochondrial dysfunction and cardiomyocytes apoptosis. Targeting the JMJD3-SESN2 signaling axis may be a potential therapeutic strategy to protect against DOX-mediated cardiomyopathy.
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