ArticleMolecular therapy. Nucleic acids2021
Cardiomyocyte mitochondrial dynamic-related lncRNA 1 (CMDL-1) may serve as a potential therapeutic target in doxorubicin cardiotoxicity.
Article in Molecular therapy. Nucleic acids, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Peroxiredoxin Ⅲ safeguards cardiac function against doxorubicin by regulating mitochondrial quality control via HRedox biology · 2026Article
- Heartbreakers and healers: RNA rebels in cardio-oncology.Seminars in cancer biology · 2026Review
- Article
- Non-Coding RNAs in the Regulation of Doxorubicin-Induced Cardiotoxicity.Biomolecules · 2025Review
- Deciphering the roles of cellular and extracellular non-coding RNAs in chemotherapy-induced cardiotoxicity.Molecular and cellular biochemistry · 2025Review
- The role and mechanism of epigenetics in anticancer drug-induced cardiotoxicity.Basic research in cardiology · 2025Review
- New insights into mitochondrial quality control in anthracycline-induced cardiotoxicity: molecular mechanisms, therapeutic targets, and natural products.International journal of biological sciences · 2025Review
- Precision Cardio-oncology: Update on Omics-Based Diagnostic Methods.Current treatment options in oncology · 2024Review
- Protective Effect of Long Noncoding RNA OXCT1-AS1 on Doxorubicin-Induced Apoptosis of Human Myocardial Cells by the Competitive Endogenous RNA Pattern.Arquivos brasileiros de cardiologia · 2024Article
- Long Non-Coding RNAs (lncRNAs) in Heart Failure: A Comprehensive Review.Non-coding RNA · 2023Review
- Modulation of lncRNA links endothelial glycocalyx to vascular dysfunction of tyrosine kinase inhibitor.Cardiovascular research · 2023Article
- DoxoDB: A Database for the Expression Analysis of Doxorubicin-Induced lncRNA Genes.Non-coding RNA · 2023Article
- Non-coding RNAs regulating mitochondrial function in cardiovascular diseases.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Recent Advances in Mitochondrial Fission/Fusion-Targeted Therapy in Doxorubicin-Induced Cardiotoxicity.Pharmaceutics · 2023Review
- Evaluation of lncRNA Expression Pattern and Potential Role in Heart Failure Pathology.Disease markers · 2023Article
- Depletion of lncRNA MEG3 Ameliorates Imatinib-Induced Injury of Cardiomyocytes via Regulating miR-129-5p/HMGB1 Axis.Analytical cellular pathology (Amsterdam) · 2023Article
- Non-coding RNAs regulate mitochondrial dynamics in the development of gastric cancer.Frontiers in molecular biosciences · 2023Review
- Long non-coding RNAs and microRNAs as crucial regulators in cardio-oncology.Cell & bioscience · 2022Review
- Mitochondrial Determinants of Anti-Cancer Drug-Induced Cardiotoxicity.Biomedicines · 2022Review
- Long non-coding RNAs in the pathogenesis of heart failure: A literature review.Frontiers in cardiovascular medicine · 2022Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (DOX)-induced cardiotoxicity has been one of the major limitations for its clinical use. Although extensive studies have been conducted to decipher the molecular mechanisms underlying DOX cardiotoxicity, no effective preventive or therapeutic measures have yet been identified. Microarray analysis showed that multiple long non-coding RNAs (lncRNAs) are differentially expressed between control- and DOX-treated cardiomyocytes. Functional enrichment analysis indicated that the differentially expressed genes are annotated to cardiac hypertrophic pathways. Among differentially expressed lncRNAs, cardiomyocyte mitochondrial dynamic-related lncRNA 1 (CMDL-1) is the most significantly downregulated lncRNA in cardiomyocytes after DOX exposure. The protein-RNA interaction analysis showed that CMDL-1 may target dynamin-related protein 1 (Drp1). Mechanistic analysis shows that lentiviral overexpression of CMDL-1 prevents DOX-induced mitochondrial fission and apoptosis in cardiomyocytes. However, overexpression of CMDL-1 cannot effectively reduce mitochondrial fission when Drp1 is minimally expressed by small interfering RNA Drp1 (siDrp1). Overexpression of CMDL-1 promotes the association between CMDL-1 and Drp1, as well as with phosphorylated (p-)Drp1, as evidenced by RNA immunoprecipitation analysis. These data indicate the role of CMDL-1 in posttranslational modification of a target protein via regulating its phosphorylation. Collectively, our data indicate that CMDL-1 may play an anti-apoptotic role in DOX cardiotoxicity by regulating Drp1 S637 phosphorylation. Thus, CMDL-1 may serve as a potential therapeutic target in DOX cardiotoxicity.
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