ArticleMolecular therapy. Nucleic acids2022
The circular RNA circNlgnmediates doxorubicin-inducedcardiac remodeling and fibrosis.
Article in Molecular therapy. Nucleic acids, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 46 citations in OpenAlex.
- Circular RNAs in Cardiovascular Diseases: From Regulatory Networks to Functional Effectors.International journal of molecular sciences · 2026Review
- CircRNA-regulated programmed cell death networks in cardiomyocytes: Molecular crosstalk and therapeutic translation.Non-coding RNA research · 2026Review
- Circular RNA-mediated regulation of key signaling pathways in cardiovascular diseases: a review.Journal of advanced research · 2026Review
- Harmine Derivative H-2-104 Alleviates Echinococcus granulosus-Induced Pulmonary Fibrosis in Mice by Inhibiting Fibroblast Activation and Inducing DNA Damage.Journal of immunology research · 2026Article
- The silent dialogue between cells: regulatory roles of non-coding RNAs in cardiovascular disease.Frontiers in cell and developmental biology · 2026Review
- Article
- Drug Repositioning in Doxorubicin-Induced Cardiotoxicity Protection.International journal of molecular sciences · 2025Review
- Mitochondrial dysfunction in oocytes: implications for fertility and ageing.Journal of ovarian research · 2025Review
- Reactivation of an embryonic cardiac neural crest transcriptional profile during zebrafish heart regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A new protein isoform encoded by human circular RNA circSLC8a1 contributes to cardiac remodelling.Cardiovascular research · 2025Article
- Sirtuin 4 accelerates heart failure development by enhancing reactive oxygen species-mediated profibrotic transcriptional signaling.Journal of molecular and cellular cardiology plus · 2025Article
- Non-Coding RNAs in the Regulation of Doxorubicin-Induced Cardiotoxicity.Biomolecules · 2025Review
- A Novel Protein NAB1-356 Encoded by circRNA circNAB1 Mitigates Atrial Fibrillation by Reducing Inflammation and Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Decoding the regulatory roles of circular RNAs in cardiac fibrosis.Non-coding RNA research · 2025Review
- The cardio-oncologic burden of breast cancer: molecular mechanisms and importance of preclinical models.Basic research in cardiology · 2025Review
- Spermine: A prospective treatment for high glucose-induced myocardial fibrosis in db/db mice.Iranian journal of basic medical sciences · 2025Article
- Circular RNAs in Heart Diseases.Advances in experimental medicine and biology · 2025Review
- Circular RNAs in Organ Fibrosis.Advances in experimental medicine and biology · 2025Review
- METTL3, m6A modification, and EGR1: interplay affecting myocardial I/R injury outcomes.Cell biology and toxicology · 2024Article
- Potential Biomarkers in Myocardial Fibrosis: A Bioinformatic Analysis.Arquivos brasileiros de cardiologia · 2024Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin is a chemotherapeutic medication commonly used to treat many types of cancers, but it has side effects including vomiting, rash, hair loss, and bone marrow suppression. The most dangerous side effects are cardiomyopathy, cardiofibrosis, and heart failure, as doxorubicin generates cytotoxicity and stops DNA replication. There is no treatment to block these side effects. We have developed a transgenic mouse line overexpressing the circular RNA circNlgn and shown that circNlgn is a mediator of doxorubicin-induced cardiofibrosis. Increased expression of circNlgn decreased cardiac function and induced cardiofibrosis by upregulating Gadd45b, Sema4C, and RAD50 and activating p38 and pJNK in circNlgn transgenic heart. Silencing circNlgn decreased the effects of doxorubicin on cardiac cell activities and prevented doxorubicin-induced expression of fibrosis-associated molecules. The protein (Nlgn173) translated by circNlgn could bind and activate H2AX, producing γH2AX, resulting in upregulation of IL-1b, IL-2Rb, IL-6, EGR1, and EGR3. We showed that silencing these molecules in the signaling pathway prevented doxorubicin-induced cardiomyocyte apoptosis, increased cardiomyocyte viability, decreased cardiac fibroblast proliferation, and inhibited collagen production. This mechanism may hold therapeutic implications for mitigating the side effects of doxorubicin therapy in cancer patients.
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