Quaking Inhibits Doxorubicin-Mediated Cardiotoxicity Through Regulation of Cardiac Circular RNA Expression
Open accessAbstract
Rationale: RBPs (RNA-binding proteins) have been described to be expressed and regulated in various organs including the heart. Little is known about the role of RBPs in heart failure induced by the chemotherapy drug doxorubicin and their interaction with circular RNAs. Objective: We aimed to identify key RBPs involved in doxorubicin-mediated heart failure and to elucidate their function. Methods and Results: Global transcriptome profiling from murine myocardium exposed to doxorubicin identified 5 differentially expressed RBPs. Expression of the RBP QKI (Quaking) in response to doxorubicin was strongly downregulated in rodent cardiomyocytes and human induced pluripotent stem cell–derived cardiomyocytes in vitro and in vivo in mice. Knockdown of Qki in primary cardiomyocytes increased apoptosis and atrophy after treatment with doxorubicin, whereas lentiviral mediated overexpression of Qki5 inhibited the doxorubicin-induced apoptosis in cardiomyocytes. In vivo, AAV9 (adeno-associated virus serotype 9)–mediated cardiac overexpression of Qki5 prevented cardiac apoptosis and cardiac atrophy induced by doxorubicin and improved cardiac function. Mechanistically, by lentiviral-based overexpression and CRISPR/Cas9-mediated silencing of Qki5 , we identified regulated expression of specific circular RNAs derived from Ttn (Titin), Fhod3 (Formin homology 2 domain containing 3), and Strn3 (Striatin, calmodulin-binding protein 3). Moreover, inhibition of Ttn -derived circular RNA increased the susceptibility of cardiomyocytes to doxorubicin. Conclusions: We here show that overexpression of Qki5 strongly attenuates the toxic effect of doxorubicin via regulating a set of circular RNAs. Qki5 is, thus, an interesting target molecule to combat doxorubicin-induced cardiotoxicity.
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DOX is a cytotoxic drug which suffers from severe side effects such as cardiotoxicity.
“Previous studies have confirmed that DOX is a cytotoxic drug which suffered from severe side effects such as cardiotoxicity.58–60”
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- Authors
- Gupta, S. K., Garg, A., Bär, C., Chatterjee, S., Foinquinos, A., Milting, H., Streckfuß-Bömeke, K., Fiedler, J., & Thum, T.
- Affiliations
- University Hospitals of the Ruhr-University of Bochum (DE)
- From the Institute of Molecular and Translational Therapeutic Strategies (S.K.G., A.G., C.B., S.C., A.F., J.F., T.T.) and Excellence Cluster REBIRTH (T.T.), Hannover Medical School, Germany; Herz- und Diabeteszentrum NRW, Universitätsklinikum der Ruhr Universität Bochum, Erich und Hanna Klessmann-Institute for Cardiovascular Research and Development, Bad Oeynhausen, Germany (H.M.); Clinic for Cardiology and Pneumology, Stem Cell Laboratory, University Medical Center, Gottingen, Germany (K.S.-B.);...
- Corresponding author
- Gupta, Shashi Kumar
- Thum, Thomas
- ORCID
- Venue
- Circulation Research
- Published
- 2018-01-19
- Volume
- 122
- Issue
- 2
- Pages
- 246-254
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- PMC
- PMC5771684
- OpenAlex
- W2770047542
- Cited by
- 227
- References
- 16
- Citations by year
- 2026: 9 · 2025: 17 · 2024: 26 · 2023: 20 · 2022: 28 · 2021: 42 · 2020: 39 · 2019: 21 · 2018: 25
- FWCI
- 17.96
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- Circulation Research (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- GoeScholar The Publication Server of the Georg-August-Universität Göttingen (Georg-August-Universität Göttingen) (submittedVersion, cc-by)
- GoeScholar The Publication Server of the Georg-August-Universität Göttingen (Georg-August-Universität Göttingen) (submittedVersion, other-oa)
- Funders
- European Commission
- Deutsche Forschungsgemeinschaft (GU-1664/1-1, 01EO1302)
- Fondation Leducq
- Bundesministerium für Bildung und Forschung (01EO1302)
- Medizinischen Hochschule Hannover
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Chemotherapy-induced cardiotoxicity and mitigation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Circular RNAs in diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- doxorubicin cardiotoxicity, Quaking (QKI), RNA-binding proteins, circular RNA, heart failure, cardiomyocyte apoptosis, cardiac atrophy, titin, striatin, AAV9 gene therapy, iPSC-derived cardiomyocytes, cardioprotection
- MeSH terms
- RNA, Circular, Animals, Antibiotics, Antineoplastic, Doxorubicin, Mice, Inbred C57BL, Random Allocation, RNA, Gene Expression, RNA-Binding Proteins, Myocytes, Cardiac, Mice, Cardiotoxicity
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