ArticleFrontiers in cardiovascular medicine2021
The Role of METTL3-Mediated N6-Methyladenosine (m6A) of JPH2 mRNA in Cyclophosphamide-Induced Cardiotoxicity.
Article in Frontiers in cardiovascular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- RBM15 Mediated m6A Modification of SRSF1 Inhibits Cuproptosis in Non-Small Cell Lung Cancer by Mediating ATP7B Alternative Splicing.The Kaohsiung journal of medical sciences · 2026Article
- The relationship between DNA damage and repair and the occurrence and development of disease.Frontiers in genetics · 2026Review
- METTL3-mediated m⁶A methylation in cardiac diseases: pathogenic roles and therapeutic potential.Cell biology and toxicology · 2025Review
- The role and mechanism of epigenetics in anticancer drug-induced cardiotoxicity.Basic research in cardiology · 2025Review
- Revisiting treatment-related cardiotoxicity in patients with malignant lymphoma-a review and prospects for the future.Frontiers in cardiovascular medicine · 2023Review
- Role of RNA modifications in carcinogenesis and carcinogen damage response.Molecular carcinogenesis · 2023Article
- Critical roles of mFrontiers in cardiovascular medicine · 2023Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
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Abstract
Cyclophosphamide (CYP)-induced cardiotoxicity is a common side effect of cancer treatment. Although it has received significant attention, the related mechanisms of CYP-induced cardiotoxicity remain largely unknown. In this study, we used cell and animal models to investigate the effect of CYP on cardiomyocytes. Our data demonstrated that CYP-induced a prolonged cardiac QT interval and electromechanical coupling time courses accompanied by JPH2 downregulation. Moreover, N6-methyladenosine (m6A) methylation sequencing and RNA sequencing suggested that CYP induced cardiotoxicity by dysregulating calcium signaling. Importantly, our results demonstrated that CYP induced an increase in the m6A level of JPH2 mRNA by upregulating methyltransferases METTL3, leading to the reduction of JPH2 expression levels, as well as increased field potential duration and action potential duration in cardiomyocytes. Our results revealed a novel mechanism for m6A methylation-dependent regulation of JPH2, which provides new strategies for the treatment and prevention of CYP-induced cardiotoxicity.
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