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Non-coding RNAs in cancer therapy-induced cardiotoxicity: Mechanisms, biomarkers, and treatments

As a result of ongoing breakthroughs in cancer therapy, cancer patients' survival rates have grown considerably. However, cardiotoxicity has emerged as the most dangerous toxic side effect of cancer treatment, negatively impacting cancer patients' prognosis. In recent years, the link betwe...

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Detalles Bibliográficos
Autores principales: Sun, Wanli, Xu, Juping, Wang, Li, Jiang, Yuchen, Cui, Jingrun, Su, Xin, Yang, Fan, Tian, Li, Si, Zeyu, Xing, Yanwei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9445363/
https://www.ncbi.nlm.nih.gov/pubmed/36082126
http://dx.doi.org/10.3389/fcvm.2022.946137
Descripción
Sumario:As a result of ongoing breakthroughs in cancer therapy, cancer patients' survival rates have grown considerably. However, cardiotoxicity has emerged as the most dangerous toxic side effect of cancer treatment, negatively impacting cancer patients' prognosis. In recent years, the link between non-coding RNAs (ncRNAs) and cancer therapy-induced cardiotoxicity has received much attention and investigation. NcRNAs are non-protein-coding RNAs that impact gene expression post-transcriptionally. They include microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs). In several cancer treatments, such as chemotherapy, radiotherapy, and targeted therapy-induced cardiotoxicity, ncRNAs play a significant role in the onset and progression of cardiotoxicity. This review focuses on the mechanisms of ncRNAs in cancer therapy-induced cardiotoxicity, including apoptosis, mitochondrial damage, oxidative stress, DNA damage, inflammation, autophagy, aging, calcium homeostasis, vascular homeostasis, and fibrosis. In addition, this review explores potential ncRNAs-based biomarkers and therapeutic strategies, which may help to convert ncRNAs research into clinical practice in the future for early detection and improvement of cancer therapy-induced cardiotoxicity.