已发表论文

抗癌药物的心脏毒性:分子机制、临床管理和创新治疗

 

Authors Gao F, Xu T, Zang F, Luo Y, Pan D

Received 17 April 2024

Accepted for publication 5 August 2024

Published 12 September 2024 Volume 2024:18 Pages 4089—4116

DOI https://doi.org/10.2147/DDDT.S469331

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Professor Manfred Ogris

Feiyu Gao,* Tao Xu,* Fangnan Zang, Yuanyuan Luo, Defeng Pan

Department of Cardiology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, 221004, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Yuanyuan Luo; Defeng Pan, Email luoyuanyuanxyfy@126.com; xzdefengpan@xzhmu.edu.cn

Abstract: With the continuous refinement of therapeutic measures, the survival rate of tumor patients has been improving year by year, while cardiovascular complications related to cancer therapy have become increasingly prominent. Exploring the mechanism and prevention strategy of cancer therapy-related cardiovascular toxicity (CTR-CVT) remains one of the research hotspots in the field of Cardio-Oncology in recent years. Cardiotoxicity of anticancer drugs involves heart failure, myocarditis, hypertension, arrhythmias and vascular toxicity, mechanistically related to vascular endothelial dysfunction, ferroptosis, mitochondrial dysfunction and oxidative stress. To address the cardiotoxicity induced by different anticancer drugs, various therapeutic measures have been put in place, such as reducing the accumulation of anticancer drugs, shifting to drugs with less cardiotoxicity, using cardioprotective drugs, and early detection. Due to the very limited treatments available to ameliorate anticancer drugs-induced cardiotoxicity, a few innovations are being shifted from animal studies to human studies. Examples include mitochondrial transplantation. Mitochondrial transplantation has been proven to be effective in in vivo and in vitro experiments. Several recent studies have demonstrated that intercellular mitochondrial transfer can ameliorate doxorubicin(DOX)-induced cardiotoxicity, laying the foundation for innovative therapies in anticancer drugs-induced cardiotoxicity. In this review, we will discuss the current status of anticancer drugs-induced cardiotoxicity in terms of the pathogenesis and treatment, with a focus on mitochondrial transplantation, and we hope that this review will bring some inspiration to you.

Keywords: cancer therapy-related cardiovascular toxicity, CTR-CVT, mitochondrial dysfunction, oxidative stress, ferroptosis, mitochondrial transplantation