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辐射诱导的心脏重塑:机制与治疗方法

Radiation-Induced Cardiac Remodeling: Mechanisms and Therapeutic Approaches.

作者信息

Ghnim Zahraa Sabah, Adhab Ayat Hussein, Mahdi Morug Salih, Kyada Ashishkumar, Roopashree R, Thakur Vishal, Kaur Manpreet, Gupta Anirudh, Mansoor Aseel Salah, Radi Usama Kadem, Abd Nasr Saadoun, Kadhim Munther

机构信息

College of Pharmacy, Alnoor University, Nineveh, Iraq.

Department of Pharmacy, Al-Zahrawi University College, Karbala, Iraq.

出版信息

Cardiovasc Toxicol. 2025 May 29. doi: 10.1007/s12012-025-10006-6.

DOI:10.1007/s12012-025-10006-6
PMID:40439873
Abstract

Radiation-induced cardiac remodeling (RICR) is one of the complications of exposure to radiotherapy. These disorders may occur for a subset of cancer patients, when the heart remains in part or in full in the radiation field. Despite advancements in radiotherapy techniques, cardiotoxicity has remained a concern after radiotherapy. RICR includes complex pathophysiological processes, which can be initiated by oxidative stress and cardiomyocyte cell death and continue with inflammation, arrhythmia, vascular and valvular abnormalities, and fibrosis, collectively contributing to structural and functional changes in the heart. Some studies have suggested strategies for RICR encompass pharmacological interventions, including angiotensin-converting enzyme (ACE) inhibitors, natural products, antioxidants, and others, which aim to mitigate cardiac damage and improve outcomes. Advanced therapies, including stem cell and gene therapy, as well as some adjuvants and novel drugs targeting specific molecular pathways, represent future directions for treatment. This review aims to elucidate the mechanisms underlying RICR, highlight early detection strategies, and discuss current and emerging therapeutic approaches.

摘要

辐射诱发的心脏重塑(RICR)是放疗暴露的并发症之一。当心脏部分或全部处于辐射野中时,这些病症可能会在一部分癌症患者中出现。尽管放疗技术有所进步,但放疗后的心脏毒性仍然是一个令人担忧的问题。RICR包括复杂的病理生理过程,其可由氧化应激和心肌细胞死亡引发,并持续伴有炎症、心律失常、血管和瓣膜异常以及纤维化,这些共同导致心脏的结构和功能变化。一些研究表明,针对RICR的策略包括药物干预,如血管紧张素转换酶(ACE)抑制剂、天然产物、抗氧化剂等,其目的是减轻心脏损伤并改善预后。先进的治疗方法,包括干细胞和基因治疗,以及一些针对特定分子途径的佐剂和新药,代表了未来的治疗方向。本综述旨在阐明RICR的潜在机制,强调早期检测策略,并讨论当前和新兴的治疗方法。

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本文引用的文献

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Coronary artery calcium score and other risk factors in patients at moderate and high risk of cancer therapy-related cardiovascular toxicity.癌症治疗相关心血管毒性中、高危患者的冠状动脉钙化评分及其他危险因素。
Cardiooncology. 2024 Sep 28;10(1):64. doi: 10.1186/s40959-024-00266-6.
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Epithelial-mesenchymal transition in chemoradiation-induced lung damage: Mechanisms and potential treatment approaches.放化疗诱导肺损伤中的上皮-间质转化:机制与潜在治疗方法。
J Biochem Mol Toxicol. 2024 Aug;38(8):e23790. doi: 10.1002/jbt.23790.
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Radiation-Induced Endothelial Ferroptosis Accelerates Atherosclerosis via the DDHD2-Mediated Nrf2/GPX4 Pathway.
辐射诱导的内皮细胞铁死亡通过 DDHD2 介导的 Nrf2/GPX4 通路加速动脉粥样硬化。
Biomolecules. 2024 Jul 22;14(7):879. doi: 10.3390/biom14070879.
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Consequences of ionizing radiation exposure to the cardiovascular system.电离辐射对心血管系统的影响。
Nat Rev Cardiol. 2024 Dec;21(12):880-898. doi: 10.1038/s41569-024-01056-4. Epub 2024 Jul 10.
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Radiation-Induced Aortic Stenosis: An Update on Treatment Modalities.放射性主动脉狭窄:治疗方式的最新进展
JACC Adv. 2023 Jan 11;2(1):100163. doi: 10.1016/j.jacadv.2022.100163. eCollection 2023 Jan.
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Dexmedetomidine ameliorates x-ray-induced myocardial injury via alleviating cardiomyocyte apoptosis and autophagy.右美托咪定通过减轻心肌细胞凋亡和自噬改善 X 射线诱导的心肌损伤。
BMC Cardiovasc Disord. 2024 Jun 26;24(1):323. doi: 10.1186/s12872-024-03988-8.
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Oxidative and Nitrous Stress Underlies Vascular Malfunction Induced by Ionizing Radiation and Diabetes.氧化应激和亚硝化应激是电离辐射和糖尿病引起的血管功能障碍的基础。
Cardiovasc Toxicol. 2024 Aug;24(8):776-788. doi: 10.1007/s12012-024-09878-x. Epub 2024 Jun 25.
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Endothelial-to-Mesenchymal Transition in Cardiovascular Pathophysiology.心血管病理生理学中的内皮细胞向间充质转化。
Int J Mol Sci. 2024 Jun 4;25(11):6180. doi: 10.3390/ijms25116180.
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Cardiovascular toxicities of radiotherapy: From practical issues to new perspectives.放射治疗的心血管毒性:从实际问题到新视角
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10
Revisiting an Inverse Dose-Fractionation Effect of Ionizing Radiation Exposure for Ischemic Heart Disease: Insights from Recent Studies.重新审视电离辐射暴露对缺血性心脏病的逆剂量分割效应:来自最近研究的启示。
Radiat Res. 2024 Jul 1;202(1):80-86. doi: 10.1667/RADE-00230.1.