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阿片肽能系统在阿霉素诱导的心脏毒性中的意义。

The significance of the apelinergic system in doxorubicin-induced cardiotoxicity.

机构信息

Department of Experimental and Clinical Physiology, Laboratory of Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland.

出版信息

Heart Fail Rev. 2024 Sep;29(5):969-988. doi: 10.1007/s10741-024-10414-w. Epub 2024 Jul 11.

Abstract

Cancer is the leading cause of death worldwide, and the number of cancer-related deaths is expected to increase. Common types of cancer include skin, breast, lung, prostate, and colorectal cancers. While clinical research has improved cancer therapies, these treatments often come with significant side effects such as chronic fatigue, hair loss, and nausea. In addition, cancer treatments can cause long-term cardiovascular complications. Doxorubicin (DOX) therapy is one example, which can lead to decreased left ventricle (LV) echocardiography (ECHO) parameters, increased oxidative stress in cellular level, and even cardiac fibrosis. The apelinergic system, specifically apelin and its receptor, together, has shown properties that could potentially protect the heart and mitigate the damages caused by DOX anti-cancer treatment. Studies have suggested that stimulating the apelinergic system may have therapeutic benefits for heart damage induced by DOX. Further research in chronic preclinical models is needed to confirm this hypothesis and understand the mechanism of action for the apelinergic system. This review aims to collect and present data on the effects of the apelinergic system on doxorubicin-induced cardiotoxicity.

摘要

癌症是全球主要的死亡原因,预计癌症相关死亡人数将会增加。常见的癌症类型包括皮肤癌、乳腺癌、肺癌、前列腺癌和结直肠癌。虽然临床研究已经改进了癌症治疗方法,但这些治疗方法往往伴随着严重的副作用,如慢性疲劳、脱发和恶心。此外,癌症治疗可能会导致长期心血管并发症。多柔比星(DOX)治疗就是一个例子,它会导致左心室(LV)超声心动图(ECHO)参数降低、细胞水平氧化应激增加,甚至导致心脏纤维化。阿片肽能系统,特别是阿片肽及其受体,具有潜在的保护心脏和减轻 DOX 抗癌治疗引起的损伤的特性。研究表明,刺激阿片肽能系统可能对 DOX 引起的心脏损伤具有治疗益处。需要在慢性临床前模型中进行进一步的研究来证实这一假设,并了解阿片肽能系统的作用机制。本综述旨在收集和呈现有关阿片肽能系统对多柔比星诱导的心脏毒性的影响的数据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d80c/11306362/bbc188361016/10741_2024_10414_Fig1_HTML.jpg

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