多柔比星诱发心脏炎症和纤维化的机制;治疗目标和方法。

IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
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引用次数: 0

摘要

多柔比星在各种恶性肿瘤的治疗中发挥着举足轻重的作用。尽管多柔比星疗效显著,但与之相关的心脏毒性却限制了其临床应用。多柔比星的心脏毒性可归因于多种机制,包括干扰线粒体功能、产生活性氧(ROS)以及随后对心肌细胞 DNA、蛋白质和脂质的损伤。此外,多柔比星还会破坏心脏特异性转录因子和信号通路的平衡,加剧心脏功能障碍。多柔比星治疗后,氧化应激、细胞死亡和其他严重变化,如线粒体功能障碍、促氧化酶激活、肾素-血管紧张素系统(RAS)、内质网(ER)应激以及免疫细胞在心脏中的浸润,都可能导致炎症和纤维化反应。纤维化和炎症可导致心脏出现一系列紊乱,造成潜在的心脏功能障碍和疾病。在临床前研究中,各种辅助剂已显示出缓解这些与心脏炎症和纤维化相关的挑战的潜力。可推荐使用抗氧化剂、植物性产品、特异性抑制剂和心脏保护药物来减轻心脏毒性。本综述探讨了多柔比星诱发心脏炎症和纤维化的复杂机制,确定了可能的细胞和分子靶点,并研究了有助于减轻这些有害影响的潜在物质。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Mechanisms of doxorubicin-induced cardiac inflammation and fibrosis; therapeutic targets and approaches

Mechanisms of doxorubicin-induced cardiac inflammation and fibrosis; therapeutic targets and approaches
Doxorubicin plays a pivotal role in the treatment of various malignancies. Despite its efficacy, the cardiotoxicity associated with doxorubicin limits its clinical utility. The cardiotoxic nature of doxorubicin is attributed to several mechanisms, including its interference with mitochondrial function, the generation of reactive oxygen species (ROS), and the subsequent damage to cardiomyocyte DNA, proteins, and lipids. Furthermore, doxorubicin disrupts the homeostasis of cardiac-specific transcription factors and signaling pathways, exacerbating cardiac dysfunction. Oxidative stress, cell death, and other severe changes, such as mitochondrial dysfunction, activation of pro-oxidant enzymes, the renin-angiotensin system (RAS), endoplasmic reticulum (ER) stress, and infiltration of immune cells in the heart after treatment with doxorubicin, may cause inflammatory and fibrotic responses. Fibrosis and inflammation can lead to a range of disorders in the heart, resulting in potential cardiac dysfunction and disease. Various adjuvants have shown potential in preclinical studies to mitigate these challenges associated with cardiac inflammation and fibrosis. Antioxidants, plant-based products, specific inhibitors, and cardioprotective drugs may be recommended to alleviate cardiotoxicity. This review explores the complex mechanisms of doxorubicin-induced heart inflammation and fibrosis, identifies possible cellular and molecular targets, and investigates potential substances that could help reduce these harmful effects.
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来源期刊
Archives of biochemistry and biophysics
Archives of biochemistry and biophysics 生物-生化与分子生物学
CiteScore
7.40
自引率
0.00%
发文量
245
审稿时长
26 days
期刊介绍: Archives of Biochemistry and Biophysics publishes quality original articles and reviews in the developing areas of biochemistry and biophysics. Research Areas Include: • Enzyme and protein structure, function, regulation. Folding, turnover, and post-translational processing • Biological oxidations, free radical reactions, redox signaling, oxygenases, P450 reactions • Signal transduction, receptors, membrane transport, intracellular signals. Cellular and integrated metabolism.
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