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调节细胞氧化还原参数以改善多发性骨髓瘤的治疗反应

Modulation of Cellular Redox Parameters for Improving Therapeutic Responses in Multiple Myeloma.

作者信息

Allegra Alessandro, Petrarca Claudia, Di Gioacchino Mario, Casciaro Marco, Musolino Caterina, Gangemi Sebastiano

机构信息

Division of Hematology, Department of Human Pathology in Adulthood and Childhood "Gaetano Barresi", University of Messina, 98125 Messina, Italy.

Center for Advanced Studies and Technology, G. D'Annunzio University, 66100 Chieti, Italy.

出版信息

Antioxidants (Basel). 2022 Feb 25;11(3):455. doi: 10.3390/antiox11030455.

Abstract

Raised oxidative stress and abnormal redox status are typical features of multiple myeloma cells, and the identification of the intimate mechanisms that regulate the relationships between neoplastic cells and redox homeostasis may reveal possible new anti-myeloma therapeutic targets to increase the effectiveness of anti-myeloma drugs synergistically or to eradicate drug-resistant clones while reducing toxicity toward normal cells. An alteration of the oxidative state is not only responsible for the onset of multiple myeloma and its progression, but it also appears essential for the therapeutic response and for developing any chemoresistance. Our review aimed to evaluate the literature's current data on the effects of oxidative stress on the response to drugs generally employed in the therapy of multiple myeloma, such as proteasome inhibitors, immunomodulators, and autologous transplantation. In the second part of the review, we analyzed the possibility of using other substances, often of natural origin, to modulate the oxidative stress to interfere with the progression of myelomatous disease.

摘要

氧化应激升高和氧化还原状态异常是多发性骨髓瘤细胞的典型特征,确定调节肿瘤细胞与氧化还原稳态之间关系的内在机制,可能会揭示新的抗骨髓瘤治疗靶点,从而协同提高抗骨髓瘤药物的疗效,或根除耐药克隆,同时降低对正常细胞的毒性。氧化状态的改变不仅是多发性骨髓瘤发病及其进展的原因,而且对治疗反应和任何化疗耐药性的产生似乎也至关重要。我们的综述旨在评估文献中关于氧化应激对多发性骨髓瘤治疗中常用药物(如蛋白酶体抑制剂、免疫调节剂和自体移植)反应影响的现有数据。在综述的第二部分,我们分析了使用其他通常来源于天然的物质来调节氧化应激以干扰骨髓瘤疾病进展的可能性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1078/8944660/fb6d1624ddba/antioxidants-11-00455-g001.jpg

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