Ubiquitination: A non-negligible modulator in doxorubicin-induced cardiotoxicity

IF 5.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Chemico-Biological Interactions Pub Date : 2025-07-15 DOI:10.1016/j.cbi.2025.111664

Can Gao , Changxu Lu , Jinwen Wei , Zhongyi Mu , Mingli Sun , Dan Dong , Zhenning Liu

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引用次数: 0

Abstract

Doxorubicin (DOX), an effective chemotherapeutic drug, is used to alleviate the progression of cancers. However, the cardiotoxic side effects of DOX significantly limit its broader clinical application. Therefore, it is extremely urgent to find effective therapeutic strategies to mitigate doxorubicin-induced cardiotoxicity (DIC). Ubiquitination, a crucial post-translational modification (PTM), is regulated by various ubiquitinases and subsequently marks and modulates the function of proteins. Notably, Numerous studies have found that ubiquitination is closely related to the progression of DIC. However, a comprehensive review of this field remains unreported. Therefore, this review will mainly summarize the critical role of ubiquitination in DIC-associated pathological mechanisms and various potential interventions. Collectively, a comprehensive understanding of ubiquitination in the progression of DIC contributes to providing a crucial theoretical basis and exploring new avenues for the management of DIC.

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泛素化：在阿霉素诱导的心脏毒性中一个不可忽略的调节剂。

阿霉素（DOX）是一种有效的化疗药物，用于缓解癌症的进展。然而，DOX的心脏毒性副作用极大地限制了其更广泛的临床应用。因此，迫切需要寻找有效的治疗策略来减轻阿霉素引起的心脏毒性（DIC）。泛素化是一种重要的翻译后修饰（PTM），由各种泛素酶调节，随后标记和调节蛋白质的功能。值得注意的是，大量研究发现泛素化与DIC的进展密切相关。然而，对这一领域的全面审查仍然没有报道。因此，本文将主要综述泛素化在dic诱导的病理机制中的关键作用以及各种可能的干预措施。总之，全面了解DIC进展中的泛素化有助于为DIC的治疗提供重要的理论基础和探索新的途径。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Chemico-Biological Interactions 生物-毒理学

CiteScore

7.70

自引率

3.90%

发文量

410

审稿时长

36 days

期刊介绍： Chemico-Biological Interactions publishes research reports and review articles that examine the molecular, cellular, and/or biochemical basis of toxicologically relevant outcomes. Special emphasis is placed on toxicological mechanisms associated with interactions between chemicals and biological systems. Outcomes may include all traditional endpoints caused by synthetic or naturally occurring chemicals, both in vivo and in vitro. Endpoints of interest include, but are not limited to carcinogenesis, mutagenesis, respiratory toxicology, neurotoxicology, reproductive and developmental toxicology, and immunotoxicology.