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NLRP3炎性小体作为阿霉素诱导的心脏毒性的治疗靶点:植物化学物质的作用

NLRP3 inflammasome as a therapeutic target in doxorubicin-induced cardiotoxicity: role of phytochemicals.

作者信息

Zhao Xiao-Peng, Duan Lian, Zhao Qian-Ru, Lv Xing, Tian Nai-Yuan, Yang Sheng-Lei, Dong Kun

机构信息

College of Exercise and Health, Shenyang Sport University, Shenyang, China.

China Volleyball College, Beijing Sport University, Beijing, China.

出版信息

Front Pharmacol. 2025 Apr 17;16:1567312. doi: 10.3389/fphar.2025.1567312. eCollection 2025.

Abstract

Doxorubicin (DOX) has received widespread attention as a broad-spectrum antitumor drug. However, it has been a recognized challenge that long-term DOX injections can lead to severe cardiotoxicity. There are numerous interventions to DOX-induced cardiotoxicity, and the most cost-effective is phytochemicals. It has been reported that phytochemicals have complex and diverse biological properties, facilitating the mitigation of DOX-induced cardiotoxicity. DOX-induced cardiotoxicity has numerous pathological mechanisms, and the nod-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome-mediated cardiomyocyte pyroptosis is one of them. This review initially presents an overview of the pathological mechanisms that underlie cardiotoxicity induced by DOX. Subsequently, we present a comprehensive elucidation of the structure and activation of the NLRP3 inflammasome. Finally, we provide a detailed summary of phytochemicals that can mitigate DOX-induced cardiotoxicity by influencing the expression of the NLRP3 inflammasome in cardiomyocytes.

摘要

阿霉素(DOX)作为一种广谱抗肿瘤药物受到了广泛关注。然而,长期注射DOX会导致严重的心脏毒性,这是一个公认的挑战。针对DOX诱导的心脏毒性有多种干预措施,其中最具成本效益的是植物化学物质。据报道,植物化学物质具有复杂多样的生物学特性,有助于减轻DOX诱导的心脏毒性。DOX诱导的心脏毒性有多种病理机制,其中含吡啉结构域的NOD样受体家族3(NLRP3)炎性小体介导的心肌细胞焦亡是其中之一。本综述首先概述了DOX诱导心脏毒性的病理机制。随后,我们全面阐述了NLRP3炎性小体的结构和激活。最后,我们详细总结了能够通过影响心肌细胞中NLRP3炎性小体的表达来减轻DOX诱导的心脏毒性的植物化学物质。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0857/12043718/969e96f43c01/fphar-16-1567312-g001.jpg

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