详细信息
Mechanisms of Doxorubicin-Induced Cardiac Senescence and Potential Therapeutic Strategies ( SCI-EXPANDED收录)
文献类型:期刊文献
英文题名:Mechanisms of Doxorubicin-Induced Cardiac Senescence and Potential Therapeutic Strategies
作者:Bai, Yanli[1];Yang, Wen[2];Wang, Zirong[2];Yang, Qianqian[2];Zhang, Zhongping[3];Liu, Jialong[2];Qi, Yafang[2];Liu, Dongling[2,4,5]
第一作者:白彦丽
通信作者:Liu, DL[1];Liu, DL[2];Liu, DL[3]
机构:[1]Gansu Univ Chinese Med, Sch Basic Med Sci, Lanzhou 730000, Peoples R China;[2]Gansu Univ Chinese Med, Sch Pharm, Lanzhou 730000, Peoples R China;[3]Tianshui Normal Univ, Sch Bioengn & Technol, Tianshui 741000, Peoples R China;[4]Gansu Univ Chinese Med, Gansu Pharmaceut Ind Innovat Res Inst, Lanzhou 730000, Peoples R China;[5]Northwest Collaborat Innovat Ctr Tradit Chinese Me, Lanzhou 730000, Peoples R China
第一机构:甘肃中医药大学基础医学院(敦煌医学研究所)
通信机构:[1]corresponding author), Gansu Univ Chinese Med, Sch Pharm, Lanzhou 730000, Peoples R China;[2]corresponding author), Gansu Univ Chinese Med, Gansu Pharmaceut Ind Innovat Res Inst, Lanzhou 730000, Peoples R China;[3]corresponding author), Northwest Collaborat Innovat Ctr Tradit Chinese Me, Lanzhou 730000, Peoples R China.|[10735]甘肃中医药大学;
年份:2026
卷号:16
期号:8
外文期刊名:BIOMOLECULES
收录:;Scopus(收录号:2-s2.0-105048493776);WOS:【SCI-EXPANDED(收录号:WOS:001859241500001)】;
基金:This project was supported by the National Natural Science Foundation of China (grant number 82360790) and the Gansu Provincial Science and Technology Plan Project (grant numbers 23JRRA1203, 23JR6KA028, and 21JR1RA256).
语种:英文
外文关键词:cardiac senescence; doxorubicin; cardiotoxicity; senescence-targeted therapy
摘要:Doxorubicin (DOX) is a widely used anthracycline chemotherapeutic agent; however, its clinical application is limited by dose-dependent cardiotoxicity, which can result in progressive cardiac dysfunction and heart failure. Increasing evidence indicates that DOX-induced cardiotoxicity is closely associated with premature cardiac senescence, a pathological process distinct from physiological cardiac aging. DOX induces senescence-associated alterations in multiple cardiac cell populations, disrupting cardiac homeostasis and contributing to pathological remodeling. In this review, we summarize current advances in DOX-induced cardiac senescence, focusing on the contributions of different cardiac cell types, the underlying molecular mechanisms, and emerging therapeutic strategies. We further discuss the challenges and future perspectives for developing effective interventions that alleviate cardiac senescence while preserving the anticancer efficacy of DOX. Understanding the mechanisms driving DOX-induced cardiac senescence may provide new opportunities to develop effective cardioprotective strategies and improve long-term cardiac outcomes after chemotherapy.
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