Liu Ao, Bai Peiyuan, You Hongmin, Zhuang Zehao, Tian Fangyan, Weng Haobo, Wei Xuemei, Tang Lu, Wang Litao, Liu Chaobao, Zhang Jinghong, Sun Minmin, Zhang Shuning, Shu Xianhong, Ge Junbo
Department of Cardiology, Zhongshan Hospital, Shanghai Institute of Cardiovascular Diseases and Institutes of Biomedical Sciences, Fudan University, Shanghai, China; State Key Laboratory of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, China; NHC Key Laboratory of Ischemic Heart Diseases, Shanghai, China; Key Laboratory of Viral Heart Diseases, Chinese Academy of Medical Sciences, Shanghai, China; National Clinical Research Center for Interventional Medicine, Shanghai, China; Department of Echocardiography, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai Institute of Medical Imaging, Shanghai, China.
Department of Cardiology, Zhongshan Hospital, Shanghai Institute of Cardiovascular Diseases and Institutes of Biomedical Sciences, Fudan University, Shanghai, China; State Key Laboratory of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, China; NHC Key Laboratory of Ischemic Heart Diseases, Shanghai, China; Key Laboratory of Viral Heart Diseases, Chinese Academy of Medical Sciences, Shanghai, China; National Clinical Research Center for Interventional Medicine, Shanghai, China.
JACC Basic Transl Sci. 2025 May 14:101256. doi: 10.1016/j.jacbts.2025.02.015.
Doxorubicin-induced cardiotoxicity (DIC) poses a significant challenge in cancer treatment. This study investigated the role of SLAMF7 in DIC, particularly in macrophage-mediated inflammation. Using SLAMF7 knockout mice, we found that SLAMF7 deficiency exacerbates DIC and amplifies inflammatory responses. Mechanistically, SLAMF7 interacts with TNF receptor-associated factor 6 to attenuate nuclear factor κB signaling, reducing oxidative stress and proinflammatory cytokines. Notably, administering recombinant SLAMF7 protein effectively mitigated DIC. These findings underscore the critical role of SLAMF7 in protecting against DIC, positioning it as a promising therapeutic target.
阿霉素诱导的心脏毒性（DIC）在癌症治疗中构成了重大挑战。本研究调查了信号淋巴细胞激活分子家族7（SLAMF7）在DIC中的作用，特别是在巨噬细胞介导的炎症中的作用。使用SLAMF7基因敲除小鼠，我们发现SLAMF7缺乏会加剧DIC并放大炎症反应。从机制上讲，SLAMF7与肿瘤坏死因子受体相关因子6相互作用，以减弱核因子κB信号传导，减少氧化应激和促炎细胞因子。值得注意的是，给予重组SLAMF7蛋白可有效减轻DIC。这些发现强调了SLAMF7在预防DIC中的关键作用，使其成为一个有前景的治疗靶点。
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