详情页 - 四川省肿瘤医院知识库

当前位置：首页 > 详情页

MIF-ACKR3 causes irreversible fat loss by impairing adipogenesis in cancer cachexia

文献详情

资源类型：

Pubmed体系：

收录情况： ◇ 自然指数

作者：

机构： [1]State Key Laboratory of Membrane Biology, Institute of Molecular Medicine, College of Future Technology, Peking University, Beijing 100871, China [2]Dazhou Central Hospital, Dazhou 635000, Sichuan, China [3]Peking-Tsinghua Center for Life Sciences, Peking University, Beijing 100871, China [4]Academy for Advanced Interdisciplinary Studies, Peking University, Beijing 100871, China [5]Beijing City Key Laboratory of Cardiometabolic Molecular Medicine, Peking University, Beijing 100871, China [6]PKU-Nanjing Institute of Translational Medicine, Nanjing 211800, China

出处：

DOI：

ISSN：

摘要：

Both exercise and cancer can cause adipose tissue shrinkage. However, only cancer-associated weight loss, namely cachexia, is characterized by profound adipose inflammation and fibrosis. Here, we identified tumor-secreted macrophage migration inhibitory factor (MIF) as a major driver that skews the differentiation of adipose stem and progenitor cells (ASPCs) toward a pro-inflammatory and pro-fibrogenic direction, with reduced adipogenic capacity in cancer cachexia. By contrast, circulating MIF is moderately reduced after exercise. Mechanistically, atypical chemokine receptor 3 (ACKR3) in ASPCs serves as the predominant MIF receptor mediating its pathological effects. Inhibition of MIF by gene ablation in tumor cells or pharmacological blockade, as well as ASPC-specific Ackr3 deficiency, markedly alleviates tumor-induced cachexia. These findings unveil MIF-ACKR3 signaling as a critical link between tumors and cachectic manifestations, providing a promising therapeutic target for cancer cachexia.Copyright © 2025 The Author(s). Published by Elsevier Inc. All rights reserved.

基金：

语种：

PubmedID：

中科院(CAS)分区：

出版当年[2025]版：

无

最新[2023]版：

大类 | 1 区

生物学

小类 | 1 区细胞生物学 1 区内分泌学与代谢

第一作者：

第一作者机构： [1]State Key Laboratory of Membrane Biology, Institute of Molecular Medicine, College of Future Technology, Peking University, Beijing 100871, China

共同第一作者：

通讯作者：

通讯机构： [1]State Key Laboratory of Membrane Biology, Institute of Molecular Medicine, College of Future Technology, Peking University, Beijing 100871, China [3]Peking-Tsinghua Center for Life Sciences, Peking University, Beijing 100871, China [4]Academy for Advanced Interdisciplinary Studies, Peking University, Beijing 100871, China [5]Beijing City Key Laboratory of Cardiometabolic Molecular Medicine, Peking University, Beijing 100871, China [6]PKU-Nanjing Institute of Translational Medicine, Nanjing 211800, China

推荐引用方式(GB/T 7714)：

APA：

MLA：