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    脂肪组织随年龄增长的异常扩张是中年代谢综合征的重要诱因,但其细胞机制长期不明。美国希望之城医学中心王琼团队联合加州大学洛杉矶分校杨霞团队于2025年4月25日在《Science》发表研究,首次发现中年特异性脂肪前体细胞(CP-A)及其调控通路,为“中年发福”提供全新解释。

    . 雄性动物“中年发福”的细胞机制揭示. 科技导报, 2025 , 43 (9) : 9 -9 .
    . Science & Technology Review, 2025 , 43 (9) : 9 -9 .
    脂肪组织随年龄增长的异常扩张是中年代谢综合征的重要诱因,但其细胞机制长期不明。美国希望之城医学中心王琼团队联合加州大学洛杉矶分校杨霞团队于2025年4月25日在《Science》发表研究,首次发现中年特异性脂肪前体细胞(CP-A)及其调控通路,为“中年发福”提供全新解释。
    研究团队通过体内谱系追踪模型结合单细胞RNA测序技术,发现中年雄性小鼠内脏脂肪中80% 以上为新生脂肪细胞,其脂肪生成速率显著高于年轻个体。进一步分析揭示,中年期(12月龄小鼠,相当于人类45岁)会激活一类新型前体细胞CP-A,该细胞具备超强增殖分化能力,其数量在中年达到顶峰。移植实验证明CP-A的高成脂活性源于细胞内在特性,而非微环境驱动。
    研究团队采用“医学版Al‐ phaGo”训练法,包括自对弈沙盒(AI医生与AI患者动态生成数万条跨专科病例对话)、反思链机制(每轮问诊即时生成鉴别诊断逻辑,增强推理透明度)和多维评价体系(包括专科医生双盲评审、患者体验问卷及AI自动评估三重验证)。
    关键机制研究中,团队鉴定出白血病抑制因子受体(LIFR)信号的关键作用:LIFR在CP-A中特异性高表达,通过激活STAT3通路促进脂肪生成;而LIFR抑制剂可选择性阻断中年内脏脂肪扩张,且不影响年轻脂肪代谢。值得注意的是,该现象存在显著性别特异性,人类男性胰周脂肪样本中同样检测到CP-A比例随年龄增长的现象。
    这项突破性研究不仅首次阐明中年脂肪增生由细胞自主程序重塑驱动,更为年龄相关的代谢疾病提供了精准干预靶点。针对中年窗口期开发LIFR抑制剂,研究团队正在探索该通路的转化应用价值,为健康老龄化策略开辟新路径。
    (来源《Science》)

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    2种不同金属材料的力学参数

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    属数
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    Number of
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    占总种数比例
    Percentage of
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    种数
    Number of
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    Percentage of total
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    鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
    小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
    多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
    红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
    小菇属 Mycena 11 5.26
    光柄菇属 Pluteus 5 2.39
    红菇属 Russula 17 8.13
    栓菌属 Trametes 5 2.39
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