撰文丨王聪 编辑丨王多鱼 排版丨水成文 胶质母细胞瘤 （GBM） 是成年人中最常见、最具侵袭性的恶性脑肿瘤。胶质母细胞瘤 表现出显著的异质 性， 患者在确诊后通常只能存活 12-18 个月。 尽管经过了几十年的研究，但该疾病尚无治愈方法，而且 已批准的治疗方法 （例如手术、放疗和化疗） 在延长预期寿命方面效果有限。 胶质母细胞瘤的 肿瘤微环境 （TME） 复杂，以 胶质母细胞瘤干细胞 （GSC） 为主，并有 肿瘤相关巨噬 细胞 （TAM） 浸润，且存在异常的代谢途径。 乳酸 （ Lactate ） 是一种关键的糖酵解代谢物，可促进 肿瘤进展；然而，胶质母细胞瘤的肿瘤微环境中 乳酸转运 和 乳酸化修饰 的作用机制仍不清楚。 2026 年 1 月 6 日，南京医科大学基础医学院 汪秀星 教授、北卡罗来纳大学教堂山分校 Jeremy N. Rich 教授、南京医科大学基础医学院 张茜 副教授、南京医科大学公共卫生学院 钱旭 教授、南京医科大学第一 附属医院 张军霞 教授作为共同通讯作者 （ 李大奇 、 崔高源 、 Kailin Yang 、 陆晨飞 、 江雨韩 、 张乐 为论文共同第一作者） ，在 Nature 子 ...

Core Insights - Recent research indicates that autophagy is activated during exercise, mediating the health benefits associated with physical activity. However, the molecular mechanisms regulating skeletal muscle autophagy during exercise remain unclear [3][5]. Group 1: Research Findings - A study published in Cell Chemical Biology reveals that lactate produced during exercise enhances autophagy in skeletal muscle by lactylation of the mTOR protein [3][5]. - Lactate is identified as a positive regulator of autophagy in muscle cells, with levels rapidly increasing after a single exercise session [5]. - The study demonstrates that lactate promotes lactylation at the K921 site of the mTOR protein, inhibiting mTORC1 activity and enhancing autophagy [5][8]. Group 2: Implications - This research fundamentally redefines lactate, transforming it from a mere metabolic byproduct into a key signaling molecule that mediates exercise-induced skeletal muscle adaptation [7][8]. - The findings provide a conceptual framework for understanding how muscle metabolism translates into adaptive responses, opening new avenues for the treatment of muscle and metabolic diseases [8].

Core Insights - Lung cancer is a leading cause of cancer-related deaths globally, with non-small cell lung cancer (NSCLC) accounting for approximately 85% of cases, and lung adenocarcinoma (LUAD) being the most common subtype. The five-year survival rate for lung adenocarcinoma patients is below 26% [2] - The study published in Cell Discovery reveals that ferroptosis-induced SUMO2 lactylation counteracts ferroptosis by enhancing the degradation of ACSL4 in lung adenocarcinoma, identifying a key regulatory factor in the resistance to ferroptosis and proposing a new strategy for cancer treatment based on ferroptosis [3][8] Group 1: Ferroptosis and Cancer Treatment - Ferroptosis is a regulated form of cell death characterized by the accumulation of reactive oxygen species (ROS), lipid peroxides, and increased levels of divalent iron (Fe2+), showing significant effectiveness in overcoming resistance to traditional cancer therapies [5] - The study indicates that ferroptosis significantly increases lactate accumulation and subsequent protein lactylation, which contributes to the resistance of lung adenocarcinoma cells to ferroptosis [6] Group 2: Key Findings of the Research - SUMO2-K11 lactylation is identified as a critical factor determining the resistance to ferroptosis in lung adenocarcinoma, as it weakens the interaction between SUMO2 and ACSL4, promoting ACSL4 degradation and disrupting lipid metabolism [6][8] - AARS1 is recognized as the lactylation transferase for SUMO2-K11la, while HDAC1 acts as the de-lactylase. The research team developed a cell-penetrating peptide that specifically inhibits SUMO2-K11la, enhancing ferroptosis and increasing the sensitivity of lung adenocarcinoma to the chemotherapy drug cisplatin [6][8]