狂揽 53 篇！陆军军医大学 2026 年高分成果爆发：肿瘤、免疫、代谢多线突破

陆军军医大学（第三军医大学）是一所具有悠久历史和光荣传统的全国重点大学。近年来，学校及西南医院、新桥医院、大坪医院等附属医疗机构持续深耕肿瘤学、免疫学、神经科学、血液学、创伤医学以及代谢性疾病等研究领域，并取得了一系列重要成果。本期文章统计了陆军军医大学 2026 年影响因子 15 分以上的部分文献，共计 53 篇。由于篇幅有限，我们从中选取 6 篇具有代表性的高水平研究进行解读，其余论文统一放在文末参考文献中，供大家查阅。

一、ACADS 通过线粒体 DNA 甲基化连接脂肪酸代谢与结直肠癌抗肿瘤免疫

2026 年 3 月 26 日，陆军军医大学高原军事医学系缪洪明团队联合西南医科大学向远彩团队在 Signal Transduction and Targeted Therapy 发表题为 Short-chain acyl-CoA dehydrogenase initiates mtDNA demethylation and leakage to fuel antitumor immunity in colorectal cancer 的研究论文。

团队整合多组结直肠癌转录组数据与 TCGA-COAD 数据筛选脂肪酸代谢相关基因，发现短链酰基辅酶 A 脱氢酶 ACADS 在结直肠癌中显著降低并与患者临床分期及生存相关。机制上，ACADS 缺失会减少线粒体 DNMT1 降解、增强 mtDNA 甲基化、抑制 mtDNA 向胞质泄漏，从而削弱 cGAS–STING–TBK1/IRF3 免疫信号、增加 MDSC 和 Treg 等免疫抑制细胞，促进肿瘤生长。提高 ACADS 或使用其结合药物 hypericin 可恢复抗肿瘤免疫并抑制肿瘤进展。该研究将脂肪酸代谢、mtDNA 表观遗传与肿瘤免疫微环境连为一条完整轴线。

图 1 相关研究

二、锁定 SOD1-K123 乳酸化，揭示乳酸促进椎间盘退变的具体机制

2026 年 2 月 28 日，陆军军医大学新桥医院新桥医院骨科李长青、刘铭汉团队在 Nature Communications 发表了题为 SOD1 lactylation impair its enzymatic activity by conformational change to aggravate intervertebral disc degeneration 的研究论文。

团队通过代谢组学、单细胞 RNA 测序和乳酸化蛋白质组学联合筛选，在退变髓核组织中鉴定出 435 个差异乳酸化蛋白和 963 个差异乳酸化位点，并锁定 SOD1 第 123 位赖氨酸乳酸化作为关键致病信号：该修饰改变 SOD1 蛋白构象并降低其酶活性，导致 ROS 积累、DNA 损伤，并激活细胞衰老程序，而 K123R 突变可减轻氧化损伤与椎间盘退变。在此基础上，团队从约 160 万个化合物中虚拟筛选出小分子 ZL-01，经 Ⅱ 型胶原靶向肽修饰的细胞外囊泡递送 ZL-01，提高髓核局部滞留并取得比直接给药更明显的椎间盘保护效果，为椎间盘退变提供了新治疗靶点。

图 2 相关研究

三、TIGAR 通过 G6PD/6PGD 乳酸化控制杯状细胞 NADPH 供给和肠黏液屏障

2026 年 3 月 3 日，陆军军医大学西南医院彭曦团队在 Nature Communications 发表题为 TIGAR regulates intestinal mucus barrier integrity by inhibiting lactylation of G6PD/6PGD in ulcerative colitis 的研究论文。

研究发现溃疡性结肠炎中杯状细胞 TIGAR 持续低表达，伴随乳酸积累，磷酸戊糖途径关键酶 G6PD 和 6PGD 分别在第 432 和 38 位赖氨酸被乳酸化修饰而失活，NADPH 供给不足。抗氧化能力随之下降，参与黏蛋白加工的 AGR2 发生 S-亚硝基化，最终影响成熟 MUC2 形成，使覆盖肠上皮表面的黏液层变薄并破坏屏障完整性；该研究提出溃疡性结肠炎中的代谢异常可通过特定位点蛋白乳酸化改变杯状细胞分泌黏蛋白的能力，为恢复肠黏液屏障提供了新的机制靶点。

图 3 相关研究

四、MG53 介导骨骼肌 — 肝脏串扰，促进酒精代谢

2026 年 2 月 13 日，陆军军医大学大坪医院曾春雨团队在国际综合性期刊 Nature Communications 发表了题为 MG53 mediates skeletal muscle-liver cross-talk and enhances alcohol metabolism in alcoholic liver disease 的研究论文。

酒精性肝病的研究通常将关注点集中在肝脏本身，但这项研究把视角转向了另一个重要的代谢器官 —— 骨骼肌。研究团队发现，骨骼肌来源的 MG53 可以参与调控肝脏酒精代谢，建立了一条此前受到关注较少的「骨骼肌 — 肝脏」器官间通讯通路。进一步研究显示，MG53 能够影响肝脏酒精代谢相关过程，并在酒精相关肝损伤中发挥保护作用。这提示骨骼肌不仅是运动和能量消耗器官，还可能通过分泌和代谢信号远程影响肝脏功能。因此，该研究从器官串扰角度拓展了人们对酒精性肝病发生机制的认识，也为通过调控骨骼肌 — 肝脏通讯改善酒精相关代谢异常提供了新的研究方向。

图 4 相关研究

五、肿瘤细胞「抢夺」氨基酸，导致 T 细胞死亡和免疫治疗耐药

2026 年 4 月 3 日，陆军军医大学大坪医院王斌团队联合西南医院卞修武院士及美国哈佛医学院魏文毅团队，在 Nature Cell Biology 发表题为 Aberrant amino acid-sensing promotes immunotherapy resistance via the inflammatory cytokine–ZBTB5–mTORC1 axis 的研究论文。

该研究发现，肿瘤微环境中的炎症细胞因子可诱导 ZBTB5 在 S127 位点磷酸化，进而形成 Cullin3-ZBTB5 E3 泛素连接酶复合物并促进 GATOR1 成员 NPRL2 降解，使原本在氨基酸不足时抑制 mTORC1 的制动机制失效，导致癌细胞在营养有限条件下仍持续激活 mTORC1 并大量摄取氨基酸；这不仅促进肿瘤生长，还使肿瘤内 CD8⁺ T 细胞因营养匮乏而生存下降、功能受损，从而削弱免疫检查点抑制剂疗效，而阻断 ZBTB5-S127 磷酸化可抑制癌细胞异常氨基酸感知、增加 T 细胞存活并提高抗 PD-1 治疗效果，由此揭示炎症因子 –ZBTB5–NPRL2–mTORC1 通路连接炎症微环境、营养竞争与免疫治疗耐药，说明肿瘤可通过抢夺氨基酸间接「饿死」T 细胞。

图 5 相关研究

六、钒重新接通糖尿病创面巨噬细胞的葡萄糖氧化代谢

2026 年 4 月 23 日，陆军军医大学西南医院罗高兴、于云龙团队联合华南理工大学朱伟团队在 Signal Transduction and Targeted Therapy 发表题为 Macrophage metabolic reprogramming by vanadium released from glucose-responsive bio-gel accelerates diabetic wound repair 的研究论文。

团队发现糖尿病创面中的炎症型巨噬细胞虽葡萄糖充足，却因糖酵解占优、葡萄糖进入线粒体 TCA 循环和氧化磷酸化不足而难以向修复型转变；掺钒介孔生物活性玻璃纳米球（V-MBG）释放的钒可激活巨噬细胞 INSR–PI3K 信号轴，增加葡萄糖摄取并恢复受抑的 TCA 循环和氧化磷酸化，推动其向修复型转变。为适应糖尿病创面持续高糖环境，团队又将 V-MBG 装入葡萄糖响应型 GCP 水凝胶以实现高糖条件下持续释放，并在糖尿病创面模型中促进修复型巨噬细胞增加、降低局部炎症、加快创面闭合与组织再生，使生物材料从被动药物载体变为主动调控免疫细胞代谢的工具。

图 6 相关研究

2026 年以来，陆军军医大学在基础医学与临床转化领域持续活跃，本次解读的 6 项研究覆盖结直肠癌、椎间盘退变、溃疡性结肠炎、酒精性肝病、肿瘤免疫治疗与糖尿病创面修复等方向。共性清晰：「代谢—疾病」交叉是主线，且普遍推进到了小分子、靶向递送与生物凝胶等干预策略，机制研究与临床转化的结合日益紧密。

注：以上仅精选了陆军军医大学 2026 年发表的部分文章，还有部分文章未报道，欢迎大家在评论区补充并挑选感兴趣的文章，我们后续继续进行解读。

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