来源：丁香学术
海军军医大学（第二军医大学），是一所历史悠久且在医学领域享有盛誉的高等学府。近年来，海军军医大学的研究团队不断深入到细胞、分子等微观层面，在涵盖了气道疾病、前列腺癌、炎症疾病、肝细胞癌、脊髓损伤、肝脏疾病细胞治疗以及急性胰腺炎等多个医学领域均取得突破性成果。
本期文章统计了海军军医大学 2025 年影响因子 10 分以上的部分文献，共计 94 篇（作者根据研究领域数量分布进行了统计，见下方词云图）。由于篇幅有限，本文选取了 7 篇进行解读，其余文章放在文末参考文献列表里供大家查阅，可能还有一些未统计到的研究，欢迎在评论区补充。
海军军医大学 2025 年高影响力研究聚焦领域一览
（涵盖癌症、免疫、神经、纳米材料等多学科前沿突破）
第一篇
2025 年 1 月 3 日， 海军军医大学白冲教授联合石荟教授及韩超峰教授共同在Nature Communications上发表了题为「
Macrophage STING signaling promotes fibrosis in benign airway stenosis via an IL6-STAT3 pathway」的研究性文章，该研究使用 scRNA 测序证明 cGAS-STING 信号传导与 BAS 有关，并伴随 dsDNA 水平升高和 STING 表达上调。
图 1: Nature Communications
良性气道狭窄（BAS）是一种由多种因素引起的气道纤维化疾病，可能导致气道阻塞和呼吸困难。尽管已有多种治疗方法，但其发病机制尚未完全阐明。该研究团队利用单细胞 RNA 测序技术，分析了 BAS 患者的气道组织样本，发现 cGAS-STING 信号传导通路在 BAS 中显著激活。
进一步实验表明，STING 激活通过 IL6-STAT3 信号轴促进巨噬细胞分泌促纤维化因子（如 TGF-β），进而刺激成纤维细胞增殖和胶原沉积，导致气道纤维化。阻断 STING 信号或 IL6-STAT3 通路可显著减轻气道纤维化程度。该研究揭示了 BAS 发病机制中的一个新环节，即巨噬细胞中的 STING 信号通过 IL6-STAT3 通路促进气道纤维化。这为开发针对 BAS 的治疗方法提供了潜在的靶点。
第二篇
2024 年 4 月 1 日，海军军医大学附属长征医院任善成教授联合华中科技大学附属同济医院谌科教授和广州医科大学附属第一医院古迪教授等共同在Nature Genetics上发表了题为
「Spatially resolved transcriptomic analysis of the adult human prostate」的研究性文章，该研究构建了首个高分辨率成人前列腺空间图谱，为前列腺癌的早期诊断和治疗提供了新的思路。
图 2: Nature Genetics
前列腺癌是男性最常见的恶性肿瘤之一，但其发病机制和细胞起源仍存在争议。传统研究多基于组织匀浆，难以解析前列腺的空间异质性和细胞亚群分布。空间转录组学技术的出现为解决这一问题提供了可能。上述研究团队整合 11 例前列腺样本，对 25.3 万个单细胞和 3.4 万个细胞核进行测序，绘制了前列腺的空间转录组图谱。发现了 126 个细胞亚群，包括新型管腔细胞、基底细胞和成纤维细胞亚型。
特别是，type2 管腔细胞和 SFTPA2+ 管腔细胞被首次鉴定为 ETS 融合阴性前列腺癌的潜在起源细胞。type2 和 SFTPA2+ 管腔细胞在外周带富集，而中央/移行带缺乏这些细胞，解释了前列腺癌在外周带高发的现象。分析了前列腺间质微环境的异质性，包括不同区域成纤维细胞的分泌特性和与管腔细胞的相互作用。该研究为前列腺癌的发病机制提供了新的见解，特别是关于前列腺癌的细胞起源和解剖区域偏好性。
第三篇
2025 年 1 月 6 日，来自海军军医大学的王品教授联合曹雪涛院士、于益芝教授共同在Cell Research期刊上发表了题为
「Nonenzymatic lysine D-lactylation induced by glyoxalase II substrate SLG dampens inflammatory immune responses」的研究性文章，该研究揭示了乙二醛酶 II（GLO2）的底物 S - D - 乳酰谷胱甘肽（SLG） 介导的细胞质蛋白乳酸化修饰的全新机制，为炎症疾病治疗提供了新靶点。
图 3: Cell Research
炎症免疫反应在抗感染和自身免疫疾病中发挥关键作用，但其过度激活会导致组织损伤。因此，揭示炎症反应的负调控机制具有重要意义。D-乳酸赖氨酸化（D-lactylation）是一种新型蛋白质翻译后修饰，但其生物学功能尚不清楚。
该研究发现 GLO2 的底物 SLG 在先天免疫激活过程中积累，诱导非酶促赖氨酸 D-乳酸化修饰蛋白质。D-乳酸赖氨酸化修饰抑制 NF-κB 和 MAPK 信号通路，从而减弱炎症因子（如 TNF-α、IL-6）的产生。在脂多糖（LPS）诱导的炎症模型中，SLG 过表达显著减轻炎症反应，而 GLO2 敲除则加剧炎症。该研究首次揭示了 SLG-GLO2-D-乳酸赖氨酸化轴在炎症免疫反应中的负调控作用，为对抗临床炎症疾病提供了新的靶点。
第四篇
2025 年 3 月 7 日，来自海军军医大学和复旦大学附属肿瘤医院/上海东方肝胆外科医院/国家肝癌科学中心的王红阳院士、陈磊研究员共同在Cell Reports Medicine上在线发表了题为
「LTA4 H improves the tumor microenvironment and prevents HCC progression via targeting the HNRNPA1/LTBP1/TGF-β axis」的研究性文章，该研究发现 LTA4 H 通过靶向 HNRNPA1/LTBP1/TGF-β 轴改善肿瘤微环境，从而抑制 HCC 的进展。
图 4: Cell Reports Medicine
肝细胞癌（HCC）是全球癌症相关死亡的主要原因之一，其肿瘤微环境（TME）中的免疫抑制和纤维化是治疗失败的重要原因。LTA4 H（白三烯 A4 水解酶）在炎症和癌症中的作用存在争议，其具体机制尚不清楚。
该研究发现 LTA4 H 通过上调 HNRNPA1（异质核核糖核蛋白 A1）的表达，促进 LTBP1（潜在 TGF-β 结合蛋白 1）的降解，从而抑制 TGF-β 的活化。LTA4 H 过表达增加 TME 中 CD8+ T 细胞的浸润，减少调节性 T 细胞（Tregs）和髓源性抑制细胞（MDSCs）的积累，逆转免疫抑制状态。在 HCC 小鼠模型中，LTA4 H 过表达显著抑制肿瘤生长和转移，延长生存期。该研究揭示了 LTA4 H 通过调控 HNRNPA1/LTBP1/TGF-β 轴改善 TME 的新机制，为 HCC 的免疫治疗提供了新的策略。
第五篇
2025 年 5 月 5 日，来自海军军医大学附属医院的刘伟医生、周许辉主任联合南京医科大学蔡卫华主任共同在Neuron上在线发表题为
「Metabolic reprogramming through histone lactylation in microglia and macrophages recruits CD8
T lymphocytes and aggravates spinal cord injury」的研究性文章，该研究发现小胶质细胞和巨噬细胞中通过组蛋白乳酸化修饰实现的代谢重编程会招募 CD8+T 淋巴细胞，进而加剧脊髓损伤。
图 5: Neuron
脊髓损伤（SCI）后继发性损伤机制复杂，涉及炎症反应、氧化应激和代谢紊乱。组蛋白乳酸化（histone lactylation）是一种新兴的表观遗传修饰，但其是否参与 SCI 的病理过程尚不清楚。
该研究团队发现，SCI 后小胶质细胞和巨噬细胞中组蛋白乳酸化水平显著升高，与炎症因子表达增加相关。组蛋白乳酸化通过激活糖酵解和线粒体代谢，促进小胶质细胞和巨噬细胞向促炎表型转化。乳酸化修饰的细胞通过分泌趋化因子（如 CXCL9、CXCL10）招募 CD8+T 细胞，加剧神经炎症和组织损伤。抑制组蛋白乳酸化或阻断 CD8+T 细胞浸润显著减轻 SCI 后的神经功能缺损。该研究首次揭示了组蛋白乳酸化在 SCI 中的作用，为开发针对 SCI 炎症反应的代谢干预策略提供了新思路。
第六篇
2025 年 5 月 20 日，来自海军军医大学的王敏君教授、高俊灵教授、陈费教授联合瑞金医院宋少华教授在Trends in Biotechnology上发表了题为
「Large-scale manufacturing of human gallbladder epithelial cell products and derived hepatocytes via a chemically defined approach」的研究性文章，该研究发现化学成分明确的培养方法可大规模制造人胆囊上皮细胞产品并诱导其分化为功能正常的肝细胞，为肝脏疾病细胞治疗提供安全可控的细胞来源。
图 6: Trends in Biotechnology
肝脏相关疾病（如肝硬化、肝癌）的细胞治疗需要大量、安全、功能正常的肝细胞。然而，传统方法依赖基质胶和动物源性成分，存在批次差异和安全隐患。该研究团队通过规模化筛选，确定了适合胆管上皮细胞生长的化学成分明确的培养基，完全替代基质胶。
在 GMP 条件下，胆管上皮细胞可稳定扩增至临床级数量，并诱导分化为功能正常的肝细胞。诱导分化的肝细胞表达肝细胞标志物（如 ALB、CYP3A4），并具有药物代谢功能。在肝损伤小鼠模型中也发现，移植的肝细胞可以显著改善肝功能。该研究建立了首个无基质胶、化学成分明确的胆管上皮细胞培养体系，为肝脏相关疾病的细胞治疗提供了安全、可控的细胞来源，推动了细胞治疗的临床转化。
第七篇
2025 年 3 月 24 日，来自海军军医大学、国家免疫和炎症实验室的孔祥毓教授联合李兆申院士及上海胰腺疾病研究所的杜奕奇教授在Microbiome上在线发表了题为
「Dietary emulsifier carboxymethylcellulose-induced gut dysbiosis and SCFA reduction aggravate acute pancreatitis through classical monocyte activation」的研究性文章，该研究首次发现膳食乳化剂 CMC 诱导肠道菌群失调和短链脂肪酸减少，进而通过激活经典单核细胞加重急性胰腺炎的机制，为急性胰腺炎的预防和治疗开辟了新的研究方向。
图 7: Microbiome
急性胰腺炎（AP）是一种严重的消化系统疾病，其发病机制涉及肠道菌群失调和免疫反应异常。膳食乳化剂（如羧甲基纤维素钠，CMC）广泛用于食品加工，但其对肠道健康的影响存在争议。该研究团队发现，长期摄入 CMC 导致小鼠肠道菌群多样性降低，拟杆菌门减少，厚壁菌门增加。
同时 CMC 摄入显著降低肠道短链脂肪酸（SCFA：如乙酸、丙酸）的水平，破坏肠道屏障功能。肠道菌群失调和 SCFA 减少通过 TLR4 信号通路激活经典单核细胞，促进其向胰腺迁移并分泌促炎因子（如 TNF-α、IL-1β），加重胰腺炎症。而补充 SCFA 或益生菌可逆转 CMC 诱导的肠道菌群失调，减轻 AP 严重程度。该研究首次揭示了膳食乳化剂 CMC 通过肠道菌群-SCFA-单核细胞轴加重 AP 的新机制，为 AP 的预防和治疗提供了新的饮食干预策略。
结语
海军军医大学科研团队今年取得的研究成果，涵盖了气道疾病、前列腺癌、炎症疾病、肝细胞癌、脊髓损伤、肝脏疾病细胞治疗以及急性胰腺炎等多个医学领域，为多种疾病的治疗提供了潜在的新靶点和新的治疗策略。彰显了海军军医大学在医学研究领域的领先地位，也为全球医学事业的发展做出了积极贡献。
注：以上仅精选了海军军医大学 2025 年发布的部分文章（影响因子高于 10 分），还有部分文章未报道，可见补充的参考文献。
精选内容的参考文献：
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