来源:丁香学术
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,陆军军医大学的研究团队在肿瘤学、神经科学、心脑血管疾病领域等均取得突出成果。本期文章统计了陆军军医大学 2025 年影响因子 10 分以上的部分文献,共计 37 篇。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,可能还有一些没有统计到的研究,欢迎在评论区补充!
一、血管内再灌注后注射替奈普酶的疗效评估
2025 年 1 月 13 日,陆军军医大学资文杰教授团队联合国内多家医院研究团队在国际顶尖医学期刊JAMA杂志发表了题为
Intra-Arterial Tenecteplase Following Endovascular Reperfusion for Large Vessel Occlusion Acute Ischemic Stroke: The POST-TNK Randomized Clinical Trial的文章。
为评估大血管闭塞性急性缺血性中风患者接受机械取栓后动脉内注射替奈普酶的安全性和有效性,这项随机对照临床试验共纳入了 34 家医院的 540 名患者。分析结果表明,血栓切除术后接受动脉内注射替奈普酶治疗的患者中,其 90 天时无残疾生存率为 49.1%,与对照组并无差异。因此,该研究表明,辅助使用动脉内注射替奈普酶治疗并没有显著提高患者 90 天无残疾生存的效能。
图 1 相关研究(图源:[1])
二、血管内再灌注后注射尿激酶的疗效评估
2025 年 1 月 13 日,陆军军医大学杨清武教授与国内多家研究团队在JAMA杂志发表了题为
Intra-Arterial Urokinase After Endovascular Reperfusion for Acute Ischemic Stroke: The POST-UK Randomized Clinical Trial的文章。
这一研究则评估了大血管闭塞性急性缺血性中风患者接受机械取栓后动脉内注射尿激酶的安全性和有效性。该研究纳入发病 24 小时内、取栓后达到近完全至完全再通的 535 例患者,并随机分为尿激酶组与对照组。分析结果显示,尿激酶组 90 天无残疾生存率为 45.1%,而对照组为 40.2%,两者之间的差异无统计学意义,安全性方面同样无显著差异。因此,本研究表明,取栓后动脉内尿激酶辅助治疗未能显著改善患者功能结局。
图 2 相关研究(图源:[2])
三、骨转移肿瘤对免疫检查点疗法耐药的新机制被揭示
2025 年 4 月 24 日,陆军军医大学朱波教授领衔的团队在肿瘤领域权威期刊Cancer Cell杂志发表了题为
Bone metastases diminish extraosseous response to checkpoint blockade immunotherapy through osteopontin-producing osteoclasts的研究论文。
研究发现,骨转移条件下的破骨细胞生成大量骨桥蛋白,其通过血液循环进入骨外肿瘤微环境,并抑制 CD8+ TCF1+ 前体细胞的分化和 T 细胞的募集,还促进髓源性抑制细胞和 M2 型巨噬细胞的浸润,形成免疫抑制微环境,最终破坏免疫检查点阻断疗法的关键环节,降低其疗效。不过,阻断破骨细胞的生成或中和血液循环中的骨桥蛋白则可恢复骨外肿瘤对免疫检查点阻断疗法的敏感性。因此,该研究证实了骨是被肿瘤转移利用的特异性免疫调节器官,还为骨转移患者的免疫联合治疗提供了新策略。
图 3 相关研究(图源:[3])
四、少突胶质前体细胞在多发性硬化症中的免疫调节与脱髓鞘机制
2025 年 4 月 2 日,陆军军医大学牛建钦领衔的团队在Science Translational Medicine杂志发表了题为
Oligodendroglial precursor cells modulate immune response and early demyelination in a murine model of multiple sclerosis的研究论文。
该研究借助自身免疫性脑脊髓炎小鼠模型,模拟多发性硬化症的病理过程,并发现少突胶质前体细胞中 Wnt 的过度激活导致病理加速和恶化,并促使病理改变向大脑实质扩展。进一步的研究还发现,一个新型细胞毒性巨噬细胞亚群在少突胶质前体细胞异常激活后显著扩增,并通过分泌促炎因子驱动神经炎症、诱导脱髓鞘等。因此,该研究阐明了多发性硬化症早期脱髓鞘的核心机制,提供了疾病干预新思路。
图 4 相关研究(图源:[4])
五、DNA 异常增多的肾小管细胞推动急性肾损伤向慢性肾病恶化
2025 年 4 月 21 日,陆军军医大学赵景宏团队在肾脏领域权威期刊Kidney International发表了题为
Single-cell analysis of proximal tubular cells with different DNA content reveals functional heterogeneity in the acute kidney injury to chronic kidney disease transition的研究论文。
该研究通过单细胞测序技术,揭示了急性肾损伤向慢性肾病转化过程中近端肾小管细胞的促进作用。经过分析,他们发现急性肾损伤后,近端肾小管细胞呈现显著的 DNA 含量差异,既包括二倍体(2N),还包括四倍体(4N)及多倍体(>4N)细胞,并且其与功能异质性具有直接关联,其中多倍体近端肾小管细胞的促炎基因和纤维化相关基因显著上调,还发现了分泌型磷蛋白 1(SPP1)是多倍体细胞的关键枢纽分子,在近端肾小管特异性敲低 SPP1 可显著改善小鼠的肾纤维化。
图 5 相关研究(图源:[5])
六、负责处理精细声音信息的丘脑皮层新通路被发现
2025 年 4 月 15 日,陆军军医大学谌小维作为最后通讯作者在神经科学权威期刊Neuron杂志发表了题为
A parallel tonotopically arranged thalamocortical circuit for sound processing的研究论文。
丘脑腹内侧核基底部是一个还未被识别的听觉相关丘脑区域。经过深入的分析,研究人员发现丘脑腹内侧核基底部可以向听觉皮层发送密集的投射,这些投射主要终止于皮层第 1 层,并且表现出强烈的频率选择性,与皮层的音频拓扑分布匹配,进一步参与了声音的精准分辨。因此,本研究发现了一条参与声音精细分辨的全新通路,为听觉神经科学添加了一个重要模块。
图 6 相关研究(图源:[6])
七、ASH2L 缺失加剧肺动脉高压
2025 年 2 月 25 日,陆军军医大学范晔作为最后通讯作者在Circulation Research发表了题为
ASH2L Deficiency in Smooth Muscle Drives Pulmonary Vascular Remodeling的研究论文。
研究团队发现,人肺动脉高压患者的 ASH2L 表达降低,并且其降低程度与肺动脉高压的临床严重程度相关。作为 SET1/MLL 甲基转移酶复合物的核心组分,ASH2L 可通过促进组蛋白 H3K4 甲基化发挥调控肺血管重塑的作用。进一步的分析发现,ASH2L 部分通过与 KLF5 和 FBXW7 形成蛋白质复合物来调节肺血管重塑,从而加速 KLF5 的降解;此外,ASH2L 的缺失还促进了 KLF5 对 NOTCH3 启动子的募集,从而增加了其转录和表达。
总之,该研究发现,ASH2L 的缺乏导致平滑肌细胞的增殖和肺血管重塑,而这一过程部分是通过 KLF5 依赖的 NOTCH3 转录介导的。因此,在未来,开发促进 ASH2L 表达或靶向 KLF5 可能是治疗肺动脉高压的潜在策略。
图 7 相关研究(图源:[7])
结语
总的来说,陆军军医大学今年的科研成果已经大放异彩,对于理解肿瘤、多发性硬化症、急性肾损伤等疾病的发病机制具有重要启示作用,并为开发新型治疗策略提供了新思路,继续期待陆军军医大学产出更加高质量的原创性科研成果,为人类健康贡献更大的力量。
注:以上仅精选了陆军军医大学 2025 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。
参考文献(上下滑动查阅)
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