海军军医大学,IF z-bio 2025-07-03 3038

　　Naval Medical University, formerly known as the Second Military Medical University, was founded in 1949. As a leader in the field of medical education, the school has strong faculty, with 6 full-time academicians, 9 Changjiang scholars, 26 national outstanding young people, and 4 national teaching teams. It also has three directly affiliated tertiary affiliated hospitals - Changhai Hospital, Changzheng Hospital, and Oriental Hepatobiliary Surgery Hospital, with rich medical resources.

　　In 2025, the scientific research team of the Naval Military Medical University continued to make progress, explored and deepened the field of medicine, and achieved a series of remarkable results. According to incomplete statistics, there are 94 documents with a total of more than 10 minutes this year. The editor selected some of the high-scoring articles published this year to share them briefly. Let’s take a look.

　　01

　　Nature Genetics (IF=29)

　　On January 6, Professor Ren Shancheng, Department of Urology at Shanghai Changzheng Hospital Affiliated to Naval Medical University, and Professor Chen Ke of Tongji Hospital Affiliated to Huazhong University of Science and Technology, and Professor Gudi of the First Affiliated Hospital of Guangzhou Medical University jointly published a paper entitled "Spatially resolved transcriptomic analysis of the adult human prostate"

　　The prostate is highly heterogeneous due to its complex cellular composition and spatial structure, which is crucial to understanding its normal function and the occurrence of diseases (such as prostate cancer). However, a comprehensive understanding of its cell type and its spatial distribution still need to be deepened.

　　The researchers conducted in-depth analysis of nearly 300,000 single cells/nuclei of prostate from multiple patients, identified 126 unique cell subpopulations, and identified four different acinar types, two of which were significantly associated with specific prostate cancer subtypes (ETS fusion negative).

　　Through multiomic integration analysis, the researchers proposed that two specific luminal cells may be cells of common origin for prostate cancer; and found that region-specific fibroblasts may shape the heterogeneity of luminal cells by affecting the microenvironment. This comprehensive map finally constructed provides an extremely valuable high-resolution reference framework for a deep understanding of the structure, function, disease mechanism of the prostate and the development of new diagnostic and treatment strategies.

　　02

　　Cell Research (IF = 25.9)

　　On January 6, Professor Wang Pin from Naval Medical University, together with Academician Cao Xuetao and Professor Yu Yizhi, jointly published a research paper entitled "Nonenzymatic lysine D-lactylation induced by glycolase II substrate SLG dampens inflammation immunoresponses".

　　Precise regulation of the immune system is crucial to prevent excessive inflammatory damage, and immune metabolism plays a key role in this process, but the self-restriction mechanism at the non-enzymatic protein modification level has not yet been clarified. The role of the glyoxalase system (especially GLO2 and its substrate SLG) in the metabolic pathway of glycolytic lysogenic byproducts in immunoregulation is poorly understood, and whether there are intermediates for inflammatory regulation of metabolic similar to mitochondrial metabolites in the cytoplasm also needs to be answered urgently.

　　Research has found that when innate immune activation, NF-κB signal downregulates GLO2 expression through TTP-mediated mRNA degradation, allowing SLG to accumulate in the cytoplasm and induce the cytoplasmic protein D-lactization modification. Among them, D-lactation at the K310 site of RelA (p65) protein can inhibit NF-κB transcriptional activity and form a negative feedback loop that limits inflammation. In vivo experiments have confirmed that destroying this regulatory axis will aggravate inflammation, and inhibiting GLO2 will relieve inflammation damage. This study reveals the negative feedback mechanism of immune metabolism composed of GLO2/SLG/D - lactation, providing a new strategy targeting GLO2 for inflammatory disease intervention.

　　03

　　Neuron (IF=15)

　　On May 5, Dr. Liu Wei and Director Zhou Xuhui, Second Affiliated Hospital of Naval Medical University, and Director Cai Weihua of Nanjing Medical University jointly published a research paper titled "Metabolic reprogramming through histone lactylation in microglia and macrophages recruits CD8+T lymphocytes and aggravates spinal cord injury" online.

　　Crosstalk between the central nervous system (CNS) and the immune system has received increasing attention in recent years, but its interaction mechanism between innate immunity and adaptive immunity after CNS injury is still unclear. As a serious CNS injury type, spinal cord injury (SCI) can affect neural function repair.

　　Through single-cell RNA sequencing, the research team found that CD8+ T lymphocytes aggregation in the cerebrospinal fluid and the spinal cord of damaged mice in SCI patients, and this phenomenon is related to deterioration of neurological function. It was further confirmed by knockout or drug intervention that CXCL16 chemokine secreted by damage activated microglia and macrophages (IAMs) recruited CXCR6+CD8+ T cells, aggravating neuronal loss after SCI.

　　Further research found that glycolytic reprogramming of IAMs enhances the transcription of Cxcl16 gene by promoting histone lactation, while knocking out the key glycolytic enzyme Pkm2 can partially reverse this process. It is worth noting that targeting inhibition of the CXCL16-CXCR6 chemokine axis with rutin significantly promotes motor function recovery after SCI.

　　This study reveals the pathological mechanisms of glycolytic reprogrammed IAMs regulating the innate/adaptive immune axis through CXCL16 and provides potential therapeutic strategies for immune intervention in SCI.

　　04

　　Nature Communications (IF=15.7)

　　On January 3 this year, Professor Bai Chong, Professor Shi Hui and Professor Han Chaofeng, Department of Respiratory and Critical Care Medicine, First Affiliated Hospital of Naval Medical University, as co-corresponding authors, published a paper entitled "Macrophage STING signaling promotes fibrosis in benign airway stenosis via an IL6-STAT3 pathway".

　　Benign airway stenosis (BAS) is a common respiratory disease caused by mechanical damage (such as tracheal intubation, incision). Acute and chronic inflammation are the core of its fibrotic pathology. Although there are currently bronchoscopic intervention and anti-fibrosis and anti-inflammatory drugs, they face problems such as secondary injury, excessive scar hyperplasia and restenosis. Therefore, in-depth exploration of the pathogenesis of BAS, especially in the inflammatory stage, is of great significance to prevent disease progress.

　　The study found for the first time through single-cell sequencing and other technologies that the cGAS-STING signaling pathway in BAS is activated (expressed by dsDNA accumulation and enhanced STING expression/activation). Mouse model experiments show that inhibition or knockout of STING can alleviate tracheal fibrosis and alleviate acute and chronic inflammation, and depletion of macrophages can also improve BAS. Mechanistically, the dsDNA released by epithelial cells after tracheal injury activates the macrophage cGAS-STING pathway, which promotes IL-6 production, which promotes fibroblast activation and fibrosis by activating the STAT3 signaling pathway. This study elucidates that the cGAS-STING-IL-6-STAT3 axis is a key mechanism driving BAS inflammation and fibrosis, providing a theoretical basis and new targets for targeting the STING pathway to prevent and treat BAS.

　　05

　　Trends in Biotechnology (IF=14.9)

　　On May 20, Professor Wang Minjun, Professor Gao Junling, Professor Chen Fei from Naval Medical University and Professor Song Shaohua from Ruijin Hospital published a research paper entitled "Large-scale manufacturing of human gallbladder epithelial cell products and derived hepatocytes via a chemically defined approach"

　　Acquisition of sufficient quantity and high quality human hepatocytes is crucial for liver disease treatment (such as cell transplantation) and drug development (such as toxicology testing), but traditional methods face bottlenecks such as limited sources, difficulty in amplification, standardized production and safety assurance.

　　The researchers successfully established an animal-free culture system with clear chemical composition and GMP specifications for large-scale production of hGBECs (a single donor can produce >10¹¹ cells) and built a main cell bank and a working cell bank. Cell products are strictly controlled to ensure safety and reliability. More importantly, the study provides a scheme to efficiently differentiate hGBECs into functional hepatocytes that possess key liver functions such as albumin secretion, urea synthesis, drug metabolism (including Cu²⁺ transport and alcohol metabolism), and successfully rescued liver failure in animal models.

　　The technology has reached TRL8, and has the advantages of low technical threshold, good repeatability and high production capacity. It not only establishes a valuable biological sample library for clinical applications (such as cell therapy), but also provides a powerful tool for drug screening and liver disease modeling.

　　06

　　Microbiome (IF=12.7)

　　On March 24, Professor Kong Xiangyu from the Naval Medical University, the National Immunology and Inflammation Laboratory, together with Academician Li Zhaoshen and Professor Du Yiqi of the Shanghai Institute of Pancreatic Diseases, published an online research paper entitled "Dietary emulsifier carboxymethylcellulose-induced gut dysbiosis and SCFA reduction aggravate acute pancreatitis through classical monocyte activation" on Microbiome.

　The above article is just a microcosm of the school's scientific research strength. These achievements embody the efforts of scientific researchers and also demonstrate the school's exploration spirit in the field of medical research. Looking forward to the future of Naval Medical University's continuous breakthroughs in scientific research and innovation!