Chinese Medical Journal最新文献

{"title":"HMGB1 induces mitochondrial dysfunction through the TLR4 and RAGE pathways to promote astrocyte autophagy and PANoptosis in intracerebral hemorrhage.","authors":"Wenzuo Shang, Jingyu Cui, Xueling Bai, Le Cao, Mangmang Xu, Shuai Jiang, Bo Wu","doi":"10.1097/CM9.0000000000004250","DOIUrl":"https://doi.org/10.1097/CM9.0000000000004250","url":null,"abstract":"<p><strong>Background: </strong>Secondary injury is an important factor that leads to a poor prognosis of intracerebral hemorrhage (ICH). Programmed cell death (PCD) plays an important role in secondary injury. After ICH, hyperactivated astrocytes transition from a protective role to a proinflammatory state, releasing neurotoxic factors that amplify neuroinflammation and exacerbate neurological deficits. Through multi-omics sequencing, we found High-mobility group box 1 (HMGB1)may be a key factor . In this study, we investigated its regulatory role in ICH and different PCDs.</p><p><strong>Methods: </strong>The ICH model was established by collagenase injection in vivo and hemoglobin treatment in vitro. Prognosis was assessed using the rotarod test and magnetic resonance imaging (MRI). Cell proliferation activity and growth status were detected using the cell counting kit 8 (CCK-8). Western blotting, enzyme-linked immunosorbent assay (ELISA), and immunofluorescence (IF) were used to detect the related proteins. Transmission electron microscopy (TEM) was used to observe pathological changes. The transferase dUTP nick end labelling (TUNEL) staining and Annexin V/Propidium Iodide (PI) assay were used to detect the apoptosis. Multi-omics experiments were conducted to identify potential pathways of HMGB1 action.</p><p><strong>Results: </strong>The results showed that after ICH, HMGB1 translocated from the nucleus to the cytoplasm and extracellular space. Extracellular HMGB1 upregulated the expression of related molecules, increased the corresponding pathological changes. Multi-omics sequencing suggested that mitochondrial function-related pathways were enriched after ICH. Results showed that increased extracellular HMGB1 aggravated mitochondrial morphology and functional damage and the expression and release of inflammatory factors. Inhibiting TLR4 and RAGE pathways alleviated the HMGB1-mediated injuries.</p><p><strong>Conclusion: </strong>In the acute phase of ICH, HMGB1 promoted poor prognosis by mediating mitochondrial dysfunction through the TLR4 and RAGE pathways, thereby promoting autophagy and PANoptosis while increasing neuroinflammation after ICH.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MOTS-c mediates remote ischemic preconditioning-induced protection against lung ischemia-reperfusion injury via NRF2-dependent mitochondrial biogenesis.","authors":"Jiaojiao Sun, Bo Xu, Dandan Wang, Meng Sui, Shengpeng Li, Yijing Chen, Jinbo Wu, Shiyong Teng, Qingfeng Pang, Chunxiao Hu","doi":"10.1097/CM9.0000000000004254","DOIUrl":"https://doi.org/10.1097/CM9.0000000000004254","url":null,"abstract":"","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism for shallow anterior chamber in eyes with primary angle-closure diseases: Trans-lenticular pressure difference.","authors":"Haishuang Lin, Shaodan Zhang, Xuanli Zheng, Huijuan Wu, David S Friedman, Nathan Congdon, Mingguang He, Ying Han, Ningli Wang, Yuanbo Liang","doi":"10.1097/CM9.0000000000004216","DOIUrl":"https://doi.org/10.1097/CM9.0000000000004216","url":null,"abstract":"","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex-specific longitudinal associations between alcohol consumption trajectories and incident cardiovascular disease in Chinese adults.","authors":"Yi Gao, Yan Liu, Wei Tian, Jiashuo Ren, Wanlu Guo, Zhirui Li, Hongbin Qiu, Bo Yu, Yiying Zhang, Shanjie Wang","doi":"10.1097/CM9.0000000000004234","DOIUrl":"https://doi.org/10.1097/CM9.0000000000004234","url":null,"abstract":"","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Score-fecal immunochemical test algorithm for early-onset colorectal neoplasia informs prioritized colonoscopy: Evidence from a nationwide prospective study.","authors":"Xiangyu Sui, Song Zhang, Zixuan He, Jiahui Wei, Xin Chang, Peng Pan, Tian Xia, Rundong Wang, Shuhuai Xu, Xinxin Huang, Youdong Zhao, Haiyang Jiang, Zhaoshen Li, Shengbing Zhao, Yu Bai","doi":"10.1097/CM9.0000000000003759","DOIUrl":"10.1097/CM9.0000000000003759","url":null,"abstract":"","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":"2827-2829"},"PeriodicalIF":9.1,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13593099/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aggressive fever suppression in septic patients without known cardiorespiratory impairment is associated with delayed SOFA score improvement.","authors":"Roman Kula, Marcela Káňová, Jan Varady, Jan Neiser, Jarmila Janišová, Klára Rusková, Kateřina Tejkalová, Roman Kula, Jiří Kalina, Jiří Jarkovský, Marcin F Osuchowski","doi":"10.1097/CM9.0000000000003892","DOIUrl":"10.1097/CM9.0000000000003892","url":null,"abstract":"","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":"2836-2838"},"PeriodicalIF":9.1,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13593053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145667486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of local spontaneous activity and hippocampal volume on the relationship between APOE genotype, ATN biomarkers, and cognitive function across the Alzheimer's disease spectrum.","authors":"Yao Zhu, Anmo Wang, Yaling Wu, Lijia Yang, Yuanhui Duan, Yaqiong Zhao, Xinyi Zhao, Wei Hu, Sen Qun","doi":"10.1097/CM9.0000000000004110","DOIUrl":"10.1097/CM9.0000000000004110","url":null,"abstract":"","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":"2839-2841"},"PeriodicalIF":9.1,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13593276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147867021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Delayed antiviral immune response in alveolar type 2 cells increases susceptibility to influenza virus in alveoli.","authors":"Xiao Shang, Zeyi Wang, Jiapei Yu, Ruiqi Zhang, Danlei Liu, Shumei Zou, Ka-Yi Leung, Ju Jia, Yujing Fan, Kwok-Hung Chan, Hui Li, Ivan Fan-Ngai Hung, Bin Cao","doi":"10.1097/CM9.0000000000004107","DOIUrl":"10.1097/CM9.0000000000004107","url":null,"abstract":"<p><strong>Background: </strong>The alveolar sac, which serves as the primary site for gas exchange, comprises alveolar type 1 (AT1) and alveolar type 2 (AT2) cells. These epithelial cells initiate immune responses upon encountering external stimuli. However, the influenza virus infection patterns and antiviral responses exhibited by different types of alveolar epithelial cells remain understudied. This study aimed to investigate the differential susceptibility and antiviral responses of AT1 and AT2 cells during influenza virus infection.</p><p><strong>Methods: </strong>Immunofluorescence staining was performed to determine the spatial distribution of influenza A virus (IAV; H1N1). Primary murine epithelial in vitro culture models, including an AT2 sphere culture and an AT1 differentiation model, were established to elucidate the mechanisms underlying cellular susceptibility to IAV. Bulk RNA sequencing and quantitative polymerase chain reaction were performed to characterize the cellular responses to viral infection.</p><p><strong>Results: </strong>Mouse AT2 cells exhibited greater susceptibility to H1N1 than did AT1 cells. The in vitro primary epithelial cell culture models mimicked the in vivo cellular phenotype. They further reproduced the in vitro finding of relatively high viral replication in AT2 cells. Mechanistically, no significant difference was observed between AT1 and AT2 cells in the expression of α-2,3 or α-2,6 sialic acid (viral receptors). However, RNA sequencing revealed that gene ontology terms such as the response to viral infection, negative regulation of the viral life cycle, and regulation of type I interferon (IFN) production were enriched in AT1 cells. This finding was validated using quantitative polymerase chain reaction. From 12 to 48 h after infection, the expression levels of types I and III IFNs, chemokines, and IFN-stimulated genes remained lower in AT2 cells than in AT1 cells.</p><p><strong>Conclusion: </strong>Our findings indicate the localization of IAV in alveoli and highlight the vulnerability of AT2 cells, which exhibit delayed immune responses, resulting in increased viral replication.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":"2780-2790"},"PeriodicalIF":9.1,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13593187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PI3K-Akt signaling network crosstalk in cerebral ischemia/reperfusion injury: Mechanisms and therapeutic implications.","authors":"Wenzhe Yang, Qian Yang, Zhihui Wang, Xu Zhao, Jingxuan Deng, Xinran Xia, Jinzheng Wang, Linhui Xia, Yanfang Wang, Fen Cui, Rubin Tan, Jinxiang Yuan","doi":"10.1097/CM9.0000000000004179","DOIUrl":"10.1097/CM9.0000000000004179","url":null,"abstract":"<p><strong>Abstract: </strong>Cerebral ischemia (CI) is an acute central nervous system disorder resulting from the abrupt interruption of blood flow to brain tissue. The restoration of blood flow during treatment is frequently accompanied by cerebral ischemia/reperfusion (CI/R) injury, a secondary injury mechanism that substantially limits the overall efficacy of reperfusion therapy. The phosphatidylinositol 3-kinase (PI3K)-protein kinase B (Akt) signaling pathway, a central regulator of cell survival, proliferation, and stress response, has attracted growing interest for its role in CI and CI/R injury. During the early ischemic phase, PI3K-Akt activation in neurons and brain microvascular endothelial cells serves as a crucial endogenous protective mechanism, inhibiting apoptosis and maintaining energy metabolic homeostasis, thereby mitigating initial brain damage. As ischemia progresses, downregulation of this pathway in microglia and infiltrating macrophages can promote excessive release of proinflammatory factors, such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), exacerbating local inflammation and tissue injury. In the reperfusion phase, reactivation of the PI3K-Akt pathway exerts multi-level neuroprotection: It counteracts neuronal apoptosis and oxidative stress, promotes angiogenesis and blood-brain barrier (BBB) repair in endothelial cells, and modulates neuroinflammation in glial cells. Importantly, the PI3K-Akt pathway does not function in isolation but engages in complex crosstalk with multiple signaling cascades, such as Wnt/β-catenin, nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1), and mammalian target of rapamycin (mTOR). Moreover, it shapes the immune microenvironment by fine-tuning the functions of immune cells, including regulatory T cells (Tregs). This intricate network dynamically governs the survival of the neurovascular unit by regulating mitochondrial function, oxidative stress, inflammation, and autophagy. This review systematically explores the dynamic changes, cell-specific functions, and interactive mechanisms of the PI3K-Akt pathway during CI and CI/R injury, and discusses its potential for precision treatment strategies and clinical translation.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":"2721-2740"},"PeriodicalIF":9.1,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13592988/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148204317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical practice guideline for the diagnosis and treatment of neonatal arterial ischemic stroke (2026).","authors":"Yang He, Jun Tang, Meng Zhang, Keren Luo, Jinxing Feng, Yuan Shi, Zhenlang Lin, Zhichun Feng, Dezhi Mu","doi":"10.1097/CM9.0000000000004227","DOIUrl":"10.1097/CM9.0000000000004227","url":null,"abstract":"","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":"2687-2689"},"PeriodicalIF":9.1,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13593102/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}