Chinese Medical Journal最新文献

{"title":"Summary of the 2024 report on gastroenterology and digestive endoscopy in China.","authors":"Zheran Chen, Yusi Xu, Lei Xin, Yifei Song, Jinfang Xu, Chu Chu, Chuting Yu, Ye Gao, Xudong Ma, Zhaoshen Li, Luowei Wang","doi":"10.1097/CM9.0000000000003810","DOIUrl":"https://doi.org/10.1097/CM9.0000000000003810","url":null,"abstract":"<p><strong>Background: </strong>China has made significant progress in medical accessibility and quality over the past decades, and quality improvements in gastroenterology and digestive endoscopy have been consistent. The study aimed to describe the status quo of gastroenterology and digestive endoscopy in the Chinese mainland based on the data from the National Clinical Improvement System (NCIS) and the Hospital Quality Monitoring System (HQMS).</p><p><strong>Methods: </strong>Data were extracted from the NCIS and the HQMS. Data analysis included general information from the Department of Gastroenterology and Endoscopy centers, management of inpatients and outpatients, and annual volume and quality indicators of digestive endoscopy. Acute pancreatitis, gastrointestinal bleeding, inflammatory bowel disease, and cirrhosis were identified as priority diseases and were subjected to detailed analysis.</p><p><strong>Results: </strong>Data from 4620 and 7074 hospitals were extracted from the NCIS and HQMS, respectively. In 2023, 9.6 gastroenterologists, 6.7 endoscopists, and 37.3 gastroenterology beds per hospital nationwide were observed, achieving 19,252.4 outpatient visits, 1615.2 hospitalizations (97.0 for acute pancreatitis, 146.1 for gastrointestinal bleeding, 40.2 for inflammatory bowel disease, and 111.4 for cirrhosis), and 9432.7 digestive endoscopic procedures per hospital. Overall, the quality of practice improved significantly. The proportion of early cancer among gastrointestinal cancers increased from 11.1% in 2015 to 23.4% in 2023, and the adenoma detection rate during colonoscopy increased from 19.3% in 2019 to 26.9% in 2023. Regarding priority diseases, hospitalizations increased, and 31-day unplanned readmission rates decreased between 2019 and 2023. The median hospitalization costs and median proportion of medication costs decreased for acute pancreatitis, gastrointestinal bleeding, and cirrhosis. However, it increased for inflammatory bowel disease.</p><p><strong>Conclusion: </strong>This report evaluates the status quo and development of gastroenterology and digestive endoscopy in the Chinese mainland, providing guidance for future quality improvements.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074545","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":"Efficacy and safety of the triple combination cream in Chinese patients with moderate to severe melasma: A multi-center, randomized, double-blind, three-arm, parallel-group, placebo-controlled clinical trial.","authors":"Li Zhang, Geyao Xu, Quanzhong Liu, Weili Pan, Lunfei Liu, Linfeng Li, Jinyan Wang, Hao Cheng, Chao Ji, Meng Pan, Xinghua Gao","doi":"10.1097/CM9.0000000000003718","DOIUrl":"https://doi.org/10.1097/CM9.0000000000003718","url":null,"abstract":"","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074548","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":"Exercise-induced angiogenesis and lymphangiogenesis: A potential therapeutic tool to fight aging and disease.","authors":"Jizong Jiang, Yongjun Zheng, Rui Wang, Hao Yang, Shihui Zang, Emeli Chatterjee, Guoping Li, Dragos Cretoiu, Cuimei Zhao, Junjie Xiao","doi":"10.1097/CM9.0000000000003831","DOIUrl":"https://doi.org/10.1097/CM9.0000000000003831","url":null,"abstract":"<p><strong>Abstract: </strong>Aging is an inevitable, physiological process of the human body, leading to deterioration in bodily function and increased susceptibility to various diseases. Effective endogenous therapeutic strategies for anti-aging and related diseases remain limited. Exercise confers multifaceted benefits to physical health by augmenting osteogenic and myogenic processes, enhancing cardiovascular and nervous system function, and attenuating chronic inflammation. Angiogenesis and lymphangiogenesis play pivotal roles in anti-aging, tissue repair, and immune response modulation, underscoring their potential as therapeutic targets for age-related diseases. Modulating angiogenic and lymphangiogenic pathways may provide a promising strategy for mitigating vascular decline and immune system dysfunction associated with aging. Exercise-induced endogenous angiogenesis and lymphangiogenesis can exert beneficial effects on physiological function, thereby representing a potential therapeutic paradigm for combating age-related decline and diseases. This review offers a thorough summary of the present knowledge regarding angiogenesis and lymphangiogenesis induced by exercise, encompassing the underlying mechanisms and the effects in different organs. In addition, it explores the potential of physical activity as a non-pharmacological intervention for anti-aging strategies and disease management, offering novel insights into the intersection of physical activity, aging, and disease progression.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074484","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":"Protein aggregation in neurodegenerative diseases.","authors":"Jiannan Wang, Lijun Dai, Zhentao Zhang","doi":"10.1097/CM9.0000000000003802","DOIUrl":"https://doi.org/10.1097/CM9.0000000000003802","url":null,"abstract":"<p><strong>Abstract: </strong>Neurodegenerative diseases constitute a group of chronic disorders characterized by the progressive loss of neurons. Major neurodegenerative conditions include Alzheimer's disease, Parkinson's disease, Huntington's disease, frontotemporal lobar degeneration, and amyotrophic lateral sclerosis. Pathologically, these diseases are marked by the accumulation of aggregates formed by pathological proteins such as amyloid-β, tau, α-synuclein, and TAR DNA-binding protein 43. These proteins assemble into amyloid fibrils that undergo prion-like propagation and dissemination, ultimately inducing neurodegeneration. Understanding the biology of these protein aggregates is fundamental to elucidating the pathophysiology of neurodegenerative disorders. In this review, we summarize the molecular mechanisms underlying the aggregation and transmission of pathological proteins, the processes through which these protein aggregates trigger neurodegeneration, and the interactions between different pathological proteins. We also provide an overview of the current diagnostic approaches and therapeutic strategies targeting pathological protein aggregates.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074493","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":"m6A-modified circCD2AP suppressed ferroptosis in bladder cancer by upregulating FOXC1 to promote PARK7 transcriptional activity.","authors":"Jinrong Wang, Jianfu Yang, Kun Yao, Jing Tan, Jun Gao, Lei Zhou","doi":"10.1097/CM9.0000000000003744","DOIUrl":"https://doi.org/10.1097/CM9.0000000000003744","url":null,"abstract":"<p><strong>Background: </strong>Bladder cancer (BCa) is the most common genitourinary malignancy and causes substantial economic losses worldwide. Recent studies suggest overexpression of circCD2AP in BCa, but its mechanistic contributions to carcinogenesis and ferroptosis regulation remain unclear.</p><p><strong>Methods: </strong>From August 2021 to January 2024, 98 pairs of BCa and adjacent normal tissue samples were collected from the Third Xiangya Hospital, Central South University. Gene/protein expression, lipid ROS levels, and cell viability were analyzed. Interactions among circCD2AP/YTH domain-containing protein 1 (YTHDC1), circCD2AP, insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3), and IGF2BP3/forkhead box C1 (FOXC1) were validated, along with circCD2AP-IGF2BP3 colocalization. FOXC1 binding sites in the Parkinson's disease protein 7 (PARK7) promoter were mapped. M6A modifications on circCD2AP were quantified via methylated RNA immunoprecipitation polymerase chain reaction.</p><p><strong>Results: </strong>circCD2AP was significantly upregulated in BCa and positively correlated with PARK7 expression (R2 = 0.1357, P = 0.0002). Patients with high circCD2AP expression showed poorer survival rates. CircCD2AP knockdown sensitized BCa cells to ferroptosis inducers (erastin and Ras-selective lethal small molecule 3). Methyltransferase-like 3 (METTL3) knockdown inhibited circCD2AP m6A modification and relative expression. YTHDC1 mediated m6A-dependent cytoplasmic export of circCD2AP (2.8-fold increase). Besides, circCD2AP stabilized FOXC1 mRNA, and FOXC1 bound the PARK7 promoter to enhance its expression. Knockdown of FOXC1 or PARK7 blocked the antiferroptotic effect of circCD2AP overexpression in BCa cells. Knockdown of METTL3 or circCD2AP reduced tumor burden in mice, decreasing both volume (approximately 48.3% or 56.4%) and weight (approximately 65.3% or 58.7%) through FOXC1/PARK7-mediated ferroptosis.</p><p><strong>Conclusions: </strong>METTL3-mediated m6A modification drives circCD2AP overexpression, which is subsequently exported to the cytoplasm with enhanced efficiency mediated by YTHDC1. Cytoplasmic circCD2AP stabilizes FOXC1 mRNA, enabling FOXC1-dependent transcriptional activation of PARK7. This axis suppresses ferroptosis and promotes BCa progression, revealing a novel therapeutic target.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074510","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":"Guidelines for the diagnosis and treatment of prurigo nodularis.","authors":"Li Zhang, Qingchun Diao, Xia Dou, Hong Fang, Songmei Geng, Hao Guo, Yaolong Chen, Chao Ji, Chengxin Li, Linfeng Li, Jie Li, Jingyi Li, Wei Li, Zhiming Li, Yunsheng Liang, Jianjun Qiao, Zhiqiang Song, Qing Sun, Juan Tao, Fang Wang, Zhiqiang Xie, Jinhua Xu, Suling Xu, Hongwei Yan, Xu Yao, Jianzhong Zhang, Litao Zhang, Gang Zhu, Fei Hao, Xinghua Gao","doi":"10.1097/CM9.0000000000003732","DOIUrl":"https://doi.org/10.1097/CM9.0000000000003732","url":null,"abstract":"","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074499","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":"Efficacy and safety of benvitimod 1% cream for atopic dermatitis in patients aged 2 years and older: A phase III randomized clinical trial.","authors":"Yan Zhao, Zhu Wei, Yanyan Feng, Lin Ma, Danhong Jiao, Yong Cui, Jun Gu, Kunpeng Bian, Chao Ci, Jianjian Zhu, Tiechi Lei, Yujie Shi, Xiaohua Tao, Xiuping Han, Xiaoli Zhang, Litao Zhang, Ying Li, Genhui Chen, Jianzhong Zhang","doi":"10.1097/CM9.0000000000003769","DOIUrl":"https://doi.org/10.1097/CM9.0000000000003769","url":null,"abstract":"<p><strong>Background: </strong>Benvitimod (tapinarof), an aryl hydrocarbon receptor (AhR) agonist approved for treating plaque psoriasis, is being investigated as a potential treatment for atopic dermatitis (AD). The aim of this study was to evaluate the efficacy and safety of benvitimod 1% cream in patients aged 2 years or older with AD.</p><p><strong>Methods: </strong>This randomized controlled trial enrolled 271 Chinese patients with AD aged ≥2 years, who received either benvitimod 1% cream (n = 183) or vehicle cream (n = 88) twice daily for 8 weeks in a 2:1 ratio at 35 sites in China from June to November 2023. The primary endpoint was the proportion of patients achieving a 75% improvement in the Eczema Area and Severity Index (EASI) 75 at week 8. Secondary endpoints included achievement of Investigator's Global Assessment (IGA) scores of 0/1, 90% EASI improvement (EASI 90), and ≥3-point reduction in Peak Pruritus Numerical Rating Scale (PP-NRS). Treatment-emergent adverse events (TEAEs) were monitored for safety evaluation. Furthermore, a subset of patients (n = 43) opted into a 44-week open-label extension.</p><p><strong>Results: </strong>At week 8, a significantly higher proportion of patients treated with benvitimod achieved EASI 75 compared to those receiving vehicle (54.4% [n = 183] vs. 25.5% [n = 88]; P <0.001). The benvitimod group also showed superior results across all secondary endpoints: IGA 0/1 (46.2% [n = 183] vs. 21.4% [n = 88]; P <0.001), EASI 90 (33.9% [58/171] vs. 13.5% [10/74]; P <0.001), and ≥3-point decrease in PP-NRS (54.0% [47/87] vs. 27.9% [12/43]; P <0.01). TEAEs occurred in 51.4% (94/183) of benvitimod-treated patients vs. 43.2% (38/88) of vehicle-treated patients, with most events being mild to moderate in severity.</p><p><strong>Conclusion: </strong>Benvitimod 1% cream demonstrated favorable efficacy and safety in adult and pediatric patients with AD, supporting its potential as a novel topical treatment option.</p><p><strong>Trial registration: </strong>chinadrugtrials.org.cn, CTR20231413.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074489","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":"H3K9 acetylation-dependent CHAC1 transcription in dihydroartemisinin-induced hepatic stellate cell ferroptosis.","authors":"Min Shen, Wenshu Han, Liangliang Cai, Weijuan Gong, Li Qian","doi":"10.1097/CM9.0000000000003788","DOIUrl":"https://doi.org/10.1097/CM9.0000000000003788","url":null,"abstract":"<p><strong>Background: </strong>The activation of hepatic stellate cells (HSCs) plays a crucial role in the progression of liver fibrosis, and eliminating activated HSCs is regarded as an effective strategy for combating fibrosis. Ferroptosis has emerged as a potential mechanism for HSC depletion. Dihydroartemisinin (DHA), a derivative of artemisinin, has shown anti-fibrotic effects, but its role in HSC ferroptosis remains unclear. This study aimed to investigate the molecular mechanism by which DHA regulates HSC ferroptosis through histone modifications to suppress liver fibrosis.</p><p><strong>Methods: </strong>RNA sequencing was employed to analyze gene expression changes in HSCs following DHA treatment. The role of glutathione-specific gamma-glutamylcyclotransferase 1 (CHAC1) in DHA-induced ferroptosis was assessed using genetic inhibition approaches. Chromatin immunoprecipitation (ChIP) and luciferase reporter assays were conducted to examine histone acetylation and transcription factor binding at the CHAC1 promoter. In vivo experiments utilized a murine liver fibrosis model to evaluate the therapeutic effects of DHA, with additional interventions targeting CHAC1 and ATF4 to validate their roles in ferroptosis and fibrosis resolution.</p><p><strong>Results: </strong>This study reported that DHA inhibited HSC activation through the ferroptosis pathway. We revealed that DHA treatment elevated CHAC1 levels in HSCs, Inhibition of CHAC1 prevented DHA-induced HSC ferroptosis, and DHA regulated the expression of CHAC1 at the transcriptional level rather than at the post-transcriptional level. Mechanistically, upregulated H3K9 acetylation was essential for the DHA-mediated transcriptional upregulation of CHAC1 through increased histone acetyltransferase P300 in HSCs. Inhibiting histone acetylation attenuated DHA-induced CHAC1 upregulation and ferroptosis. Aactivating transcription factor 4 (ATF4) was identified as a key transcription factor in the transcriptional activation of CHAC1. Interfering with ATF4 inhibited the transcriptional upregulation of CHAC1 by DHA. Notably, the -212 to -199 bp and -269 to -257 bp promoter regions in CHAC1 were essential for the initiation of transcription of ATF4. In mice, treatment with DHA alleviated murine liver fibrosis by inducing HSC ferroptosis. Inhibition of CHAC1 or ATF4 impaired DHA-induced HSC ferroptosis in murine liver fibrosis.</p><p><strong>Conclusion: </strong>The transcriptional activation of CHAC1, which is regulated by H3K9 acetylation, was essential for the ability of DHA to trigger HSC ferroptosis and, consequently, to suppress liver fibrosis.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063632","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":"Development and validation of a prediction score for subtype diagnosis of primary aldosteronism.","authors":"Ping Liu, Wei Zhang, Jiao Wang, Hongfei Ji, Haibin Wang, Lin Zhao, Jinbo Hu, Hang Shen, Yi Li, Chunhua Song, Feng Guo, Xiaojun Ma, Qingzhu Wang, Zhankui Jia, Xuepei Zhang, Mingwei Shao, Yi Song, Xunjie Fan, Yuanyuan Luo, Fangyi Wei, Xiaotong Wang, Yanyan Zhao, Guijun Qin","doi":"10.1097/CM9.0000000000003741","DOIUrl":"https://doi.org/10.1097/CM9.0000000000003741","url":null,"abstract":"","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063594","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":"Single-cell analysis identifies PI3+S100A7+ keratinocytes in early cervical squamous cell carcinoma with HPV infection.","authors":"Peiwen Fan, Danning Dong, Yaning Feng, Xiaonan Zhu, Ruozheng Wang","doi":"10.1097/CM9.0000000000003795","DOIUrl":"https://doi.org/10.1097/CM9.0000000000003795","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Cervical squamous cell carcinoma (CESC), the most common subtype of cervical cancer, is primarily caused by the high-risk human papillomavirus (HPV) infection and genetic susceptibility. Single-cell RNA sequencing (scRNA-seq) has been widely used in CESC research to uncover the diversity of cell types and states within tumor tissues, enabling a detailed study of the tumor microenvironment (TME). This technology allows precise mapping of HPV infection in cervical tissues, providing valuable insights into the initiation and progression of HPV-mediated malignant transformation.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We performed the scRNA-seq to characterize gene expression in tumor tissues and paired adjacent para-cancerous tissues from four patients with early-stage CESC using the 10× Genomics platform. The HPV infection and its subtypes were identified using the scRNA data and viral sequence mapping, and trajectory analyses were performed using HPV+ or HPV- cells. Interactions between different types of keratinized cells and their interactions with other cell types were identified, and pathways and specificity markers were screened for proliferating keratinized cells. The Cancer Genome Atlas (TCGA) dataset was used to verify the prognostic correlation between tumor-specific PI3+S100A7+ keratinocyte infiltration and CESC, and the localization relationship between PI3+S100A7+ keratinocytes and macrophages was verified by immunofluorescence staining.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Various types of keratinocytes and fibroblasts were the two cell types with the most significant differences in percentage between the tumor tissue samples and paired adjacent non-cancerous tissue samples in the early stages of CESC. We found that PI3+S100A7+ keratinocytes were associated with early HPV-positive CESC, and PI3+S100A7+ keratinocytes were more abundant in tumors than in adjacent normal tissues in the TCGA-CESC dataset. Analysis of clinical information revealed that the infiltration of PI3+S100A7+ keratinocytes was notably higher in tumors with poor prognosis than in those with good prognosis. Additionally, multiplex immunofluorescence analysis showed a specific increase in PI3+S100A7+ expression within tumor tissues, with PI3+S100A7+ keratinocytes and CD163+ macrophages being spatially very close to each other. In the analysis of cell-cell interactions, macrophages exhibited strong crosstalk with PI3+S100A7+ proliferating keratinocytes in HPV-positive CESC tumors, mediated by tumor necrosis factor (TNF), CCL2, CXCL8, and IL10, highlighting the dynamic and tumor-specific enhancement of macrophage-keratinocyte interactions, which are associated with poor prognosis and immune modulation. Using CIBERSORTx, we discovered that patients with high infiltration of both PI3+S100A7+ proliferating keratinocytes and macrophages had the shortest overall survival. In the analysis of cell-cell interactions, PI3+S100A7+ proliferating keratinocytes an","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063570","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}