Current Medical Science最新文献

{"title":"Development and Validation of a Nomogram Prediction Model for Sepsis-Induced Coagulopathy: A Multicenter Retrospective Study.","authors":"Wen-Hao Ma, Ze-Yu Yang, Xing-Xing Fan, Lei Tian, Tuo Zhang, Ming-da Wang, Ji-Yuan Gao, Jian-le Xu, Wei Fang, Hui-Min Hou, Man Chen","doi":"10.1007/s11596-025-00093-5","DOIUrl":"https://doi.org/10.1007/s11596-025-00093-5","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to develop a prediction model to assess the risk of sepsis-induced coagulopathy (SIC) in sepsis patients.</p><p><strong>Methods: </strong>We conducted a retrospective study of septic patients admitted to the Intensive Care Units of Shandong Provincial Hospital (Central Campus and East Campus), and Shenxian People's Hospital from January 2019 to September 2024. We used Kaplan-Meier analysis to assess survival outcomes. LASSO regression identified predictive variables, and logistic regression was employed to analyze risk factors for pre-SIC. A nomogram prediction model was developed via R software and evaluated via receiver operating characteristic (ROC) curves, calibration curves, and decision curve analysis (DCA).</p><p><strong>Results: </strong>Among 309 patients, 236 were in the training set, and 73 were in the test set. The pre-SIC group had higher mortality (44.8% vs. 21.3%) and disseminated intravascular coagulation (DIC) incidence (56.3% vs. 29.1%) than the non-SIC group. LASSO regression identified lactate, coagulation index, creatinine, and SIC scores as predictors of pre-SIC. The nomogram model demonstrated good calibration, with an AUC of 0.766 in the development cohort and 0.776 in the validation cohort. DCA confirmed the model's clinical utility.</p><p><strong>Conclusion: </strong>SIC is associated with increased mortality, with pre-SIC further increasing the risk of death. The nomogram-based prediction model provides a reliable tool for early SIC identification, potentially improving sepsis management and outcomes.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances and Challenges in Adeno-Associated Virus Gene Therapy Applications of Localized Delivery Strategies.","authors":"Jin-Hao Chen, Li-Jun Zhan, Cun-Ming Lv, Jun-Bo Teng, Chun-Yu Cao","doi":"10.1007/s11596-025-00084-6","DOIUrl":"https://doi.org/10.1007/s11596-025-00084-6","url":null,"abstract":"<p><p>In recent years, adeno-associated viruses (AAVs) have emerged as leading vectors in gene therapy, with several FDA-approved treatments and ongoing clinical trials demonstrating their effectiveness in treating inherited retinal diseases, hemophilia, and Duchenne muscular dystrophy, among others. However, AAV-based therapies still face challenges, including immune responses and side effects, due to high viral doses. To address these challenges, various strategies have been developed, such as creating new viral capsids, optimizing gene expression regulation, and improving delivery methods. Localized delivery is a promising direction, utilizing the tissue tropism of AAVs to reduce systemic side effects and lower the required viral dose, thus improving targeting and efficiency, especially for organs that are difficult to treat with conventional methods. These innovations have opened new pathways for the clinical application of AAVs. This review aims to provide a comprehensive summary of the various applications of AAVs, offer valuable insights for future research directions, and holds significant importance for researchers and clinicians in the field. As AAV therapy continues to evolve, this article emphasizes its transformative potential in treating genetic diseases, indicating the central role of AAV in the future of gene therapy.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NEP1-40 Regulates the Development of Hippocampal Neural Stem Cells in Schizophrenic Mice.","authors":"Yu Shao, Yan-Bo Liu, Dong-Kun Yu, Zhi-Lun Yang, Zi-Qi Feng, Xiao-Juan Mi, Juan Liu","doi":"10.1007/s11596-025-00078-4","DOIUrl":"https://doi.org/10.1007/s11596-025-00078-4","url":null,"abstract":"<p><strong>Objective: </strong>Schizophrenia is a complex neuropsychiatric disorder characterized by cognitive, affective, and behavioral abnormalities. Existing treatments have yielded limited effects on improving cognitive function. Recent studies have identified the abnormal differentiation of hippocampal neural stem cells (NSCs), neuronal loss, and dysregulated proliferation of astrocytes as significant pathological mechanisms contributing to the symptoms of schizophrenia. Impaired hippocampal neurogenesis may lead to emotional and cognitive deficits and biases in learning and memory, indicating that NSC differentiation is critical. NEP1-40, a Nogo-A receptor inhibitor, has shown promise for nerve protection and repair promotion. However, the effects of NEP1-40 on stem cell differentiation, the reduction in neuronal apoptosis, and the amelioration of schizophrenia-like behaviors have not been adequately investigated. This study examined the influence of NEP1-40 on NSC differentiation, hippocampal neuronal apoptosis, and proliferation in adolescent mice, along with its potential to enhance cognitive and behavioral outcomes in MK-801-induced schizophrenia mouse models.</p><p><strong>Methods: </strong>In in vivo experiments, a schizophrenia mouse model was successfully established. Subsequently, behavioral tests were conducted, followed by Western blotting (WB) and immunofluorescence (IF) analyses. In in vitro settings, NSCs were cultured and transfected. Flow cytometry, along with WB and IF assays, was employed to evaluate the effects of NEP1-40.</p><p><strong>Results: </strong>Schizophrenia-like behaviors in mice were significantly improved with the overexpression of NEP1-40. Compared with the model group, the NEP1-40 treatment group presented increased expression of a neuronal marker (Tuj1), reduced expression of an astroglial marker (GFAP), and decreased hippocampal neuronal apoptosis. NSC differentiation was assessed by quantifying the number of BrdU-positive cells coexpressing Tuj1 and GFAP in the hippocampal dentate gyrus. NEP1-40 treatment led to an increase in BrdU/Tuj1-positive cells and a reduction in BrdU/GFAP-positive cells. In cellular studies, NEP1-40 overexpression similarly increased the number of Tuj1-positive cells, reduced the number of GFAP-positive cells, decreased the degree of neuronal apoptosis, and promoted neuronal proliferation.</p><p><strong>Conclusion: </strong>These findings demonstrated the neurogenic effects of NEP1-40 on NSCs and their potential to mitigate schizophrenia-like behaviors in vivo.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expert Consensus on Clinical Application of Implantable Biventricular Assist Devices.","authors":"Nian-Guo Dong, David D'Alessandro, Jamshid Karimov, I-Wen Wang, Liang-Wan Chen, Ying-Bin Xiao, Chun-Sheng Wang, Qiang Zhao, Jia-Wei Shi, Shun-Zhou Yu, Cheng Zhou, Pascal Leprince, Minoru Ono, Jan Schmitto, Ming Gong, Yong-Feng Shao, Xian-Qiang Wang, Xing Hao, Xiao-Tong Hou, Xin Li, Wei Wang, Ting Wu, Hai-Tao Zhang, Cheng-Bin Zhou, Ping Li, Yin Wang, Yi-Xuan Wang, Jing Zhang","doi":"10.1007/s11596-025-00087-3","DOIUrl":"https://doi.org/10.1007/s11596-025-00087-3","url":null,"abstract":"<p><p>While biventricular assist devices (BiVADs) remain underutilized in Western countries for biventricular heart failure (BHF), their application is expanding in China. This consensus synthesizes international guidelines, medical evidence, and Chinese clinical expertise to establish standardized protocols for BiVAD management. Key recommendations include: (1) Preoperative right heart catheterization and echocardiography for central venous pressure (CVP): pulmonary capillary wedge pressure (PCWP) ratio and pulmonary artery pulsatility index (PAPi) assessment (Class I); (2) BiVAD indication in refractory BHF or high-risk right heart failure post-left ventricular assist device (LVAD) implantation (Class IIa); (3) Right atrial implantation as the preferred surgical approach (Class IIa); (4) Warfarin-based anticoagulation (INR 2.0-2.5) with aspirin, avoiding direct oral anticoagulants (DOACs) (Class III). The guidance addresses critical gaps in patient selection, pump speed titration, and complication management, positioning integrated BiVAD systems as a promising solution for complex BHF.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-146a Regulates Neuroinflammation and Immune Cell Function in Neurodegenerative Diseases.","authors":"Jia-Rui Xiong, Zi-Yi Yan, Meng-Qiong Shi, Gang Zhou, Ji-Hong Zhang, Jie Xu, Yong Liao, Hai-Ming Tang","doi":"10.1007/s11596-025-00080-w","DOIUrl":"https://doi.org/10.1007/s11596-025-00080-w","url":null,"abstract":"<p><p>Neurodegenerative diseases (NDDs) are characterized primarily by progressive impairments in cognition, behavior, and memory. MicroRNAs (miRNAs) are abundantly expressed in the central nervous system and are vital for the normal function and survival of neurons. Mature miRNAs are naturally occurring small noncoding single-stranded RNA molecules that are approximately 21-25 nucleotides in length. They regulate gene expression by pairing with target mRNAs and undergo significant alterations in various physiological and pathological processes. miR-146a, a miRNA dependent on nuclear factor κB (NF-κB), is highly expressed in neurons and functions as an anti-inflammatory miRNA via the Toll-like receptor (TLR) pathway, which is an essential regulatory factor for neuroinflammation expression during the development of NDDs. In this review, we summarize and emphasize the pivotal role of miR-146a in NDDs, highlighting the association between miR-146a polymorphisms and the risk of NDDs. We also discuss how alterations in miR-146a expression levels represent a critical event in the pathogenesis of numerous NDDs. Furthermore, the target genes of miR-146a are involved in regulating the pathophysiological processes of these diseases, particularly in the context of neuroinflammatory responses. In conclusion, miR-146a plays a central role in the progression of NDDs, with its primary function in neuroinflammation. These findings suggest that miR-146a holds promise as both a biomarker and a potential therapeutic target. A deeper understanding of how miR-146a influences neuroinflammatory responses across different types of neurological damage, cell types, and even various stages of certain NDDs will pave the way for its use as a therapeutic target in treating these conditions. Therefore, this article reviews the mechanism of miR-146a in NDDs and discusses the future therapeutic prospects for this type of disease. miR-146a regulates the related genes of the inflammatory signaling pathway and its influence on the development of NDDs. (Created in https://BioRender.com ).</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interplay Between Vestibular Dysfunction and Sleep Disorders.","authors":"Xi-Xi Yu, E Tian, Jun Wang, Ouk Synadet, Zhao-Qi Guo, Jing-Yu Chen, Jia-Qi Guo, Zhang-Hong Zhou, Shi-Yu Shi, Hua-Jing Yang, Yi-Sheng Lu, Su-Lin Zhang","doi":"10.1007/s11596-025-00085-5","DOIUrl":"https://doi.org/10.1007/s11596-025-00085-5","url":null,"abstract":"<p><p>Recent years have seen a burgeoning interest in elucidating the intricate relationship between vestibular dysfunction and sleep disorders, owing to their substantial impact on daily functioning and overall health. Despite significant advancements, the precise mechanisms underpinning this interplay remain elusive. This review aims to synthesize the current literature on the association between vestibular dysfunction and sleep disorders, focusing on potential causal mechanisms and therapeutic implications. We systematically examine various sleep disorders, including insomnia, circadian rhythm disorders, and sleep apnea, in association with specific vestibular dysfunctions, such as Meniere's disease (MD), vestibular migraine (VM), benign paroxysmal positional vertigo (BPPV), vestibular neuritis (VN), and persistent postural perceptual dizziness (PPPD). By exploring these complex interactions, our goal is to provide a comprehensive understanding that contributes to the ongoing discourse in this field. We seek to encourage further investigations into innovative diagnostic and therapeutic strategies, ultimately aiming to improve the clinical management and enhance the quality of life for patients affected by both vestibular dysfunction and sleep disorders.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144574992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dapagliflozin Suppressed Cuproptosis and Myocardial Fibrosis in Myocardial Infarction Through HIF-1α/TGF-β Pathway.","authors":"Yu-Ze Zhang, Ting-Ting Lin, Shu-Min Fan, Yan-Qing Wu","doi":"10.1007/s11596-025-00076-6","DOIUrl":"https://doi.org/10.1007/s11596-025-00076-6","url":null,"abstract":"<p><strong>Background: </strong>Myocardial infarction (MI) and postmyocardial remodeling are the most common causes of heart failure worldwide and seriously affect the quality of life and prognosis of patients. Dapagliflozin, a sodium glucose cotransporter 2 (SGLT2) inhibitor, is a novel class of hypoglycemic drug that has been proven to have cardiovascular protective effects. However, the underlying mechanisms by which dapagliflozin affects MI have yet to be elucidated.</p><p><strong>Methods: </strong>An MI mouse model was created by ligating the left anterior descending branch of the coronary artery. Hematoxylin‒eosin (HE) and Masson's trichrome (Masson) staining were used to assess myocardial damage. The levels of fibrosis-related and cuproptosis-related markers were assessed via Western blot analysis. A hypoxia-induced cardiomyocyte fibrosis model was constructed in vitro. The DCFH-DA probe was used to measure the levels of reactive oxygen species (ROS), and flow cytometry was used to identify cell apoptosis.</p><p><strong>Results: </strong>Dapagliflozin improved heart function, ameliorated fibrosis in the myocardium, and alleviated myocardial injury. Moreover, dapagliflozin reduced the copper ion concentration and ROS accumulation and inhibited the expression of cuproptosis-related markers. Dapagliflozin suppressed the expression of HIF-1α/TGF-β signal and the overexpression of HIF-1α effectively reversed the dapagliflozin-mediated myocardial protective effects.</p><p><strong>Conclusion: </strong>Dapagliflozin reduced myocardial fibrosis by suppressing HIF-1α/TGF-β-mediated cuproptosis.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144574991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Key Transcription Factors: Avenue for Treating Alcoholic Liver Disease.","authors":"Min Guo, Jian-Nan Cao, Xiao-Dong Li, Ling Jin","doi":"10.1007/s11596-025-00079-3","DOIUrl":"https://doi.org/10.1007/s11596-025-00079-3","url":null,"abstract":"<p><p>Alcoholic liver disease (ALD), which includes a range of diseases, ranging from alcoholic steatosis, hepatitis, and fibrosis to cirrhosis and hepatocarcinoma, is a process of epigenetic remodeling involving multiple genes and metabolic pathways. ALD is involved in various transcriptional regulatory mechanisms, including lipid metabolism disorders, inflammatory responses, autophagy, fibrogenesis, oxidative stress, fatty acid metabolism, iron metabolism, and endoplasmic reticulum stress. In the occurrence of ALD and its response to the microenvironment, various transcription factors (TFs) play important roles. Targeted therapy involving these TFs may pave a novel avenue for the treatment of ALD. Here, we summarize the molecular characteristics of TFs and their involvement in the biological and pathological processes of ALD. We further discuss the current pharmaceutical treatments targeting these TFs and their mediators. This study provides detailed and accurate regulation maps of TFs for the targeted therapy of ALD.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144574993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of the Subnucleus Reticularis Dorsalis (SRD) in Pain Modulation: A Literature Review.","authors":"Zi-Yan Zhang, Jia-le Mei, Yi-Qing Rao, Ke-Xing Wan, Jia-Jia Huang, Ling-Ling Yu, Xiang-Hong Jing, Man Li, Zheng-Tao Lv","doi":"10.1007/s11596-025-00082-8","DOIUrl":"https://doi.org/10.1007/s11596-025-00082-8","url":null,"abstract":"<p><p>The subnucleus reticularis dorsalis (SRD), also known as the dorsal reticular nucleus (DRt) or dorsal medullary reticular nucleus (MdD), which resides at the caudal end of the medulla, plays a pivotal role in regulating pain perception. Despite extensive research efforts to unravel its mechanisms, the operational intricacies of SRD remain poorly understood. Advances in experimental methodologies such as brain imaging and chemogenetics have facilitated deeper investigations into the involvement of SRD in various pain disorders. This comprehensive review aims to analyze 36 years (1989-2024) of preclinical research highlighting the critical role of SRD in diffuse noxious inhibitory control (DNIC), also known as conditioned pain modulation (CPM) in humans, and its interconnected neural circuits. Moreover, this review explores the neural circuits related to SRD, including locus coeruleus (LC)-SRD, parabrachial nucleus (PBN)-SRD, rostroventromedial medulla (RVM)-ventrolateral medulla (VLM)-SRD, anterior cingulate cortex (ACC)-SRD, medial medullary reticular formation (mMRF)-SRD, and dorsal striatum (DS)-SRD. Their activation also plays a significant role in analgesia. The pivotal roles of neurotransmitters such as μ-opioid receptor (MOR), noradrenaline, and metabotropic glutamate receptor 7 (mGluR7) in modulating SRD responsiveness to pain stimuli are also discussed, as are the influences of SRD on different pain types. This review identified promising avenues for innovative analgesic treatments by shedding light on potential therapeutic strategies targeting SRD.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144574994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of ZWINT Expression with Clinicopathologic Characteristics and Prognosis in Breast Cancer Patients.","authors":"Bei Liu, Qin Wang, Xiao-Hong Min, Han-Han Liu, Huan Wu, Hui Xu, Jun-Bo Hu, Yong-Qing Tong, Zi-Ming Huang","doi":"10.1007/s11596-025-00081-9","DOIUrl":"https://doi.org/10.1007/s11596-025-00081-9","url":null,"abstract":"<p><strong>Objective: </strong>ZW10 interacting kinetochore protein (ZWINT) has been demonstrated to play a pivotal role in the growth, invasion, and migration of cancers. Nevertheless, whether the expression levels of ZWINT are significantly correlated with clinicopathological characteristics and prognostic outcomes of patients with breast cancer remains elusive. This study systematically investigated the clinical significance of ZWINT expression in breast cancer through integrated molecular subtyping and survival analysis.</p><p><strong>Methods: </strong>We systematically characterized the spatial expression pattern of ZWINT across various breast cancer subtypes and assessed its prognostic significance using an integrated bioinformatics approach that involved multi-omics analysis. The approach included the Breast Cancer Gene-Expression Miner v5.1 (bc-GenExMiner v5.1), TNMplot, MuTarget, PrognoScan database, and Database for Annotation, Visualization, and Integrated Discovery (DAVID).</p><p><strong>Results: </strong>Our analysis revealed consistent upregulation of ZWINT mRNA and protein expression across distinct clinicopathological subtypes of breast cancer. ZWINT overexpression demonstrated significant co-occurrence with truncating mutations in cadherin 1 (CDH1) and tumor protein p53 (TP53), suggesting potential functional crosstalk in tumor progression pathways. The overexpression of ZWINT correlated with adverse clinical outcomes, showing 48% increased mortality risk (overall survival: HR 1.48, 95% CI 1.23-1.79), 66% higher recurrence probability (relapse-free survival: 1.66, 95% CI 1.50-1.84), and 63% elevated metastasis risk (distant metastasis-free survival: HR 1.63, 95% CI 1.39-1.90). Multivariate Cox regression incorporating TNM staging and molecular subtypes confirmed ZWINT as an independent prognostic determinant (P < 0.001, Harrell's C-index = 0.7827), which was validated through bootstrap resampling (1000 iterations).</p><p><strong>Conclusion: </strong>ZWINT may serve as a potential biomarker for prognosis and a possible therapeutic target alongside TP53/CDH1 in breast cancer.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}