Biomolecules & biomedicine最新文献

{"title":"Retraction: Tocilizumab inhibits neuronal cell apoptosis and activates STAT3 in cerebral infarction rat model.","authors":"Shaojun Wang, Jun Zhou, Weijie Kang, Zhaoni Dong, Hezuo Wang","doi":"10.17305/bb.2025.12568","DOIUrl":"10.17305/bb.2025.12568","url":null,"abstract":"<p><p>Retracted article: https://www.bjbms.org/ojs/index.php/bjbms/article/view/853 Following publication, concerns were raised by readers and the public regarding the integrity of the data presented in two figures of this article: Figure 2B: An unexpected overlap was found between an image presented in this study and figures published in other articles. Figure 4: An unexpected overlap was detected within the Western blot panels, suggesting potential duplication or manipulation. The editorial office contacted all authors on 13 January 2025 and 30 January 2025 to clarify these concerns. On 4 March 2025, the corresponding author was specifically approached through both the e-mail address provided upon article submission and an institutional e-mail located online. However, no response or explanation was ever received. Following our journal's policies and guidelines from the Committee on Publication Ethics (COPE), the editors have decided to retract the article from publication due to serious concerns about the reliability and originality of the data. This retraction is intended to maintain the integrity of the scientific record. We apologize to the readership for any inconvenience caused. We thank the individuals who brought these concerns to our attention. The Editor-in-Chief has approved this retraction note.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1897"},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447746/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144043823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TCF12 enhances angiogenesis and affects sorafenib response in liver cancer via HIF-1α interaction.","authors":"Yuanbin Chen, Xiaolong Wang, Jin Chen, Min Dai, Xinyue Zhang, Jie Yin, Xiao He","doi":"10.17305/bb.2025.12022","DOIUrl":"10.17305/bb.2025.12022","url":null,"abstract":"<p><p>Transcription factor 12 (TCF12), a member of the basic Helix-Loop-Helix (bHLH) protein family, plays a crucial role in regulating cell growth and differentiation. It has been implicated in the development and progression of malignant tumors; however, its specific mechanisms in vascularization and drug resistance in liver cancer remain poorly understood. This study aims to explore how the interaction between TCF12 and Hypoxia-Inducible Factor 1-alpha (HIF-1α) affects vascularization and drug sensitivity in liver cancer. Using bioinformatics analysis (n = 374 TCGA samples and n = 50 clinical specimens), we assessed TCF12 expression levels in liver cancer and evaluated their association with patient prognosis. Gene Set Enrichment Analysis (GSEA) was employed to identify related signaling pathways. The expression of TCF12 in liver cancer tissues was examined via Western blotting and immunohistochemistry, while Kaplan-Meier survival analysis was used to analyze the relationship between TCF12 expression and overall survival. Functional assays-including scratch wound repair, tube formation, and endothelial cell permeability tests-were conducted to assess TCF12's role in angiogenesis. Cell viability assays were performed to evaluate the impact of TCF12 on sorafenib sensitivity, and co-immunoprecipitation experiments were carried out to investigate the interaction between TCF12 and HIF-1α. Our bioinformatics analysis revealed that both TCF12 and HIF-1α are significantly overexpressed in liver cancer and are associated with poor prognosis. Immunohistochemical staining showed a positive correlation between TCF12 expression and the vascularization marker CD31. Furthermore, survival analysis demonstrated that patients with elevated TCF12 expression had significantly shorter overall survival. Functional assays indicated that TCF12 knockdown suppressed blood vessel formation and reduced endothelial cell permeability. Moreover, reducing TCF12 expression increased the sensitivity of liver cancer cells to sorafenib. Notably, overexpression of HIF-1α reversed these effects, and co-immunoprecipitation experiments confirmed a direct interaction between TCF12 and HIF-1α. In summary, this study demonstrates that TCF12 is highly expressed in liver cancer and is associated with poor prognosis. TCF12 promotes angiogenesis by stabilizing HIF-1α and modulates tumor sensitivity to sorafenib, highlighting its potential as a therapeutic target in liver cancer.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1868-1881"},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447747/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143797338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The influence of sodium-glucose co-transporter-2 inhibitors on the risk of cancer therapy-related cardiac dysfunction: A meta-analysis.","authors":"Zhitao Yan, Xiaona Xing, Jinmei Huang","doi":"10.17305/bb.2025.11847","DOIUrl":"10.17305/bb.2025.11847","url":null,"abstract":"<p><p>Cancer therapy-related cardiac dysfunction (CTRCD) is a major concern for patients undergoing cardiotoxic cancer treatments. Sodium-glucose co-transporter-2 (SGLT2) inhibitors have shown cardioprotective effects in both diabetic and non-diabetic populations. However, their impact on CTRCD risk remains uncertain. This meta-analysis aimed to assess the association between SGLT2 inhibitor use and CTRCD in cancer patients receiving cardiotoxic treatments. A systematic search of PubMed, Embase, and Web of Science was conducted to identify relevant studies. Cohort studies comparing CTRCD incidence in cancer patients with and without SGLT2 inhibitor use were included. Risk ratios (RRs) were pooled using a random-effects model, and subgroup and meta-regression analyses were performed to explore potential effect modifiers. Ten cohort studies involving 34,847 cancer patients met the inclusion criteria. Overall, SGLT2 inhibitor use was associated with a significantly reduced risk of CTRCD (RR: 0.47, 95% confidence interval: 0.33-0.68, P < 0.001), though significant heterogeneity was observed (I² = 70%). Subgroup analysis indicated a stronger protective effect in patients receiving anthracyclines (RR: 0.26) compared to those undergoing other treatments (RR: 0.73, P for subgroup difference = 0.001). Additionally, the cardioprotective effect was more pronounced in cohorts with a lower proportion of men (<55%, RR: 0.27) compared to those with a higher proportion (≥55%, RR: 0.75, P < 0.001). Sensitivity analyses, conducted by excluding one study at a time, consistently supported these findings, reinforcing their robustness. In conclusion, SGLT2 inhibitor use is associated with a lower risk of CTRCD in cancer patients, particularly those receiving anthracyclines. These findings highlight the potential role of SGLT2 inhibitors in mitigating cardiotoxicity during cancer therapy.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1723-1736"},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447736/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143617681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction:  LKB1 suppression promotes cardiomyocyte regeneration via LKB1-AMPK-YAP axis.","authors":"Shuang Qu, Qiao Liao, Cheng Yu, Yue Chen, Han Luo, Xuewei Xia, Duofen He, Zaicheng Xu, Pedro A Jose, Zhuxin Li, Wei Eric Wang, Qing Rex Lyu, Chunyu Zeng","doi":"10.17305/bb.2025.12567","DOIUrl":"10.17305/bb.2025.12567","url":null,"abstract":"<p><p>Corrected article: https://www.bjbms.org/ojs/index.php/bjbms/article/view/7225 In the published article [Qu S, et al. LKB1 suppression promotes cardiomyocyte regeneration via LKB1-AMPK-YAP axis. Bosn J Basic Med Sci. 2022; DOI: 10.17305/bjbms.2021.7225], an error was identified in Figure 4D1. Specifically, the immunofluorescence image originally belonging to the \"vector\" group was mistakenly used for the \"LKB1 OE\" group during figure preparation. This was an inadvertent error in image placement. The corrected version of Figure 4 is shown below. This correction does not affect the statistical analysis, interpretation, or the overall conclusions of the study.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1895"},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144043197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adefovir anticancer potential: Network pharmacology, anti-proliferative and apoptotic effects in HeLa cells.","authors":"Muzammal Mateen Azhar, Tahir Maqbool, Fatima Ali, Awais Altaf, Muhammad Atif, Zulfiqar Ali, Zahid Habib Qureshi, Muhammad Naveed, Tariq Aziz, Rania Ali El Hadi Mohamed, Fakhria A Al-Joufi, Maher S Alwethaynani","doi":"10.17305/bb.2025.12058","DOIUrl":"10.17305/bb.2025.12058","url":null,"abstract":"<p><p>Cervical cancer presents a significant healthcare challenge due to recurrent disease and drug resistance, highlighting the urgent need for novel therapeutic strategies. Network pharmacology facilitates drug repurposing by elucidating multi-target mechanisms of action. Adefovir, an acyclic nucleotide analog, has shown promising potential in cervical cancer treatment, particularly in HeLa cells. In vitro studies have demonstrated that adefovir inhibits HeLa cell proliferation by enhancing apoptosis while maintaining a low cytotoxicity profile at therapeutic concentrations, making it an attractive candidate for further exploration. A combined network pharmacology and in vitro study was conducted to investigate the molecular mechanism of adefovir against cervical cancer. Potential gene targets for adefovir and cervical cancer were predicted using database analysis. Hub targets were identified, and protein-protein interaction (PPI) networks were constructed. Molecular docking assessed adefovir's binding affinity to key targets. In vitro cytotoxic assays, including 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and crystal violet assays, were performed using 96-well plates to evaluate anti-proliferative effects in HeLa cells. Apoptosis was assessed via p53 immunocytochemistry Enzyme-Linked Immunosorbent Assay (ELISA), while Vascular Endothelial Growth Factor ELISA (VEGF ELISA) was used to measure cell proliferation. Venn analysis identified 144 common targets between adefovir and cervical cancer. Network analysis revealed key hub targets involved in oncogenic pathways. Molecular docking demonstrated strong binding between adefovir and Mitogen-Activated Protein Kinase 3 (MAPK3) and SRC proteins. In vitro, adefovir significantly suppressed HeLa cell viability, with an Inhibitory Concentration 50 (IC50) of 7.8 µM, outperforming 5-Fluorouracil (5-FU). Additionally, it induced apoptosis via p53 activation and inhibited cell proliferation through VEGF suppression. These integrated computational and experimental findings suggest that adefovir exerts multi-targeted effects against cervical cancer. Its promising preclinical efficacy warrants further investigation as a potential alternative therapy.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1751-1764"},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143659794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-omics reveals that ST6GAL1 promotes colorectal cancer progression through LGALS3BP sialylation.","authors":"Yuanchao Shi, Zhenzhong Pan, Jingwei Duan, Zexing Wang, Yiliang Fang, Bo Tang, Quanlin Guan","doi":"10.17305/bb.2025.11663","DOIUrl":"10.17305/bb.2025.11663","url":null,"abstract":"<p><p>ST6 β-galactoside α2,6-sialyltransferase 1 (ST6GAL1), a crucial enzyme for tumor-associated sialic acid modification, has been reported to positively correlate with colorectal cancer (CRC) tumorigenesis; however, the underlying mechanism remains unclear. To elucidate the protumor mechanisms of ST6GAL1, we performed transcriptomic and N-glycoproteomic analyses and in vitro assays. We found that ST6GAL1 was significantly upregulated in tumor samples than in matched normal samples by analyzing fresh clinical samples from public databases (mean mRNA expression level: tumor vs. normal samples = 0.002712:0.000966, P < 0.05, n = 22). The in vitro results revealed that ST6GAL1 overexpression promoted CRC cell proliferation, migration, and chemoresistance, which were significantly blocked by its knockdown. Transcriptomic data showed that many genes related to the four modules (proliferation/cell cycle, migration, motility, and epithelial-mesenchymal transition (EMT) were upregulated after ST6GAL1 overexpression but downregulated after ST6GAL1 knockdown. Furthermore, the N-glycoproteomic data revealed that 25 substrates that were sialylated upon ST6GAL1 overexpression were related to protumor activity. Importantly, we found that knockdown of lectin galactoside-binding soluble 3-binding protein (LGALS3BP), a newly identified secreted substrate of ST6GAL1, significantly blocked the proliferation, invasion, and chemoresistance of CRC cells induced by ST6GAL1 overexpression. Treatment with sialidases (neuraminidases, NAs) also blocked the protumor activity of ST6GAL1. Thus, ST6GAL1-induced increased sialylation of substrates, such as LGALS3BP and upregulation of protumor genes promote CRC tumorigenesis and chemoresistance, which provides important perspectives and new targets for the treatment of CRC.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1853-1867"},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447743/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143400809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumor hypoxia: Classification, detection, and its critical role in cancer progression.","authors":"Yan Zhao, Bing Zhong, Jing-Yi Cao, Qian Wang, Jie Liang, Ke Lu, Sheng-Ming Lu","doi":"10.17305/bb.2025.12318","DOIUrl":"10.17305/bb.2025.12318","url":null,"abstract":"<p><p>Hypoxia is a common feature of solid tumors and plays a critical role in cancer progression. A thorough understanding of tumor hypoxia is essential for gaining deeper insights into various aspects of cancer biology. This review examines the key factors contributing to tumor hypoxia, such as inadequate blood supply and oxygen delivery resulting from rapid tumor growth. We present a detailed classification of hypoxic regions and provide an overview of current methods used to identify these areas-from molecular techniques to imaging approaches-offering a comprehensive and multifaceted perspective. Additionally, we explore the mechanisms by which hypoxia drives tumor progression. Under low-oxygen conditions, tumor cells can alter their biological behavior, influencing processes such as cell proliferation, immune evasion, and the maintenance of tumor stem cells. By addressing these dimensions, we aim to enhance understanding of how hypoxia contributes to cancer development. Through this in-depth exploration, we hope this review will offer valuable insights to guide future research and clinical applications.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1672-1690"},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447734/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144043202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Passenger lymphocyte syndrome - Epidemiology, pathogenesis, diagnosis, treatment and future directions: A review.","authors":"Yingfang Pan, Aiping Zhao, Xiujiao Jiang, Na Zhou, Jing Wang, Changkui Sun, Fang Zhou","doi":"10.17305/bb.2025.12548","DOIUrl":"10.17305/bb.2025.12548","url":null,"abstract":"<p><p>Passenger lymphocyte syndrome (PLS) is a hematological complication that can occur following transplantation, characterized by donor-derived memory B lymphocytes producing antibodies against the recipient's blood cells. This review examines the pathophysiology, diagnostic approaches, and treatment strategies aimed at enhancing clinical management and standardizing therapeutic protocols for PLS. A literature search was conducted using Web of Science and PubMed to identify relevant publications on PLS, resulting in 79 studies. Studies were selected based on predefined criteria, including a focus on human donor-derived alloimmunity, documented blood group antigen-antibody interactions, transplantation context, clinical data on outcomes or management, and methodological validity. Only studies containing actual patient data and substantive discussions about PLS were included. PLS commonly presents as hemolytic anemia, accompanied by elevated lactate dehydrogenase (LDH) levels, indirect hyperbilirubinemia, and reduced haptoglobin levels. Diagnosis is primarily based on clinical manifestations and laboratory tests, including the direct antiglobulin test (DAT) and antibody screening. Differential diagnosis is crucial for excluding drug-induced hemolytic anemia and thrombotic microangiopathy. Current treatment strategies for PLS focus on halting hemolysis and restoring hematological balance. First-line treatment includes donor-compatible red blood cell transfusions and high-dose corticosteroids, while refractory cases may necessitate rituximab or plasmapheresis. Despite advancements in PLS management, challenges persist, including delayed diagnosis due to self-limiting cases and a lack of standardized treatment protocols. Future research should incorporate genomic and proteomic biomarkers for accurate diagnosis and risk prediction. Developing mechanism-driven therapies targeting donor lymphocytes and establishing global consensus frameworks can enhance monitoring, improve graft survival, and optimize transplant recipient outcomes.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"215-226"},"PeriodicalIF":0.0,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12505524/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144755182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diabetes-induced redistribution of mast cells to the adventitia in ascending aortic aneurysms.","authors":"Aleš Pleskovič, Ruda Zorc-Pleskovič, Marjeta Zorc, Aleksandra Milutinović","doi":"10.17305/bb.2025.12772","DOIUrl":"10.17305/bb.2025.12772","url":null,"abstract":"<p><p>Mast cells (MCs) are inflammatory cells that reside mainly in the intima of healthy and early- atherosclerotic abdominal aortas but migrate to the adventitia in advanced atherosclerosis and abdominal aortic aneurysms. We compared MC infiltration in the intima, media, and adventitia of ascending aortic aneurysms from patients with diabetes mellitus (DM) or arterial hypertension (AH). Fifty-one patients (36-81 years) undergoing surgical repair were enrolled and allocated to a DM group without AH (n = 9) or an AH group without DM (n = 42). Aortic specimens were stained with hematoxylin-eosin and immunohistochemically labeled with anti-CD117 to detect MCs and anti-vWF to visualize blood vessels. Compared with the AH group, the DM group had fewer MCs in the intima and more in the adventitia (Mann-Whitney test, p < 0.05). In both groups, intact MCs outnumbered degranulated MCs in the adventitia, whereas no such difference was observed in the intima or media (p < 0.05). Medial vascular density did not differ between groups (p < 0.05). In the AH group, medial vascularization correlated positively with intact, degranulated, and total MC counts, whereas in the DM group it correlated only with degranulated MCs (Spearman, p < 0.05). These findings suggest that DM-associated aneurysms exhibit a distinct MC distribution and vascular response, indicating a pathogenesis that differs from that of AH-associated aneurysms.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"2827-2834"},"PeriodicalIF":0.0,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12461267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144746314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of serum Netrin-1, NSE, and S100β with brain injury severity and prognosis in patients with sepsis-associated encephalopathy.","authors":"Bo Zhang, Qiong Wu, Jing Wu","doi":"10.17305/bb.2025.12215","DOIUrl":"10.17305/bb.2025.12215","url":null,"abstract":"<p><p>Sepsis-associated encephalopathy (SAE) represents the most prevalent neurological complication of sepsis and is frequently linked to unfavorable patient outcomes. This study aimed to evaluate the prognostic significance of serum Netrin-1, neuron-specific enolase (NSE), and S100β levels in patients diagnosed with SAE. A retrospective analysis was performed on 120 SAE patients, measuring serum levels of Netrin-1, NSE, and S100β and correlating these with Acute Physiology and Chronic Health Evaluation II (APACHE-II) scores. Independent risk factors for short-term mortality were identified, and the predictive values of these biomarkers were assessed both individually and in combination. Kaplan-Meier analysis was utilized to compare short-term mortality based on biomarker levels. Netrin-1 was found to be significantly downregulated, while NSE and S100β levels were upregulated in SAE patients. Lower levels of Netrin-1, alongside higher levels of NSE and S100β, correlated with elevated APACHE-II scores and increased short-term mortality. Multivariate analysis confirmed that all three biomarkers serve as independent predictors of short-term mortality. The combined assessment of Netrin-1, NSE, and S100β demonstrated superior prognostic value compared to individual biomarker. Therefore, serum levels of Netrin-1, NSE, and S100β are closely associated with the severity of brain injury in SAE and serve as effective predictors of short-term mortality, enhancing prognostic accuracy in clinical practice.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"2755-2765"},"PeriodicalIF":0.0,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12461284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144719230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}