{"title":"Immune Dysregulation and Hub Gene Identification in Non-Pulmonary Sepsis-Induced Acute Lung Injury: Insights from Transcriptomic and Experimental Analyses.","authors":"Chen Yan, Wen Li, Yang-Ming Cai, Wei-Yi Cai, Nian-Dan Hu, Yang-Yi-Yan Song, Wen-Qiang Li, Zhou Sun, Qing Geng","doi":"10.1007/s11596-025-00083-7","DOIUrl":"https://doi.org/10.1007/s11596-025-00083-7","url":null,"abstract":"<p><strong>Objective: </strong>Sepsis-induced acute lung injury (ALI) poses a critical challenge in critical care, yet its immunoregulatory mechanisms remain poorly defined. This study aimed to delineate immune dysregulation networks and identify therapeutic targets through multiomics data integration.</p><p><strong>Methods: </strong>Transcriptomic datasets (GSE40180 and GSE165226) were analyzed through a multiphase bioinformatics workflow, including gene set enrichment analysis (GSEA), immune cell deconvolution (CIBERSORT), differential gene expression profiling (|log2FC|> 1.5, P.adj < 0.05), and pathway annotation (GO/KEGG). Protein-protein interaction (PPI) networks were constructed to identify hub genes. Experimental validation was done using a murine cecal ligation and puncture (CLP) model with histopathological lung injury scoring and RT-qPCR-based hub gene verification.</p><p><strong>Results: </strong>Integrated analysis revealed 26 consensus biological processes (24 upregulated, 2 downregulated) dominated by innate immune activation. CIBERSORT revealed significant infiltration of M1 macrophages, neutrophils, activated dendritic cells (DCs), and activated natural killer (NK) cells in septic lungs, which was concurrent with Th17/naive CD8+ T-cell dysregulation. Among the 58 differentially expressed genes (DEG), 7 hub genes (Cxcl1, Cxcl2, Ccl3, Cd14, Saa3, Timp1, and Socs3) were significantly correlated with immune cell dynamics. CLP modeling confirmed severe alveolar damage (lung injury score: 8.11 ± 1.17 vs. 1.97 ± 0.29; P < 0.0001) and upregulated hub gene expression (all P < 0.01) in septic lungs, with hub gene expression levels strongly correlated with the lung injury score (Pearson's r > 0.85, P < 0.001).</p><p><strong>Conclusion: </strong>Innate adaptive immune crosstalk, particularly dysregulated immune cell infiltration, drives sepsis-induced ALI pathogenesis. The 7 hub genes mechanistically connect immune dyshomeostasis to tissue injury, suggesting novel targets for precision immunomodulation and biomarker development in critical care.</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":"144539357","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":"Maternal Electronic Cigarette Exposure Induces Dysregulation of Autophagy via Oxidative Stress/DNA Methylation in Pulmonary Hypertension Offspring.","authors":"Ze-Wen Chen, Yi-Fan Li, Hai-Long Qiu, Wen Xie, Tian-Yu Chen, Yong Zhang, Ji-Mei Chen, Jian Zhuang, Shu-Sheng Wen","doi":"10.1007/s11596-025-00074-8","DOIUrl":"https://doi.org/10.1007/s11596-025-00074-8","url":null,"abstract":"<p><strong>Objective: </strong>Electronic cigarettes (ECs) differ from traditional tobacco smoke but may contribute to cardiopulmonary remodeling. Pulmonary hypertension (PH), characterized by pulmonary artery and right ventricle remodeling, poses a significant risk of mortality in infants, children, and adolescents. However, the impact of maternal EC exposure on PH development in offspring remains unclear. To address this, we established a PH rat model with maternal EC exposure.</p><p><strong>Methods: </strong>Maternal EC exposure was initiated on gestation day 12 via electronic nicotine delivery systems. Offspring were administered monocrotaline (MCT) at 6 weeks of age (6-wo) to induce PH. Mechanistic experiments were conducted at 10-week-old (10-wo). Protein expression of NADPH oxidases, DNA methyltransferases, and autophagy-related markers was analyzed by Western blot. Morphological changes and the severity of PH were evaluated via hematoxylin and eosin (HE) staining and echocardiography, respectively. Furthermore, the involvement of the oxidative stress/DNA methylation/autophagy axis in response to maternal EC exposure was confirmed through a combination of ELISA, Western blot, HE staining, and echocardiography. Additionally, ATG5 mRNA expression was measured by qRT-PCR.</p><p><strong>Results: </strong>Compared with control conditions, maternal EC exposure significantly worsened MCT-induced PH in male offspring. This was associated with increased oxidative stress, DNA hypomethylation, and anomalous autophagy in the offspring. In vivo treatment with chloroquine inhibited autophagy and ameliorated PH development in offspring exposed to maternal EC. Furthermore, N-acetylcysteine (NAC), an antioxidant, attenuated maternal EC exposure-induced oxidative stress, DNA hypomethylation, and excessive autophagy, thereby improving PH. DNA hypermethylation also reversed PH development, accompanied by reduced oxidative stress and suppressed autophagy. ATG5, a key regulator of autophagy, was identified as a potential therapeutic target, as its repression mitigated PH in maternal EC-exposed offspring.</p><p><strong>Conclusion: </strong>Maternal EC exposure induces oxidative stress and DNA hypomethylation in offspring, leading to anomalous autophagy and exacerbation of PH development. Targeting ATG5-mediated autophagy may represent a novel therapeutic approach for improving PH outcomes in offspring exposed to maternal EC.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144474182","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}
Dan Lv, Shi-Yao Chen, Xu-Fang Li, Praseth Leakana, Jia-Qi Han, Jun-Rong Xian, Fan-Fan Li, Meng-Zhou He, Yao Fan, He-Ze Xu, Li Liu, Wei Li, Xing-Guang Lin, Fang Ye, Dong-Rui Deng
{"title":"Long Sleep Duration Is Associated with Fetal Brain Parameter Extreme Values: A Prospective Cohort Study.","authors":"Dan Lv, Shi-Yao Chen, Xu-Fang Li, Praseth Leakana, Jia-Qi Han, Jun-Rong Xian, Fan-Fan Li, Meng-Zhou He, Yao Fan, He-Ze Xu, Li Liu, Wei Li, Xing-Guang Lin, Fang Ye, Dong-Rui Deng","doi":"10.1007/s11596-025-00073-9","DOIUrl":"https://doi.org/10.1007/s11596-025-00073-9","url":null,"abstract":"<p><strong>Objective: </strong>Sleep is fundamental to the physical and mental health of both the general population and pregnant women. Most studies have focused on the impact of certain trimester sleep behaviors on gestational complications and birth outcomes. This study aimed to explore the association between maternal sleep duration and fetal growth development from as early as 23 gestational weeks to birth.</p><p><strong>Methods: </strong>A total of 803 pregnant women were prospectively enrolled. The self-reported maternal nocturnal sleep duration during all 3 trimesters was recorded. The outcome measures were reference-population-based Z-scores of fetal biometric measurements obtained through routine ultrasonographic examination.</p><p><strong>Results: </strong>Using multiple linear regression, a marginally significant negative association was observed between second-trimester sleep duration and second-trimester fetal head circumference (HC) and third-trimester fetal biparietal diameter (BPD). Then the associations of long sleep duration in each trimester with fetal biometry extreme values were evaluated. A significant impact of second-trimester long sleep duration on the second-trimester BPD below the 10th percentile of the reference population was observed. Longitudinal analysis reported similar results for BPD and HC.</p><p><strong>Conclusions: </strong>Overall, a negative association between sleep duration and fetal biometric measurements was observed. Long sleep durations in the second trimester might negatively impact fetal growth, particularly brain parameters, including BPD and HC.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144474181","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":"Genotype Identification of Complete Hydatidiform Moles without a Maternal Component: Attempts at a Novel 26-plex STR System.","authors":"Yi-Na Jiang, Lu-Yao Li, Peng-Fei Nan, Fu-Quan Jia, Li-Qin Chen","doi":"10.1007/s11596-025-00071-x","DOIUrl":"https://doi.org/10.1007/s11596-025-00071-x","url":null,"abstract":"<p><strong>Objective: </strong>Current autosomal short tandem repeat (STR) assays can analyze the zygotic composition by comparing the allelic genes at each locus of complete hydatidiform moles (CHM), with a maternal genotype serving as an essential reference for comparative analysis. However, their application in pathology represents a challenge because of deficiency or contamination of maternal-origin tissues. This study aimed to develop a novel STR genotyping method for identifying CHM genotypes without a maternal component.</p><p><strong>Methods: </strong>Samples with the pathologic description of molar pregnancy were collected. Routine hematoxylin-eosin (HE) staining and p57 immunohistochemistry staining were conducted in accordance with standard guidelines. A novel 26-plex system was explored to classify CHM and diploid pregnancies. The system combined 22 STRs on chromosomes 21/18/13/X, 3 sex loci, and 1 quality control marker (TAF9L), enabling molecular diagnosis in the absence of maternal tissue. At last, traditional DNA typing based on villi and decidua (maternal component) of each case was used for result consistency analysis.</p><p><strong>Results: </strong>CHM and nonmolar abortus could not be distinguished by the basic HE staining with no fetal evidence or other prominent features. DNA typing was successfully processed for all cases according to the novel 26-plex and traditional system. CHM (46XX) diagnosis required single A-STR/X-STR peaks and absent Y-chromosome markers, excluding chromosomal abnormalities via TAF9L analysis. When the villous tissue analysis revealed single peaks at X-STR/SRY loci, a 1:1 amelogenin ratio, and a 2:1 TAF9L peak ratio, these results overlapped with those of 46XY hydropic abortus or CHM. Notably, p57 immunohistochemical staining resolved the ambiguity. Consistency with traditional DNA genotyping confirmed system accuracy. This multiplex assay enhanced reliability in mole diagnosis, supporting clinical differentiation and genetic counseling.</p><p><strong>Conclusion: </strong>This study presents a rapid and cost-effective assay for the genotypic identification of CHM without the need for a maternal component. The method combined the characteristics of STR loci distributed across different chromosomes and developed the clinic application of forensic biomarkers.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144474180","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}
Chun Hoe Tan, Haresh Sivakumar, Da-Gui Luo, Yu-Xin Cen
{"title":"Integrative Network Pharmacology and Molecular Docking Analyses on the Mechanisms of San-Zhong-Kui-Jian-Tang in Treating Oral Squamous Cell Carcinoma.","authors":"Chun Hoe Tan, Haresh Sivakumar, Da-Gui Luo, Yu-Xin Cen","doi":"10.1007/s11596-025-00067-7","DOIUrl":"https://doi.org/10.1007/s11596-025-00067-7","url":null,"abstract":"<p><strong>Objective: </strong>Oral squamous cell carcinoma (OSCC) is an aggressive cancer with a high mortality rate. San-Zhong-Kui-Jian-Tang (SZKJT), a Chinese herbal formula, has long been used as an adjuvant therapy in cancer clinical practice. Although its therapeutic effects and molecular mechanisms in OSCC have been previously elucidated, the potential interactions and mechanisms between the active phytochemicals and their therapeutic targets are still lacking.</p><p><strong>Methods: </strong>The present study employed network pharmacology and topology approaches to establish a \"herbal ingredients-active phytochemicals-target interaction\" network to explore the potential therapeutic targets of SZKJT-active phytochemicals in the treatment of OSCC. The role of the target proteins in oncogenesis was assessed via GO and KEGG enrichment analyses, and their interactions with the active phytochemicals of SZKJT were calculated via molecular docking and dynamic simulations. The pharmacokinetic properties and toxicity of the active phytochemicals were also predicted. RESULTS: A total of 171 active phytochemicals of SZKJT fulfilled the bioavailability and drug-likeness screening criteria, with the flavonoids quercetin, kaempferol, and naringenin having the greatest potential. The 4 crucial targets of these active phytochemicals are PTGS2, TNF, BCL2, and CASP3, which encode cyclooxygenase-2, tumor necrosis factor (TNF), BCL-2 apoptosis regulator, and caspase-3, respectively. The interactions between phytochemicals and target proteins were predicted to be thermodynamically feasible and stable via molecular docking and dynamics simulations. Finally, the results revealed that the IL-6/JAK/STAT3 pathway and TNF signaling via NF-κB are the two prominent pathways targeted by SZKJT.</p><p><strong>Conclusion: </strong>In summary, this study provides computational data for in-depth exploration of the mechanism by which SZKJT activates phytochemicals to treat OSCC.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316066","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}
Current Medical SciencePub Date : 2025-06-01Epub Date: 2025-04-23DOI: 10.1007/s11596-025-00042-2
Xiao-Ya Cai, Gui-Qin Huang, Ye-Ming Zhou, Deng-Ju Li
{"title":"Targeting Calprotectin S100A8/A9 to Overcome AML Progression in DNMT3A-Mutant Cells.","authors":"Xiao-Ya Cai, Gui-Qin Huang, Ye-Ming Zhou, Deng-Ju Li","doi":"10.1007/s11596-025-00042-2","DOIUrl":"10.1007/s11596-025-00042-2","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effects of calprotectin (S100A8/A9) on the biological activity of acute myeloid leukemia (AML) cells harboring a DNA methyltransferase 3A (DNMT3A) mutation and to explore the underlying molecular mechanisms involved.</p><p><strong>Methods: </strong>AML monoclonal cell lines harboring the DNMT3A<sup>R882H</sup> mutation were generated via lentiviral transduction and limiting dilution. RNA sequencing was used for differential gene expression analysis, followed by bioinformatic pathway enrichment and gene correlation analyses. The biological effects of paquinimod, a selective S100A8/A9 inhibitor, on DNMT3A<sup>R882H</sup> AML cells were assessed via Cell Counting Kit (CCK-8) proliferation assays, Annexin V/PI staining, cell cycle analysis, cell adhesion assays, and transwell migration assays.</p><p><strong>Results: </strong>Differential gene expression analysis revealed 442 upregulated and 535 downregulated genes in DNMT3A-mutated (DNMT3A<sup>mut</sup>) cells compared with those in DNMT3A wild-type (DNMT3A<sup>wt</sup>) cells, with the S100A8/A9 complex recurrently enriched in Reactome pathway analysis. Compared with healthy controls, patients with AML presented increased expression of S100A8 and S100A9 and increased expression of DNMT3A<sup>mut</sup> cells relative to DNMT3A<sup>wt</sup> cells, which was correlated with poor prognosis in patients with AML. There were no notable differences in proliferation among the DNMT3A<sup>mut</sup>, DNMT3A<sup>wt</sup>, and empty vector cells under normal or starvation conditions. However, paquinimod treatment notably inhibited the proliferation, migration, and adhesion of DNMT3A<sup>mut</sup> AML cells in a dose-dependent manner, causing G0/G1 cell cycle arrest, whereas no significant effects on apoptosis were observed. Paquinimod also downregulated key adhesion molecules, including intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), monocyte chemoattractant protein-1 (MCP-1), and matrix metalloproteinase-2 (MMP-2). Additionally, S100A8 and S100A9 expression was upregulated in a dose-dependent manner in response to cytarabine treatment.</p><p><strong>Conclusion: </strong>Elevated S100A8/A9 expression contributes to the abnormal proliferation, migration, adhesion, and chemoresistance of DNMT3A<sup>mut</sup> AML cells. Targeting S100A8/A9 alone or in combination with other treatments represents a promising therapeutic strategy for DNMT3A<sup>mut</sup> AML.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"458-468"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967670","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}
Current Medical SciencePub Date : 2025-06-01Epub Date: 2025-06-16DOI: 10.1007/s11596-025-00065-9
Miao Li, Wei Chen, Yao-Bing Chen, Lei Wang, Liu Huang
{"title":"Effects of Thymidine Phosphorylase and Sine Oculis Homeobox Homologue 1 on the Prognosis and Immune Microenvironment of Gastric Cancer.","authors":"Miao Li, Wei Chen, Yao-Bing Chen, Lei Wang, Liu Huang","doi":"10.1007/s11596-025-00065-9","DOIUrl":"10.1007/s11596-025-00065-9","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the combined effects of thymidine phosphorylase (TYMP) and sine oculis homeobox homologue 1 (Six1) on the tumor microenvironment and their role in promoting metastasis in gastric cancer (GC).</p><p><strong>Methods: </strong>A total of 674 GC patients who underwent surgical resection were enrolled. Correlations between TYMP/Six1 expression and the clinicopathological characteristics and overall survival of patients were analysed. The expression of TYMP, Six1 and vascular endothelial growth factor C (VEGFc) was quantified via immunohistochemistry and quantitative real-time polymerase chain reaction. Cell transfection, wound-healing assays and bioinformatics analyses were used to explore the potential underlying mechanisms involved.</p><p><strong>Results: </strong>Compared with the other groups, the Six1+ /TYMP+ patients exhibited poor differentiation, advanced tumor stage, a higher rate of lymphatic vessel invasion and shorter survival. Additionally, the protein expression of TYMP and Six1 was positively correlated with the VEGFc level. A significant increase in VEGFc expression was observed in cells transfected with TYMP, Six1, and TYMP/Six1 vectors. The results of the wound-healing assay indicated that the synergistic effect of TYMP and Six1 enhanced the migratory ability of GC cells. Furthermore, bioinformatics analysis revealed that TYMP and Six1 were positively correlated with immunosuppressive immune cell subsets and elevated the expression of inhibitory immune checkpoints in GC.</p><p><strong>Conclusions: </strong>The combination of TYMP and Six1 is a good predictive and prognostic biomarker for GC. This combination enhances the expression of VEGFc, facilitates the invasion of GC cells, and may be linked to inhibitory immune cells and the tumor immune microenvironment.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"616-625"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144301310","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}
Current Medical SciencePub Date : 2025-06-01Epub Date: 2025-04-17DOI: 10.1007/s11596-025-00016-4
Shou-Kang Li, Nai-Cheng Song, Quan Liu, Zhi-Kun Zheng, Jin-Song Li
{"title":"Risk Factors for Lymph Node Metastasis in Stage pT1 Invasive Lung Adenocarcinoma.","authors":"Shou-Kang Li, Nai-Cheng Song, Quan Liu, Zhi-Kun Zheng, Jin-Song Li","doi":"10.1007/s11596-025-00016-4","DOIUrl":"10.1007/s11596-025-00016-4","url":null,"abstract":"<p><strong>Objective: </strong>To analyze the risk factors for lymph node metastasis (LNM) in patients with stage pT1 lung adenocarcinoma to select a more appropriate surgical option.</p><p><strong>Methods: </strong>In this retrospective study, 294 patients with postoperative pathologically confirmed stage pT1 invasive lung adenocarcinoma were collected and divided into two groups according to whether they had mediastinal or hilar LNM. Patient tumor imaging, pathological features and gene mutations were analyzed, and risk factors that might predict LNM were derived via univariate and multivariate logistic analyses. LNM-related variables were screened by Boruta and least absolute shrinkage and selection operator regression analysis.</p><p><strong>Results: </strong>Among the 294 patients, 45 (15.3%) had positive mediastinal or hilar lymph nodes. There were no significant differences between the two groups in terms of sex, age, or underlying disease. The difference in the percentage of solidity between the two groups was significant, with the higer percentage group showing a more significant difference. The results of multivariate logistic analysis revealed that a high percentage of solid components and wild-type epidermal growth factor receptor (EGFR) were risk factors for LNM. The nomogram for predicting LNM included the consolidation tumor ratio, tumor size, micropapillary and EGFR, with an area under the curve of 93.4% (95% CI: 88.7-99.1) in the derivation cohort and 92.3% (95% CI: 84.6-99.9) in the validation cohort.</p><p><strong>Conclusions: </strong>A high proportion of solid components and wild-type EGFR were risk factors for pT1 stage lung adenocarcinoma, suggesting that the choice of lung segmentectomy needs to be evaluated and selected more cautiously.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"449-457"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143987095","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}
Current Medical SciencePub Date : 2025-06-01Epub Date: 2025-04-28DOI: 10.1007/s11596-025-00048-w
Yi-Qing Rao, Zi-Yu Zhou, Zi-Qi Yang, Meng-Xin Liu, Xiao-Yu Gan, Xue-Fei Hu, Hong-Yang Wang, Hao Li, Man Li
{"title":"Unraveling the Molecular Underpinnings: The Therapeutic Impact of Aerobic Exercise on Anxiety Disorders.","authors":"Yi-Qing Rao, Zi-Yu Zhou, Zi-Qi Yang, Meng-Xin Liu, Xiao-Yu Gan, Xue-Fei Hu, Hong-Yang Wang, Hao Li, Man Li","doi":"10.1007/s11596-025-00048-w","DOIUrl":"10.1007/s11596-025-00048-w","url":null,"abstract":"<p><p>Anxiety disorders, characterized by persistent apprehension, somatic symptoms and fatigue, are leading causes of disability worldwide. The burgeoning therapeutic potential of aerobic exercise has gained prominence as a leading non-pharmacological strategy, with evidence supporting its effectiveness in alleviating anxiety across diverse conditions. This review synthesizes current research to clarify the molecular mechanisms through which aerobic exercise ameliorates anxiety in terms of the effects of exercise on the hypothalamic-pituitary-adrenal (HPA) axis, the hepatic-brain axis and epigenetics; electroencephalographic alterations; inflammatory pathways; the balance between oxidative and nitrogenous stress; various substances, such as brain-derived neurotrophic factor (BDNF), atrial natriuretic peptide (ANP), and opioid peptides; and the 5-HT2C receptor and cannabinoid receptor type-1 (CB1R), among others, reflecting the positive modulatory effects of aerobic exercise on anxiety. As a non-pharmacological intervention, aerobic exercise has been demonstrated to be useful in a variety of medical applications and has considerable potential for ameliorating symptoms of anxiety.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"405-414"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143961618","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}
Current Medical SciencePub Date : 2025-06-01Epub Date: 2025-05-28DOI: 10.1007/s11596-025-00055-x
Xiao-Ning Lu, Jun Chen, Guang Han, Cheng Ding, Chang Li, Chun Xu, Yuan Cui, Sheng Ju, Xin Tong, Jun Zhao
{"title":"FOXM1 Promotes Non-Small Cell Lung Cancer Progression by Increasing CHEK1 Expression.","authors":"Xiao-Ning Lu, Jun Chen, Guang Han, Cheng Ding, Chang Li, Chun Xu, Yuan Cui, Sheng Ju, Xin Tong, Jun Zhao","doi":"10.1007/s11596-025-00055-x","DOIUrl":"10.1007/s11596-025-00055-x","url":null,"abstract":"<p><strong>Objective: </strong>Non-small cell lung cancer (NSCLC) is a leading cause of cancer-associated mortality. This study aimed to investigate the role of checkpoint kinase 1 (CHEK1) in NSCLC progression and its regulatory relationship with forkhead box protein M1 (FOXM1).</p><p><strong>Methods: </strong>Transwell assays were used to evaluate the migration and invasion capabilities of NSCLC cells with either CHEK1 overexpression or knockdown. The expression of epithelial-mesenchymal transition (EMT) markers in NSCLC cells under CHEK1 overexpression or knockdown conditions was analyzed via Western blotting. Proliferative capacity was assessed using CCK-8 assays in NSCLC cells with modulated CHEK1 expression. Additionally, real-time quantitative PCR was employed to measure CHEK1 and FOXM1 expression levels in NSCLC tissues. The effects of CHEK1 knockdown on tumor growth were further validated in animal models. The binding of FOXM1 to the CHEK1 promoter region was examined using dual-luciferase reporter assays and chromatin immunoprecipitation (ChIP) assays.</p><p><strong>Results: </strong>FOXM1 and CHEK1 were upregulated in NSCLC tissues. CHEK1 overexpression promoted NSCLC cell proliferation, while its knockdown suppressed proliferation, inhibited EMT, and reduced tumor growth in vivo. FOXM1 was shown to directly bind to CHEK1 promoter, thereby upregulating CHEK1 expression.</p><p><strong>Conclusion: </strong>CHEK1 promotes NSCLC cell proliferation and tumor growth, and its expression is regulated by FOXM1. These findings suggest CHEK1 and FOXM1 are potential therapeutic targets for NSCLC treatment.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"525-538"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144157268","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}