Current medicinal chemistry最新文献

{"title":"Myoferlin Regulates Cell Proliferation and Migration through the ERK and PI3K/Akt Signaling Pathways in Airway Smooth Muscle Cells.","authors":"Zongnan He, Dayan Cao, Xiuzhen Li, Yixiong Zhan, Hongru Lin","doi":"10.2174/0109298673503885260928073609","DOIUrl":"https://doi.org/10.2174/0109298673503885260928073609","url":null,"abstract":"<p><strong>Background: </strong>The migration and proliferation of airway smooth muscle (ASM) cells are critical processes in the pathogenesis of asthma; however, the underlying regulatory mechanisms remain unclear. Myoferlin (MYOF), a protein known for its involvement in membrane repair, vesicle trafficking, and cancer progression, has recently been associated with enhanced cell migration and proliferation. Nevertheless, the specific role of MYOF in ASM phenotype remains unclear.</p><p><strong>Methods: </strong>Human airway smooth muscle cells (HASMCs) were stimulated with tumor necrosis factor-alpha (TNFα), interleukin-1 beta (IL-1β), or platelet-derived growth factor BB (PDGF-BB) to assess myoferlin expression. Genetic knockdown and the specific pharmacological inhibitor HJ445A were performed to evaluate myoferlin's role in cell proliferation (assessed via CCK-8 and proliferating cell nuclear antigen expression) and migration (evaluated by wound-healing assay). Signaling pathway activation, including MAPK and PI3K/Akt, was examined by Western blot.</p><p><strong>Results: </strong>The expression of myoferlin was markedly upregulated in airway smooth muscle cells (ASMCs) upon stimulation with tumor necrosis factor-alpha (TNF-α), interleukin- 1 beta (IL-1β), and platelet-derived growth factor BB (PDGF-BB). The knockdown or inhibition of myoferlin significantly suppressed PDGF-BB-induced proliferation and migration of ASMCs. Mechanistically, myoferlin depletion or inhibition selectively attenuated PDGF-BB-induced phosphorylation of extracellular signal-regulated kinase (ERK) and Akt, suggesting that these signaling pathways are potentially involved in MYOF- mediated ASMC proliferation and migration.</p><p><strong>Discussion: </strong>This study identifies myoferlin as a key contributor to PDGF-BB-induced ASMC proliferation and migration, and suggests that MYOF inhibition may have therapeutic potential in airway remodeling. However, whether MYOF directly modulates the ERK and PI3K/Akt pathways or acts indirectly through upstream receptor regulation remains to be determined and requires further investigation.</p><p><strong>Conclusion: </strong>Myoferlin is upregulated in activated airway smooth muscle cells (ASMCs) and drives their proliferation and migration via activation of the ERK and PI3K/Akt signaling pathways. Targeted inhibition of myoferlin significantly suppresses these pathological processes.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135300","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":"Five Spermatogenesis-Associated Candidate Biomarker Genes and Computational Identification of Acetaminophen-RNASE4 Interaction Provide New Insights into Cryptorchidism Pathogenesis and Treatment Potential.","authors":"Dashuai Miao, Shiqi Ren, Tingting Huang, Zimeng Wu, Yifang Sun, Yuanyuan Pan, Hua Li, Runfeng Sun, Wenliang Ge","doi":"10.2174/0109298673527009260923055958","DOIUrl":"https://doi.org/10.2174/0109298673527009260923055958","url":null,"abstract":"<p><strong>Introduction: </strong>Cryptorchidism is a frequent congenital anomaly of the genitourinary system in male children. This study aimed to identify candidate biomarker genes and potential therapeutic agents for cryptorchidism based on spermatogenesis-associated pathways.</p><p><strong>Methods and materials: </strong>The GSE25518 and GSE16191 datasets containing the expression profile of cryptorchidism were retrieved from the GEO database. SPERMATOGENESIS scores were calculated using the ssGSEA algorithm. Differential expression analysis was performed using the limma package for both cryptorchidism and control groups. Key module genes were screened using WGCNA and then subjected to functional enrichment analysis using the clusterProfiler package. Furthermore, core hub genes were determined by applying machine learning algorithms, and their case-control discrimination performance was evaluated based on single-gene ROC curves. Immune infiltration was analyzed utilizing ssGSEA, ESTIMATE, and MCPcounter algorithms. Molecular docking between candidate drugs and target protein was performed applying Auto- Dock4 software, followed by molecular dynamics simulation using GROMACS software.</p><p><strong>Results: </strong>SPERMATOGENESIS-related pathway activity was markedly reduced in cryptorchidism. Five hub genes (FBXL7, RNASE4, CTCFL, CRHBP, and RGCC) were identified as candidate molecular signatures with promising discriminatory potential. These genes exhibited close association with the infiltration of several immune cells. Acetaminophen showed a stable binding affinity with RNASE4 protein.</p><p><strong>Discussion: </strong>This study screened five candidate molecular signatures with promising discriminatory potential for cryptorchidism, identified dysregulated spermatogenic pathways, and predicted acetaminophen as a candidate therapeutic compound targeting RNASE4 based on computational simulations.</p><p><strong>Conclusion: </strong>This research provided five candidate spermatogenesis-related biomarker genes for cryptorchidism and predicted acetaminophen as an in silico-predicted candidate compound drug targeting RNASE4.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135333","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":"Chlorogenic Acid Attenuates Liver Fibrosis in Mice via HIF-1α Inhibition and M2 Macrophage Polarization.","authors":"Yongqin Zhang, Ling Feng, Ting Tang, Die Shi, Yiying Yang, Jun Li","doi":"10.2174/0109298673472200260904114536","DOIUrl":"https://doi.org/10.2174/0109298673472200260904114536","url":null,"abstract":"<p><strong>Introduction: </strong>Liver fibrosis, a key pathological step preceding cirrhosis, is characterized by the abnormal accumulation of extracellular matrix (ECM) components, a process largely driven by hepatic stellate cell activation and persistent chronic inflammation. Chlorogenic acid (CGA), a natural polyphenolic compound, has exhibited promising anti-fibrotic activity. However, the precise mechanisms underlying its effects are still not fully elucidated. This study investigates CGA's therapeutic effects and underlying pathways in carbon tetrachloride (CCl4)-induced liver fibrosis in mice.</p><p><strong>Methods: </strong>In this study, a mouse liver fibrosis model was established using CCl4. After treatment with different concentrations of CGA, the biochemical indicators related to liver fibrosis were detected. The pathological changes of liver tissues were examined by HE, Masson, and Sirius Red staining. The expression of related genes was analyzed by RNA-seq, immunohistochemistry, and immunofluorescence techniques to explore the molecular mechanism of CGA in anti-liver fibrosis.</p><p><strong>Results: </strong>CGA dose-dependently ameliorated liver fibrosis, as evidenced by reduced serum markers of liver injury and decreased collagen deposition in hepatic tissues. Histopathological examination confirmed that CGA treatment attenuated hepatocyte necrosis, inflammatory infiltration, and fibrotic lesions. At the molecular level, CGA inhibited Hepatic Stellate Cells (HSCs) activation, indicated by down-regulation of α-SMA, mitigated oxidative stress through restoration of SOD and GSH activities and reduction of MDA, and suppressed the expression of pro-inflammatory cytokines. Transcriptomic analysis identified 338 differentially expressed genes modulated by CGA, which were primarily enriched in immune regulation and metabolic pathways. Further mechanistic investigation revealed that CGA suppressed HIF-1α signaling, restored macrophage morphology, and promoted M2 polarization (up-regulation of CD206), thereby facilitating the clearance of activated HSCs.</p><p><strong>Discussion: </strong>This study found that CGA exerts multi-target anti-fibrotic effects by synergistically inhibiting HSC activation, reprogramming macrophage phenotypes, and alleviating oxidative stress. This synergistic mechanism provides a new basis for developing CGA-based targeted therapeutic strategies for liver fibrosis.</p><p><strong>Conclusion: </strong>This study demonstrates that CGA effectively reverses CCl4-induced liver fibrosis by promoting macrophage polarization toward the M2 phenotype, which in turn facilitates the elimination of HSCs. Its ability to reprogram macrophage function underscores its potential for clinical translation in treating chronic liver fibrosis.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149105417","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":"Novel Approaches in Bladder Cancer Diagnosis and Treatment.","authors":"Arifa Naz Shaikh, Islana Ginayatova, Ilona Malikova, Marina Kriajevska","doi":"10.2174/0109298673474262260909061628","DOIUrl":"https://doi.org/10.2174/0109298673474262260909061628","url":null,"abstract":"<p><p>Bladder Cancer (BC) is among the most prevalent malignancies globally, and the number of new BC cases is expected to increase. The muscle-invasive form of BC is particularly aggressive and often lethal. Conventional treatment options for BC include nontargeted chemotherapy, vaccination-based immunotherapy, and surgical interventions, which may involve complete removal of the bladder. Many patients develop resistance to conventional chemotherapies and immunotherapies and experience significant side effects, leading to poor clinical outcomes. Recent advancements in molecular biology and biotechnology are changing the landscape of BC treatment. This review evaluates whether novel targeted and nontargeted therapies can alleviate toxicity, minimize side effects, and prevent resistance associated with conventional treatments for BC. Furthermore, an overview of the molecular classification system for BC is provided, emphasizing its advantages over traditional histopathological classification. We survey the current diagnostic landscape, from cystoscopy, TURBT-based tissue analysis, and urine cytology to protein-based urinary tests, circulating tumor DNA, and emerging biosensor platforms for minimally invasive point-of-care testing, and we consider how these modalities differ in sensitivity, invasiveness, and resource requirements. The potential impact of new diagnostic markers and preclinical models on BC treatment protocols is further discussed. Finally, this review summarizes the growing understanding of the role of ferroptosis in BC, highlighting its potential as a novel avenue for treatment development. In conclusion, it is asserted that innovative treatment strategies, improved diagnostic markers, advanced preclinical models, and deeper insights into the molecular foundations of BC can significantly improve clinical outcomes for a broad spectrum of BC patients.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149105443","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":"Bioinformatics Identification and Functional Validation of Mitochondrial Homeostasis-Related Genes in Nasopharyngeal Carcinoma Metastasis.","authors":"Zhen Guo, BinSheng He, DanFeng Cao","doi":"10.2174/0109298673481654260903105403","DOIUrl":"https://doi.org/10.2174/0109298673481654260903105403","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Metastatic spread remains the leading cause of death in Nasopharyngeal Carcinoma (NPC); however, the role of mitochondrial homeostasis in this process remains largely unclear.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Objective: &lt;/strong&gt;This study aims to identify key genes associated with mitochondrial homeostasis and NPC metastasis, and to further explore their potential regulatory mechanisms, correlations with the immune microenvironment, and prognostic values.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Focusing on metastasis- and mitochondrial homeostasis-related genes (MMHRGs), we sequentially conduct screening for hub genes, construct regulatory networks, predict drug binding, explore correlations with immunity and prognosis, and perform in vitro functional verification. Candidate hub genes were prioritized using LASSO regression combined with Random Forests. Putative druggable compounds targeting these genes were identified through the Drug Gene Interaction Database (DGIdb) and further examined by molecular docking. Immune infiltration and Tumor Immune Dysfunction and Exclusion (TIDE) analyses were performed to characterize the tumor immune microenvironment and predict immunotherapy response. A prognostic nomogram incorporating these genes was developed, and its predictive accuracy was assessed using time-dependent ROC curve analysis. Finally, the functional roles of the hub genes were experimentally validated in NPC cell lines using wound-healing assays and transmission electron microscopy.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;A mitochondrial homeostasis-related gene signature, highlighted by four hub genes (FKBP4, ATN1, CDKAL1, GPR25), was identified in NPC metastasis. These genes were embedded within extensive post-transcriptional and transcriptional regulatory networks (ceRNA, RNA-binding proteins, TFs, PPIs) to deeply illustrate the molecular mechanism in NPC. Molecular docking revealed SAR260301 with high binding affinity to FKBP4, suggesting potential binding clues. Consensus clustering stratified NPC into two subtypes (Cluster_A/B), with Cluster_B showing enhanced immune checkpoint expression and TIDE-based features. A prognostic model incorporating HNMT, TAGLN3, CSF2RA, and LYZ demonstrated high predictive accuracy for NPC with AUC values of 0.854, 0.860, and 0.920 for 1-, 2-, and 3-year overall survival in the training cohort, and 0.778, 0.914, and 0.846 in the internal validation cohort. Crucially, functional validation showed that overexpression of GPR25 or knockdown of ATN1, CDKAL1, or FKBP4 significantly inhibited NPC cell migration and disrupted mitochondrial morphology.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Discussion: &lt;/strong&gt;The study demonstrated mitochondrial homeostasis-related genes- FKBP4, ATN1, CDKAL1, and GPR25 as candidate hub genes in NPC metastasis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;This study identified four novel mitochondrial homeostasis-associated hub genes involved in NPC metastasis, established a mitochondria-based molecular subtyping s","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149180003","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":"Structure-Based Virtual Screening and Computational Evaluation of Putative Mushroom-Associated Natural Compounds as Janus Kinase 1 (JAK1) Inhibitors: An In Silico Study.","authors":"Bushra Shakoor, Ali Irfan, Muhammed Tilahun Muhammed, Huma Hameed, Ayesha Amin, Sadaf Ahmad, Mahwish Arshad, Aisha Sethi, Laila Rubab, Yousef A Bin Jardan","doi":"10.2174/0109298673453564260829142839","DOIUrl":"https://doi.org/10.2174/0109298673453564260829142839","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction/objective: &lt;/strong&gt;Janus kinase 1 (JAK1) is a key controller and regulator of cytokinemediated immune responses and an effective therapeutic target in autoimmune and inflammatory diseases. In the present study, an in silico workflow was implemented to identify secondary metabolites of mushrooms as prospective JAK1-binding compounds. This integrated computational-aided drug discovery (CADD) approach was used to evaluate their binding affinity scores, interactions, pharmacokinetic properties, structural stability, toxicity, and electronic characteristics.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;An in-silico workflow was employed by employing molecular docking against two JAK1 crystal structures (PDB IDs: 6DBN and 6N7A) in a focused virtual library, and then pharmacokinetic absorption, distribution, metabolism, and excretion (ADME) prediction, toxicity analysis, molecular dynamics (MD) simulation, MM/PBSA binding free energy estimation, and density functional theory (DFT) analysis were performed.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Various compounds, such as Vibralactone Z1, SF2738 B, and Lumichrome, showed rather promising docking scores compared to the reference inhibitor Tofacitinib at the ATP-binding pocket of JAK1. ADME profiling and toxicity modeling predicted acceptable oral drug-like properties and high gastrointestinal absorption for the selected candidates. Although Terreumol A produced the highest docking score against one JAK1 structure, integrated evaluation of docking performance, ADME characteristics, toxicity predictions, and drug-likeness properties identified Vibralactone Z1, Vibrolactone X, SF2738 B, and Lumichrome as the most promising overall lead compounds. Furthermore, MM/PBSA calculations suggested energetically favorable binding, particularly for the 6DBN-SF2738 B complex, while 200-ns molecular dynamics simulations demonstrated moderate structural stability of the selected ligand-protein complexes. DFT analysis showed that Lumichrome and SF2738B had lower HOMO-LUMO energy gaps and good electronic descriptors, indicating increased electronic flexibility in the catalytic pocket.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Discussion: &lt;/strong&gt;The integrated computational findings suggest that selected mushroom-derived metabolites possess favorable binding affinity, pharmacokinetic properties, structural stability, and electronic characteristics that support their potential as JAK1 inhibitor scaffolds. These structurally diverse natural compounds provide valuable starting points for the rational design and optimization of novel JAK1-targeted therapeutics. However, the findings are based entirely on computational predictions and should be interpreted as hypothetical until experimentally validated.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;This CADD approach identified Vibralactone Z1, SF2738 B, and Lumichrome as the most promising and putative mushroom-derived lead compounds for JAK1 inhibition based on data presented in this study through computation","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149105486","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":"SLC7A11 as a Prognostic Biomarker and Therapeutic Target in Renal Cell Carcinoma: Insights into Tumor Microenvironment Remodeling and Immune Infiltration.","authors":"Xinyang Cheng, Jun Zhang, Jixin Yuan, Jingze Xu, Wenjuan Gan, Zhifei Cao, Yongsheng Zhang","doi":"10.2174/0109298673487882260908065601","DOIUrl":"https://doi.org/10.2174/0109298673487882260908065601","url":null,"abstract":"<p><strong>Introduction: </strong>SLC7A11 is part of the solute carrier family and encodes the transporter xCT. However, its functional role in renal cell carcinoma (RCC) progression and associated tumor microenvironment (TME) modulation remains poorly characterized and requires further investigation. This study aimed to explore SLC7A11 expression patterns and their prognostic value, focusing on changes in TME and immune cell infiltration dynamics.</p><p><strong>Methods: </strong>Multi-omics data from TCGA, GTEx, and four GEO cohorts were analyzed, followed by immunohistochemical validation on 498 clinical renal specimens. Bioinformatic tools, including co-expression networks, GSEA, ESTIMATE, CIBERSORT, TIMER2.0, and Kaplan-Meier survival analysis, were applied to dissect signaling pathways and immune infiltration. SiRNA-mediated SLC7A11 knockdown in 786-O and OSRC2 cell lines was conducted to detect cell proliferation, migration, invasion, and cell cycle changes.</p><p><strong>Results: </strong>SLC7A11 was significantly upregulated in KIRC, KIRP and KICH compared with normal renal tissues (P<0.05). SLC7A11-related genes were enriched in cell cycle, DNA replication, p53, ferroptosis, and IL-17 pathways. High SLC7A11 correlated with elevated tumor-associated macrophages and reduced CD8+ T cells, predicting poor overall survival. Knocking down SLC7A11 suppressed malignant phenotypes of RCC cells, induced G0/G1 arrest, and downregulated Cyclin D1/Cyclin B1.</p><p><strong>Discussion: </strong>SLC7A11 exerted oncogenic effects across all primary RCC subtypes. SLC7A11 remodeled the TME by recruiting and polarizing tumor-associated macrophages. Mechanistically, it promoted RCC progression by activating cell cycle pathways to sustain unrestrained cell proliferation. The crosstalk among SLC7A11, ferroptosis, and immune signaling provides new evidence for combining ferroptosis induction with immunotherapy in RCC treatment.</p><p><strong>Conclusion: </strong>SLC7A11 was an adverse prognostic biomarker overexpressed in all main RCC subtypes. It remodeled the TME by weakening the immune response via macrophages and disrupting normal cell growth regulation. Targeting SLC7A11 was a promising combinatorial therapeutic strategy for RCC.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149105430","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":"Zinc Selenide Nanostructures: A Review of Electronic and Biomedical Applications.","authors":"Narimann Neamah Hussein, Kahtan A Mohammed, Ali J Khalaf, Taghreed N Jamil, Nibras Hayder, Shubham Sharma, Jasmina Lozanovic","doi":"10.2174/0109298673415233251130180731","DOIUrl":"https://doi.org/10.2174/0109298673415233251130180731","url":null,"abstract":"<p><p>Zinc selenide nanostructures (ZnSe) hold enormous potential in various technical fields, especially electronics and biomedical applications. Their broad bandgap and quantum confinement effects give them unique physical and chemical characteristics that make them suitable for a wide range of uses. This section discusses ZnSe and its applications in electronics and biomedical fields. It covers the distinctive physical and chemical properties of these structures, such as: Optical properties: Because of their large energy gap and quantum confinement effects, ZnSe can emit light in the bluegreen region of the spectrum, making it useful in light-emitting diodes, microelectronic devices, and lasers. Applications in solar cells: ZnSe is used to create efficient solar cells, making it an attractive material for photovoltaics. Biomedical applications: ZnSe is widely used in fluorescent sensors for in vitro biological imaging, enabling high-resolution imaging of tissues and cells. Their demonstrated antibacterial properties have created new opportunities for developing antimicrobial treatments. Biosensor applications: ZnSe nanostructures can be used to create sensitive biosensors capable of identifying a range of biological materials. Overall, this article discusses the various uses of ZnSe nanostructures and the special properties that make them important across multiple sectors.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149105498","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":"Integrated Single-Cell and Machine-Learning Analysis Identifies Antigen-Presenting Macrophage-Associated Genes in Pediatric Community-Acquired Pneumonia.","authors":"Chu Chu, Yuqin Li, Qian Qian, Chunyu Lu, Ying Ding, Zhe Wang","doi":"10.2174/0109298673515116260907052230","DOIUrl":"https://doi.org/10.2174/0109298673515116260907052230","url":null,"abstract":"<p><strong>Introduction: </strong>Community-Acquired Pneumonia (CAP) is a major global threat with mortality driven by immune dysregulation. The potential role of antigen-presenting macrophages in coordinating immune responses remains poorly defined in CAP. This study aimed to characterize their cellular landscape and intercellular communication and to identify candidate CAP-associated genes through an integrated computational framework.</p><p><strong>Methods: </strong>Single-cell RNA-seq (scRNA-seq) data were analyzed using Seurat, followed by functional enrichment, CellChat, and hdWGCNA analyses. Four machine-learning classifiers were trained and evaluated using a stratified training/test split and repeated cross-validation. Gene set enrichment analysis was performed using the MSigDB Hallmark collection. Molecular docking and a 100-ns molecular dynamics simulation were conducted to explore the predicted interaction between estradiol and SAT1. The expression of SAT1, SERPINB1, and IFITM3 was further examined by qRT-PCR in an LPS/ IFN-γ-stimulated THP-1-derived macrophage model.</p><p><strong>Results: </strong>Antigen-presenting macrophages were identified, whose markers were enriched in antigen processing pathways. CellChat indicated extensive communication between these macrophages and other immune cells. hdWGCNA identified M9/M10 as key modules, while XGBoost achieved the highest test-set performance and prioritized SAT1, SERPINB1, and IFITM3 as candidate genes associated with interferon and inflammatory pathways. Molecular docking predicted interactions of estradiol with SAT1 and SERPINB1, and the 100-ns simulation suggested relative dynamic stability of the predicted SAT1-estradiol complex. qRT-PCR showed that LPS/IFN-γ stimulation significantly increased SAT1, SERPINB1, and IFITM3 mRNA expression in THP-1-derived macrophages.</p><p><strong>Discussion: </strong>This study characterized antigen-presenting macrophages as potentially important immune-cell populations in pediatric CAP and prioritized three candidate genes. The estradiol findings remain exploratory and require direct mechanistic and functional validation.</p><p><strong>Conclusion: </strong>Antigen-presenting macrophages were identified as potential immune regulators in CAP. SAT1, SERPINB1, and IFITM3 represent candidate CAP-associated genes supported by preliminary in vitro transcriptional validation, whereas the predicted interaction with estradiol should be regarded as a hypothesis warranting further investigation.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149105424","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":"HTRA1 and RGS3 as Candidate Genes Associated with Shared Stromal-Immune Dysregulation across Atherosclerotic Plaques and Premature Ovarian Insufficiency.","authors":"Qianqian Ma, Han Zheng, Ailing Chen, Yunzhao Xu, Yanfang Gu","doi":"10.2174/0109298673533900260911093332","DOIUrl":"https://doi.org/10.2174/0109298673533900260911093332","url":null,"abstract":"<p><strong>Introduction/objective: </strong>Endothelial dysfunction and altered stromal-immune crosstalk are implicated in chronic inflammatory diseases. However, their roles in atherosclerotic plaque (AP) and premature ovarian insufficiency (POI) remain unclear.</p><p><strong>Methods: </strong>The single-cell RNA-seq (scRNA-seq) data of AP and human follicular aspirates and bulk RNA-seq data for POI were obtained the Gene Expression Omnibus (GEO) database. Single-- cell analysis was performed using the Seurat package. Differential expression analysis was performed using DESeq2. High-dimensional weighted gene co-expression network analysis (hdWGCNA) was used to identify endothelial-associated modules, and the hub genes were then integrated with differentially expressed genes (DEGs). The CellChat package was used to infer cell-cell communication. Functional enrichment analysis was conducted using the clusterProfiler package.</p><p><strong>Results: </strong>Single-cell analysis showed reduced endothelial cell abundance but increased macrophages and CD4+/CD8+ T cells in AP. Endothelial cells displayed extensive ligand-receptor crosstalk with immune and stromal cells, thereby orchestrating angiogenic and inflammatory responses. hdWGCNA identified three endothelial-associated gene modules, and integrating these modules with bulk differential expression prioritized high-temperature requirement protein A1 (HTRA1) and regulator of G protein signaling 3 (RGS3) as candidate genes. Both genes were downregulated in POI samples, and their expression levels were positively correlated with E2F/MYC/G2M cell-cycle programs and were negatively associated with IL-6/JAK-STAT3 signaling. Within the follicular niche, HTRA1 localized to theca/stromal-like follicular cells, while RGS3 was enriched in cytotoxic lymphocytes. CellChat analysis further revealed extensive bidirectional ligand-receptor interactions between theca/stromal-like follicular cells and immune populations.</p><p><strong>Discussion: </strong>These findings suggest that endothelial dysfunction in AP and POI may share common stromal-immune features mediated by HTRA1 and RGS3. However, given the limited sample sizes and the computational nature of this study, these associations should be further validated.</p><p><strong>Conclusion: </strong>This study developed a transcriptional gene model for AP and POI and preliminarily found that downregulation of HTRA1 and RGS3 may be associated with cell cycle and inflammatory signaling pathways.</p>","PeriodicalId":10984,"journal":{"name":"Current medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149105453","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}