Current molecular medicine最新文献

{"title":"Melatonin Attenuates H₂O₂-Induced Muscle Atrophy and Promotes Hypertrophy: Morphological, Redox, and Gene Evidence.","authors":"Nazlı Karimi Ahmadi, Adnan Berk Dinçsoy","doi":"10.2174/0115665240509060260627094405","DOIUrl":"https://doi.org/10.2174/0115665240509060260627094405","url":null,"abstract":"<p><strong>Introduction: </strong>Disuse muscle atrophy is strongly associated with oxidative stress, with antioxidants such as melatonin emerging as potential therapeutic agents, particularly due to their protective effects on mitochondrial function. This study aimed to investigate the effects of melatonin on redox balance, cellular morphology, and expression of atrophy-related genes, Atrogin-1 and MuRF1, in an H2O2-induced muscle atrophy model using the C2C12 cell line.</p><p><strong>Materials and methods: </strong>Four experimental groups were established, namely Control, Melatonin, H2O2, and Melatonin + H2O2. Morphological alterations were evaluated by measuring myotube diameters. Redox status was assessed using the Oxidative Stress Index (OSI), calculated from Total Antioxidant Status (TAS) and Total Oxidant Status (TOS). The expression levels of Atrogin-1 and MuRF1 were analyzed using quantitative real-time PCR.</p><p><strong>Results: </strong>Significant differences in myotube diameters were observed among the groups (p < 0.05). The Melatonin + H2O2 group exhibited the lowest OSI values, indicating improved redox balance. Although the differences were not statistically significant, melatonin treatment was associated with lower expression levels of Atrogin-1 and MuRF1 compared to other groups.</p><p><strong>Discussion: </strong>The findings suggest that melatonin may alleviate oxidative stressinduced muscle atrophy by preserving myotube morphology and improving cellular redox balance. The observed trends in Atrogin-1 and MuRF1 expression indicate a potential modulatory effect of melatonin on atrophy-related pathways; however, additional time-course and protein-level analyses are needed to further clarify these mechanisms.</p><p><strong>Conclusion: </strong>Melatonin demonstrated protective effects against HⁿOⁿ-induced muscle atrophy in C2C12 cells, particularly through the preservation of myotube morphology and enhancement of cellular antioxidant status. These findings support the potential role of melatonin as a therapeutic candidate for oxidative stress-related muscle atrophy.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148600036","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":"Calycosin Attenuates Endoplasmic Reticulum Stress Injury in Human Renal Glomerular Endothelial Cells by Inhibiting SRC/SYKDependent Reactive Oxygen Species.","authors":"Yutian Wang, Xiaolin Bai, Ruixia Pei, Wen Lei, Zequn Zhang, Pei Dai","doi":"10.2174/0115665240473729260504092344","DOIUrl":"https://doi.org/10.2174/0115665240473729260504092344","url":null,"abstract":"<p><strong>Introduction: </strong>Diabetic Nephropathy (DN), a severe complication, involves endoplasmic reticulum stress. Calycosin, an isoflavone derived from Mongolian Milkvetch Root, may mitigate DN by targeting proto-oncogene tyrosine-protein kinase SRC (SRC)/Spleen Tyrosine Kinase (SYK)-dependent Reactive Oxygen Species (ROS)-mediated ER stress.</p><p><strong>Methods: </strong>Human Renal Glomerular Endothelial Cells (HRGECs) were exposed to high glucose to mimic DN, and then treated with calycosin or transfected with SRC overexpression plasmids. Quantitative real-time PCR was performed to assess transfection efficiency, and a western blot was conducted to examine the expression of proteins associated with endothelial dysfunction and endoplasmic reticulum stress. Cell viability, cytotoxicity, apoptosis, and ROS levels were assessed via cell counting kit-8, lactate dehydrogenase assay, flow cytometry, and DCFH-DA probes.</p><p><strong>Results: </strong>Calycosin barely affected HRGEC viability in normal glucose medium, but apparently reversed high glucose-induced suppression of viability. High glucose increased cytotoxicity, apoptosis, ROS content, and levels of intercellular cell adhesion molecule-1 (ICAM-1), Glucose-Regulated Protein 78 kD (GRP78), Phosphorylated (P)- Protein Kinase RNA-Like Endoplasmic Reticulum Kinase (PERK)/ total (t)-PERK ratio, C/EBP-Homologous Protein (CHOP), SYK, and SRC protein, which were all counteracted by calycosin. Overexpression of SRC attenuated the effects of calycosin on promoting cell viability and repressing apoptosis, ROS, ICAM-1, and endoplasmic reticulum stress-related proteins in high-glucose-treated HRGECs.</p><p><strong>Discussion: </strong>These findings are in line with prior research linking SRC/SYK-ROS signaling to endoplasmic reticulum stress in the context of DN, highlighting the therapeutic potential of calycosin, although the lack of in vivo evidence necessitates future investigation using animal models.</p><p><strong>Conclusion: </strong>Calycosin attenuates high glucose-induced endoplasmic reticulum stress injury in HRGECs by inhibiting SRC/SYK-dependent ROS.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148600027","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":"Integrative Analysis Identifies Key Genes Associated with Immune Responses in Non-Alcoholic Fatty Liver Disease Via Single-Cell Sequencing and Bulk RNA Analysis.","authors":"Nan Shen, Binghan Bi, Yucheng Fang, Hongyu Miao, Peimin Pu, Zhidong Liu, Xiao Yu, Lianjun Xing","doi":"10.2174/0115665240509801260710112828","DOIUrl":"https://doi.org/10.2174/0115665240509801260710112828","url":null,"abstract":"<p><strong>Introduction: </strong>Liver inflammation in Non-Alcoholic Fatty Liver Disease (NAFLD) is shaped by immune regulation. This study examines the contribution of immune-related genes to NAFLD pathogenesis.</p><p><strong>Methods: </strong>Single-cell analysis identified key immune cell clusters and subtypes. Differential expression, machine learning, and expression profiling were used to screen key genes, which were then used to construct a nomogram predicting NAFLD risk. Immune infiltration analysis characterized immune states, and pseudotime analysis tracked key gene expression along T-cell differentiation. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blotting were used to validate gene expression.</p><p><strong>Results: </strong>T cells were identified as the key immune cells, with regulatory T cells (Tregs) as the critical subtype. CXCR4, DUSP1, and ID2 were downregulated in NAFLD and supported a nomogram with good predictive performance. Immune infiltration analysis showed differences in six immune cell types, including Tregs, between NAFLD and controls. Pseudotime analysis showed increased CXCR4, DUSP1, and ID2 expression in Tregs and cytotoxic T lymphocytes (CTLs) at late differentiation, while NAFLD samples showed reduced DUSP1 and ID2 expression in RT-qPCR and Western blot assays.</p><p><strong>Discussion: </strong>Treg-centered immune dysregulation and the downregulation of CXCR4, DUSP1, and ID2 are closely linked to NAFLD pathology. The context-dependent nature of these genes precludes simple protective or pathogenic labels. The nomogram capturing single-cell-derived immune signatures outperforms conventional clinical predictors and offers mechanistic insight. Pseudotime analysis provides the first continuous view of T-cell activation trajectories in NAFLD. A ceRNA network involving NEAT1/XIST and miR-15b-5p may explain DUSP1 suppression. However, small validation cohorts (n = 3/group), the absence of functional experiments, and PBMC-based profiling limit causal inference; replication in larger intrahepatic cohorts is necessary before clinical translation.</p><p><strong>Conclusion: </strong>T cells, especially Tregs, and CXCR4, DUSP1, and ID2 are central to Non-Alcoholic Fatty Liver Disease and may serve as diagnostic and therapeutic targets.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148600022","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 Bioinformatics and Experimental Validation Reveal Shared Molecular Targets for Diagnosis and Intervention in Type 2 Diabetes Mellitus and Diabetic Nephropathy.","authors":"Syed Shah Zaman Haider Naqvi, Zhitong Li, Ruixue Duan, Jiaojiao Li, Wenxia Ren, Muhammad Zaeem, Shoaib Muhammad, Imran Ali, Shiwei Liu","doi":"10.2174/0115665240446197260120100411","DOIUrl":"https://doi.org/10.2174/0115665240446197260120100411","url":null,"abstract":"<p><strong>Introduction: </strong>Type 2 diabetes mellitus (T2DM) is a major risk factor for diabetic nephropathy (DN), yet the molecular mechanisms connecting these conditions remain unclear. Identifying shared hub genes and regulatory networks may provide insight into common pathogenic pathways.</p><p><strong>Methods: </strong>Four GEO microarray datasets associated with T2DM (GSE23343, GSE29226) and DN (GSE30528, GSE142153) were analyzed using limma in R to identify differentially expressed genes (DEGs). Overlapping DEGs were assessed using Venn analysis and integrated into a STRING-based protein-protein interaction network. Hub genes were identified in Cytoscape. Their expression under high-glucose conditions was validated in HK-2 and NRK-52E cells using RT-qPCR and Western blotting. Predicted miRNAs were obtained from TargetScan and evaluated experimentally. Functional assays assessed the effects of hub gene overexpression.</p><p><strong>Results: </strong>Thirty-six common DEGs were identified, with APP, RHEB, FRYL, and SOS1 exhibiting highest network connectivity. All four genes were consistently downregulated in patient datasets and high-glucose cell models. ROC analyses indicated moderate discriminatory capacity within datasets. Four candidate miRNAs (miR-26b-5p, miR-18a-5p, miR-199a-5p, miR-148a-3p) were elevated under highglucose conditions. Functional enrichment linked hub genes to mTOR, PI3K-Akt, and cytoskeletal pathways. Overexpression of hub genes reduced proliferation, clonogenicity, and migration in vitro.</p><p><strong>Discussion: </strong>The convergence of transcriptomic and experimental findings suggests that reduced expression of these hub genes may contribute to glucose-induced cellular dysfunction. However, miRNA-gene relationships remain correlative, and validation in additional renal cell types and independent patient cohorts is needed.</p><p><strong>Conclusion: </strong>APP, RHEB, FRYL, and SOS1 represent shared molecular signatures of T2DM and DN and may offer potential targets for future mechanistic and therapeutic studies.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148600069","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":"VSIG2 Promotes Osteosarcoma Cisplatin Resistance Via Activating PI3K/AKT/mTOR Pathway.","authors":"Xueren Zhong, Jing Xiang, Xiaoyu Yang, Shuangquan Gao, Qihui Lin, Pengyu Lai, Konghe Hu, Dan Li, Zhengyun Zhang, Yongzheng Bao, Qiang Wu, Xinhua Xi","doi":"10.2174/0115665240450935260508061942","DOIUrl":"https://doi.org/10.2174/0115665240450935260508061942","url":null,"abstract":"<p><strong>Introduction: </strong>Chemotherapy resistance is one of the main reasons for osteosarcoma (OS) relapses. Understanding the regulatory mechanisms of cisplatin resistance is critical for developing potential therapeutic strategies for OS. This study aimed to examine the role of VSIG2 in OS chemotherapy resistance.</p><p><strong>Methods: </strong>Cell viability assay, colony formation assay, LDH cytotoxicity assay, and a subcutaneous xenograft model were used to explore VSIG2's role in OS cisplatin resistance in vitro and in vivo. A luciferase reporter assay was carried out to determine the pathways regulated by VSIG2. Co-Immunoprecipitation was carried out to investigate the interaction of VSIG2.</p><p><strong>Results: </strong>VSIG2 is upregulated in OS tissues with poor response to neoadjuvant chemotherapy. Functionally, VSIG2 promoted cisplatin resistance determined by cell models and animal models. Mechanistically, VSIG2 activated the PI3K/AKT pathway. Moreover, VSIG2 interacted with mTOR and increased p70 S6 Kinase phosphorylation. Furthermore, inhibition of mTOR significantly reversed the effect of VSIG2 on cisplatin resistance.</p><p><strong>Discussion: </strong>Our findings emphasize the key role of VSIG2 in chemoresistance of OS, deepening the understanding of the molecular mechanisms of OS chemoresistance generation.</p><p><strong>Conclusion: </strong>In summary, our findings suggested that VSIG2 may confer novel platinum resistance via activating the PI3K/AKT/mTOR pathway, providing a potential target for OS therapy.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148560953","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":"Nebulized Inhalation of Bacillus Calmette-Guerin Polysaccharide Nucleic Acid Attenuates Airway Hyperresponsiveness in Asthma by Inhibiting the Notch3/NF-Κb Signaling Pathway to Regulate MUC5AC Expression.","authors":"Hao Zhu, Rongfang Tu, Shaoze Zhang, Guang Li, Fang Hu, Lifu Wu, Wei Liu, Chaoqian Li","doi":"10.2174/0115665240445931260619112752","DOIUrl":"10.2174/0115665240445931260619112752","url":null,"abstract":"<p><strong>Introduction: </strong>Bacillus Calmette-Guerin polysaccharide nucleic acid (BCGPSN) has potential efficacy in asthma. We aim to investigate the mechanisms by which BCG-PSN attenuates asthma.</p><p><strong>Methods: </strong>Ovalbumin (OVA) was used to establish asthma mouse models and simulate asthma injury in BEAS-2B cells. After BCG-PSN nebulization and Notch3 overexpression, acetylcholine provocation tests and immunoblotting were used to assess airway hyperresponsiveness (AHR) in mice. Hematoxylin and eosin staining was used to evaluate bronchial pathology in mice. The Mucin 5AC (MUC5AC) expression was analyzed through mRNA quantification. The Notch3/Nuclear Factor- Kappa B (NF-κB) signaling pathway in mouse lung tissues and BEAS-2B cells was analyzed by immunoblotting. The morphology and cell viability of BEAS-2B cells were examined through morphological analysis and CCK-8 assay.</p><p><strong>Results: </strong>OVA-induced mice showed increased AHR, a thickened bronchial basement membrane, goblet cell hyperplasia, inflammatory infiltration, and elevated lung MUC5AC. Nebulized inhalation of BCG-PSN reduced AHR and the level of MUC5AC in the lung tissues of asthmatic mice. In vivo and in vitro experiments showed that BCG-PSN treatment partially reversed the effects induced by OVA, leading to restored cell morphology, increased cell viability, and decreased expression levels of Notch3, pp65Ser276/ p65, and MUC5AC. However, overexpression of Notch3 partially counteracted the action of BCG-PSN.</p><p><strong>Discussion: </strong>The findings suggest that the Notch3/NF-κB pathway plays a key role in OVA-induced airway epithelial injury and MUC5AC overexpression. BCG-PSN appears to exert its protective effects by modulating this signaling axis.</p><p><strong>Conclusion: </strong>BCG-PSN inhalation alleviates asthma-related AHR primarily by downregulating MUC5AC via the Notch3/NF-κB pathway.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148430100","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":"Dynamic Expression of Fibroblast Activation Protein (FAP) During Chronic Pancreatitis (CP) Progression in Mice and Evaluation of FAP-targeted Tracers for Early CP Diagnosis.","authors":"Xiao-Lou Zhang, Xing-da Xu, Xiao-Kang Ma, Wang Xiao, Jian-Ping Qian, Wan-Jun Yang, Hao Xu, Guo-Wei Zhang","doi":"10.2174/0115665240385783260617105756","DOIUrl":"https://doi.org/10.2174/0115665240385783260617105756","url":null,"abstract":"<p><strong>Introduction: </strong>Currently, effective methods for the early diagnosis of Chronic Pancreatitis (CP) remain limited. PANCREATIC STELLATE CELLS (PSCs) in pancreatitis are critical drivers of CP progression, and PSCs are known to overexpress Fibroblast Activation Protein (FAP) in inflamed pancreatic tissue. This study aims to investigate the correlation between the dynamic changes in FAP expression by PSCs and CP progression, and to evaluate the feasibility of three FAP inhibitor (FAPI)-based tracers for early CP diagnosis.</p><p><strong>Method: </strong>Caerulein-treated PRSS1 transgenic mice (PRSS1Tg) were categorized into four groups based on the development stage of CP. The pancreatic pathology was observed using HE and Masson staining. Moreover, immunohistochemistry, immunofluorescence, and qRT-PCR were employed to further analyze the pancreas. Additionally, near-infrared in vivo fluorescence imaging was performed with ICG-FAPI- 04, whereas Micro-PET/CT was performed with 68Ga-FAPI-04 and 18F-FAPI-42. The results were subsequently observed and analyzed.</p><p><strong>Results: </strong>Experiments revealed that FAP was overexpressed in CP, with its expression peaking at 2 weeks. In vivo near-infrared imaging using ICG-FAPI-04 failed to effectively assess pancreatic morphology and fibrosis at the 2-week time point in the CP model mice. In micro-PET/CT evaluations of CP model mice at two weeks, 18FFAPI- 42 demonstrated superior visualization of pancreatic morphology and fibrosis compared to 68Ga-FAPI-04.</p><p><strong>Discussion: </strong>The near-infrared probe ICG-FAPI-04 shows limited efficacy, but its performance could be improved by increasing hydrophilicity or adopting NIR-II imaging. In comparison, FAPI-based PET/CT-especially using 18F-FAPI-42-offers clear visualization of pancreatic morphology, positioning it as a highly promising tool for CP detection.</p><p><strong>Conclusion: </strong>This study demonstrated dynamic FAP expression during CP progression. FAP-targeted tracers were shown to sensitively visualize the pancreatic morphology reflecting fibrosis severity, validating their feasibility for early CP diagnosis.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148307389","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":"Therapeutic Potential of Pistacia Atlantica Gum in Aspirin-Induced Peptic Ulcers: A Dose-Dependent Approach to Mucosal Protection and Hepatorenal Safety.","authors":"Kourosh Sayehmiri, Somayeh Heidarizadi, Kamyar Sayehmiri, Monireh Azizi","doi":"10.2174/0115665240445451260611091700","DOIUrl":"https://doi.org/10.2174/0115665240445451260611091700","url":null,"abstract":"<p><strong>Introduction: </strong>Aspirin-induced peptic ulcers present a major clinical challenge, driving the search for safer, natural gastroprotective agents. This study evaluated the therapeutic potential and safety of Pistacia atlantica gum (PAG) in a rat model of aspirin-induced gastric damage.</p><p><strong>Materials and methods: </strong>Forty-nine male Wistar rats were divided into seven groups (n=7): normal control, aspirin control, aspirin + vehicle, aspirin + PAG (3, 6, or 12 mg/kg), and aspirin + sucralfate (70 mg/kg, positive control). Ulcers were induced by oral aspirin (200 mg/kg for 3 days). Treatments were administered for two weeks. Assessments included ulcer scoring, serum biochemical markers (ALT, AST, ALP, GGT, BUN, creatinine), oxidative/antioxidant status (MDA, SOD), inflammatory cytokines (IL-6, TNF-α), and blinded histopathological evaluation.</p><p><strong>Results: </strong>PAG exhibited a dose-dependent reduction in ulcer severity, with the 12 mg/kg dose achieving efficacy comparable to sucralfate. Biochemically, PAG 12 mg/kg significantly ameliorated aspirin-induced hepatotoxicity (reduced ALT, AST, ALP, and GGT) and nephrotoxicity (reduced BUN and creatinine), surpassing sucralfate, which showed no renal benefit. PAG treatment also mitigated oxidative stress (increased SOD, decreased MDA) and suppressed pro-inflammatory cytokines (IL-6, TNF-α). Histopathological analysis confirmed significant mucosal preservation in PAG-treated groups.</p><p><strong>Discussion: </strong>The study highlights PAG's multifaceted therapeutic profile, aligning with its traditional use in Kurdish medicine. Its efficacy is likely associated with phytochemicals such as α-pinene and flavonoids, which are suggested to modulate oxidative stress, inflammation, and apoptosis pathways. Notably, PAG may offer a safer profile, as it lacks nephrotoxic effects and exhibits hepatorenal protective properties.</p><p><strong>Conclusion: </strong>PAG emerges as a potent natural remedy for aspirin-induced ulcers, combining mucosal protection with systemic safety.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148276341","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":"Causal Relationship Between 91 Inflammatory Factors and Gastritis: A Two-Sample Bidirectional Mendelian Randomization Study.","authors":"Tong Wang, Lu Lin","doi":"10.2174/0115665240441630260530222919","DOIUrl":"https://doi.org/10.2174/0115665240441630260530222919","url":null,"abstract":"<p><strong>Introduction: </strong>Emerging evidence from recent pathological investigations has demonstrated that inflammation plays a critical role in the progression of gastrointestinal diseases. However, the causal relationships between inflammation and gastritis still lack further validation.</p><p><strong>Methods: </strong>Mendelian Randomization (MR) was used to evaluate the causal effects of inflammatory factors on gastritis. The datasets of 91 inflammatory factors were obtained from the Genome-Wide Association Study (GWAS) database, and the genetic datasets of Acute Gastritis (AG) and Chronic Gastritis (CG) were obtained from the GWAS database and the FinnGen database, respectively. Heterogeneity and pleiotropy were assessed with Cochran's Q test and MR-Egger's intercept test, respectively.</p><p><strong>Results: </strong>After accounting for heterogeneity and horizontal pleiotropy, MR analysis identified Axin-1, C-X-C motif chemokine 10 (CXCL10), and Fms-related tyrosine kinase 3 ligand to be significantly associated with acute gastritis, while linking CXCL10, glial cell line-derived neurotrophic factor, Leukemia Inhibitory Factor Receptor (LIFR), hepatocyte growth factor, and fibroblast growth factor 19 to chronic gastritis. Furthermore, reverse MR analysis revealed that CG could significantly downregulate the levels of Interleukin-2 receptor subunit beta, Interleukin-15 receptor subunit alpha, Interleukin-20 receptor subunit alpha, LIFR, and Interleukin-1-alpha.</p><p><strong>Discussion: </strong>This study found that AG and CG were associated with distinct inflammatory factors and that CG could reverse the levels of inflammatory factors. CXCL10 and LIFR may be potential biomarkers for gastritis.</p><p><strong>Conclusion: </strong>This study systematically identified causal relationships between inflammatory factors and gastritis. The identified inflammatory factors offer new insights into potential targets for gastritis.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148276415","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":"Identification and Characterization of MicroRNAs Associated with Borax-mediated Anti-tumor Activity through High-throughput Technology.","authors":"Wenbo Zhou, Fen Sheng, Jiao Zhou, Jinjin Wang, Xuefei Huang, Qinhua Chen, Jinchao Li, Huizhen Li, Mingxing Liu, Junying Zhu, Jingjian Liu, Ying Wei, Lun Wu","doi":"10.2174/0115665240373591251126101819","DOIUrl":"https://doi.org/10.2174/0115665240373591251126101819","url":null,"abstract":"<p><strong>Objective: </strong>The primary aim of this study was to explore the involvement of miRNAs in the anti-tumor effects of borax through high-throughput sequencing analysis.</p><p><strong>Methods: </strong>Total RNA was extracted and purified from HepG2 cells treated with 4 mM borax for 2 or 24 hours. The samples were subjected to microarray analysis using a human miRNA array. Differentially expressed miRNAs were identified through a volcano plot and heatmap analysis and validated using quantitative PCR. A proteinprotein interaction (PPI) network was constructed, and hub genes were identified using Cytoscape software.</p><p><strong>Results: </strong>Exposure to borax significantly altered miRNA expression levels in HepG2 cells. After 2 or 24 hours of borax treatment, 14 miRNAs were upregulated, respectively, while 3 miRNAs were downregulated compared to the control group (≥2- fold change, P<0.05). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses revealed that the target genes of differentially expressed miRNAs were primarily involved in the MAPK, TGF-β, and NFκB signaling pathways in the 2-hour treatment group. In contrast, the 24-hour treatment group showed involvement in the Ras signaling pathway, the forkhead box O signaling pathway, and cellular senescence. PPI network analysis identified NACC2, CACNB1, and FZD6 as hub genes in the 2-hour treatment group, while CDK6, BCL-2, IGF1R, BTG2, AGO2, and DLGAP3 were identified as hub genes in the 24-hour treatment group.</p><p><strong>Discussion: </strong>The findings suggested that the anti-tumor effects of borax may be associated with changes in miRNA expression.</p><p><strong>Conclusion: </strong>This study established a potential miRNA-mRNA regulatory network related to tumor biology, providing a comprehensive understanding of the molecular mechanisms and offering new therapeutic targets for liver cancer.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148263483","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}