Korean Journal of Physiology & Pharmacology最新文献

{"title":"Deciphering the role of nicotinamide metabolism and melanin-related genes in acute myocardial infarction: a machine learning approach integrating bioinformatics analysis.","authors":"Jun Li, Chao Li, Tao Qian","doi":"10.4196/kjpp.24.431","DOIUrl":"https://doi.org/10.4196/kjpp.24.431","url":null,"abstract":"<p><p>Acute myocardial infarction (AMI) represents a significant global mortality factor. Alterations in nicotinamide metabolism within the myocardium post-AMI can influence the progression of the condition. Additionally, melanin plays a crucial role in nicotinamide metabolism and exhibits anti-inflammatory properties. Nevertheless, the diagnostic biomarkers for AMI that are based on nicotinamide metabolism and melanin-associated genes remain poorly defined. In this study, the AMI transcriptomic data from the Gene Expression Omnibus were analyzed to identify differentially expressed genes (DEGs) intersecting with nicotinamide metabolism and melatonin-related genes. Machine learning algorithms, including RandomForest, least absolute shrinkage and selection operator, and support vector machinerecursive feature elimination, were applied to select feature genes. Diagnostic markers were further evaluated based on area under the curve from receiver operating characteristic analysis. We identified 14 candidate genes, refined to 4 key genes, with NAMPT and BST1 ultimately selected as diagnostic biomarkers. These were used to classify AMI into two molecular subtypes. Immune landscape analysis revealed increased infiltration of monocytes, neutrophils, macrophages, and parainflammation in AMI. Enrichment analyses showed DEGs were mainly involved in innate immune response and cytokine production. Additionally, hsa-miR-34a-5p and hsa-miR-181b-5p were identified as potential regulators of NAMPT and BST1. In summary, NAMPT and BST1 are promising diagnostic biomarkers associated with nicotinamide metabolism and melatonin in AMI. The molecular subtyping based on these genes will enhance the management and hierarchical treatment of AMI, offering significant implications for clinical diagnosis and therapeutic strategies.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144144422","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":"Phytochemicals as promising agents in Axl-targeted cancer treatment.","authors":"ChuHee Lee","doi":"10.4196/kjpp.25.006","DOIUrl":"https://doi.org/10.4196/kjpp.25.006","url":null,"abstract":"<p><p>Axl, a receptor tyrosine kinase, plays a critical role in various cellular processes, such as survival, proliferation, migration, and immune response regulation. Dysregulation of Axl, particularly its overexpression and activation, is implicated in several cancers, where it has been found to facilitate tumor growth, metastasis, and the development of resistance to chemotherapy. Consequently, the inhibition of Axl has garnered significant interest as a potential strategy for cancer treatment. Natural compounds, known for their structural diversity and inherent bioactivity, are a valuable resource for drug discovery. These compounds offer a vast array of chemical structures that can serve as potential inhibitors of Axl, thereby providing novel approaches to modulate its activity. Researchers have identified various natural compounds that exhibit inhibitory effects on Axl, which underscore their potential for developing effective therapies. This review strives to provide a comprehensive overview of natural compounds that have been identified as Axl inhibitors. It will examine the mechanisms through which these natural compounds exert their inhibitory effects on Axl and discuss their potential applications in therapeutic settings. By compiling and analyzing existing research, this review seeks to advance the understanding of natural compounds as viable candidates in the development of effective Axl-targeted therapies, ultimately contributing to improved outcomes in diseases marked by Axl dysregulation.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082085","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":"Amorfrutin A ameliorates cerebral ischemia/reperfsion injury <i>in vivo</i> and <i>in vitro via</i> modulating Nrf2/HO-1 signaling pathway.","authors":"Youxi Yang, Liying Shi, Xiaoting Xu, Bilan Luo, Xing Cui, Lei Tang, Jianta Wang","doi":"10.4196/kjpp.24.304","DOIUrl":"https://doi.org/10.4196/kjpp.24.304","url":null,"abstract":"<p><p>Ischemic stroke is a leading cause of death and disability worldwide. Amorfrutin A (AA), a small molecule compound found in <i>Amorpha fruticosa</i> L. (bastard indigo), possesses various activities, including blood glucose regulation, antiinflammatory, analgesic, and tumor suppression. In this study, we used the middle cerebral artery occlusion/reperfusion (MCAO/R) model and the oxygen glucose deprivation/ reoxygenation (OGD/R) model to mimic the ischemia/reperfusion process <i>in vivo</i> and <i>in vitro</i>, respectively. The role of AA in ischemic stroke was evaluated by CCK-8 assay, ELISA, TTC staining, hematoxylin-eosin staining and Western blot assay. AA increased the survival of BV2 or PC12 cells following OGD/R injury. Meanwhile, AA effectively suppressed the release of reactive oxygen species, nitric oxide, and tumor necrosis factor-α (TNF-α) in BV2 or PC12 cells subjected to OGD/R. After 24 h of MCAO/R surgery, AA significantly reduced the neurological deficit score, diminished the cerebral infarct volume, and attenuated brain pathological injury in rats. AA administration significantly increased superoxide dismutase and glutathione peroxidase levels, reduced malondialdehyde production, and inhibited the release of inflammatory cytokines interleukin-1β and TNF-α in the ischemic brain tissue of MCAO/R rats. In addition, AA suppressed Kelch-like ECH-associated protein 1 expression and promoted nuclear factor erythroid 2-related factor 2 (Nrf2), NAD(P)H quinone oxidoreductase 1, and heme oxygenase 1 (HO-1) expression in rat ischemic brain. AA may be a potential drug for the treatment of ischemic stroke. Its antioxidant and anti-inflammatory effects in cerebral ischemia-reperfusion injury may be related to Nrf2/HO-1 signaling pathway.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082081","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":"Emerging role of circular RNAs in diabetic retinopathy.","authors":"Hyunjong Kim, Juhee Ryu","doi":"10.4196/kjpp.24.389","DOIUrl":"https://doi.org/10.4196/kjpp.24.389","url":null,"abstract":"<p><p>Diabetic retinopathy (DR), a significant complication that affects the retina of individuals with diabetes, poses a severe threat to their visual health. DR is classified into stages ranging from non-proliferative to proliferative forms. As the disease progresses, pathological neovascularization and hemorrhage in the retina or vitreous can occur, potentially leading to vision impairment or blindness. Current treatments for DR include intravitreal injections of anti-vascular endothelial growth factor drugs and surgical interventions such as laser photocoagulation. However, these treatments are associated with various complications and side effects. Therefore, cellular and epigenetic studies are necessary to better understand the pathogenesis of DR, which may lead to the development of novel therapeutic strategies. Several studies have demonstrated the role of circular RNAs (circRNAs) in the pathogenesis and progression of DR. CircRNAs have been shown to regulate the expression of genes involved in the proliferation, differentiation, or angiogenesis of different retinal cells, thereby influencing their function. Therefore, this review aims to investigate the role of circRNAs in different retinal cell types in DR and evaluate their potential as diagnostic and therapeutic targets for the disease.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082083","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":"Quetiapine competitively inhibits 5-HT₃ receptor-mediated currents in NCB20 neuroblastoma cells.","authors":"Yong Soo Park, Gyu Min Kim, Ho Jun Sung, Ju Yeong Yu, Ki-Wug Sung","doi":"10.4196/kjpp.24.363","DOIUrl":"10.4196/kjpp.24.363","url":null,"abstract":"<p><p>The 5-hydroxytryptamine type₃ (5-HT₃) receptor, a ligand-gated ion channel, plays a critical role in synaptic transmission. It has been implicated in various neuropsychiatric disorders. This study aimed to elucidate the mechanism by which quetiapine, an atypical antipsychotic, could inhibit 5-HT₃ receptor-mediated currents in NCB20 neuroblastoma cells. Whole-cell patch-clamp recordings were used to study effects of quetiapine on receptor ion channel kinetics and its competitive antagonism. Co-application of quetiapine shifted 5-HT concentration-response curve rightward, significantly increasing the EC50 without altering the maximal response (E_max), suggesting a competitive inhibition. Quetiapine's IC₅₀ varied with 5-HT concentration and treatment condition. The IC₅₀ value of quetiapine was 0.58 μM with 3 μM 5-HT and 25.23 μM with 10 μM 5-HT, indicating an inverse relationship between quetiapine efficacy and agonist concentration. Pretreatment of quetiapine significantly enhanced its inhibitory potency, reducing its IC₅₀ from 25.23 μM to 0.20 μM. Interaction kinetics experiments revealed an IC₅₀ of 5.17 μM for an open state of the 5-HT₃ receptor, suggesting weaker affinity during receptor activation. Quetiapine also accelerated receptor deactivation and desensitization, suggesting that it could stabilize the receptor in non-conducting states. Additionally, quetiapine significantly prolonged recovery from desensitization without affecting recovery from deactivation, demonstrating its selective impact on receptor kinetics. Inhibition of the 5-HT₃ receptor by quetiapine was voltage-independent, and quetiapine exhibited no use-dependency, further supporting its role as a competitive antagonist. These findings provide insights into inhibitory mechanism of quetiapine on 5-HT₃ receptor and suggest its potential therapeutic implications for modulating serotonergic pathways in neuropsychiatric disorders.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"373-384"},"PeriodicalIF":1.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12012313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142848235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aspirin-induced acetylation of APE1/Ref-1 enhances RAGE binding and promotes apoptosis in ovarian cancer cells.","authors":"Hao Jin, Yu Ran Lee, Sungmin Kim, Eun-Ok Lee, Hee Kyoung Joo, Heon Jong Yoo, Cuk-Seong Kim, Byeong Hwa Jeon","doi":"10.4196/kjpp.24.273","DOIUrl":"10.4196/kjpp.24.273","url":null,"abstract":"<p><p>The role of acetylated apurinic/apyrimidinic endonuclease 1/redox factor 1 (APE1/Ref-1) in ovarian cancer remains poorly understood. Therefore, this study aimed to investigate the combined effect of recombinant human APE1/Ref-1 (rhAPE1/Ref-1) and aspirin (ASA) on two ovarian cancer cells, PEO-14, and CAOV3. The viability and apoptosis of ovarian cancer cells treated with rhAPE1/Ref-1 or ASA were assessed. Our results demonstrated that ASA induced rhAPE1/Ref-1 acetylation and widespread hyperacetylation in PEO-14 cells. Additionally, co-treatment with rhAPE1/Ref-1 and ASA substantially reduced cell viability and induced PEO-14 cell apoptosis, not CAOV3, in a dose-dependent manner. ASA increased the expression and membrane localization of the receptor for advanced glycation endproducts (RAGEs). Acetylated APE1/Ref-1 showed enhanced binding to RAGEs. In contrast, RAGE knockdown reduced cell death and poly(ADP-ribose) polymerase cleavage caused by rhAPE1/Ref-1 and ASA combination treatment, highlighting the importance of the APE1/Ref-1-RAGE interaction in triggering apoptosis. Moreover, combination treatment with rhAPE1/Ref-1 and ASA effectively induced apoptosis in 3D spheroid cultures of PEO-14 cells, a model that better mimics the tumor microenvironment. These results demonstrate that acetylated APE1/Ref-1 and its interaction with RAGE is a potential therapeutic target for ovarian cancer. Thus, the combination of ASA and APE1/Ref-1 may offer a promising new strategy for inducing cancer cell death.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"293-305"},"PeriodicalIF":1.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12012317/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143574687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Geraniin attenuates isoproterenol-induced cardiac hypertrophy by inhibiting inflammation, oxidative stress and cellular apoptosis.","authors":"Jiaqi Ding, Shenjie Zhang, Qi Li, Boyu Xia, Jingjing Wu, Xu Lu, Chao Huang, Xiaomei Yuan, Qingsheng You","doi":"10.4196/kjpp.24.200","DOIUrl":"10.4196/kjpp.24.200","url":null,"abstract":"<p><p>Geraniin, a polyphenol derived from the fruit peel of <i>Nephelium lappaceum</i> L., has been shown to possess anti-inflammatory and antioxidant properties in the cardiovascular system. The present study explored whether geraniin could protect against an isoproterenol (ISO)-induced cardiac hypertrophy model. Mice in the ISO group received an intraperitoneal injection of ISO (5 mg/kg) once daily for 9 days, and the administration group were injected with ISO after 5 days of treatment with geraniin or spironolactone. Potential therapeutic effects and related mechanisms analysed by anatomical coefficients, histopathology, blood biochemical indices, reverse transcription-PCR and immunoblotting. Geraniin decreased the cardiac pathologic remodeling and myocardial fibrosis induced by ISO, as evidenced by the modifications to anatomical coefficients, as well as the reduction in collagen I/III á1mRNA and protein expression and cross-sectional area in hypertrophic cardiac tissue. In addition, geraniin treatment reduced ISO-induced increase in the mRNA and protein expression levels of interleukin (IL)-6, IL-1β and tumor necrosis factor-α, whereas ISO-induced IL-10 showed the opposite behaviour in hypertrophic cardiac tissue. Further analysis showed that geraniin partially reversed the ISO-induced increase in malondialdehyde and nitric oxide, and the ISO-induced decrease in glutathione, superoxide dismutase and glutathione. Furthermore, it suppressed the ISO-induced cellular apoptosis of hypertrophic cardiac tissue, as evidenced by the decrease in B-cell lymphoma-2 (Bcl-2)-associated X/caspase-3/caspase-9 expression, increase in Bcl-2 expression, and decrease in TdT-mediated dUTP nick-end labeling-positive cells. These findings suggest that geraniin can attenuate ISO-induced cardiac hypertrophy by inhibiting inflammation, oxidative stress and cellular apoptosis.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"307-319"},"PeriodicalIF":1.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12012319/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142689684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhancing doxorubicin's anticancer impact in colorectal cancer by targeting the Akt/Gsk3β/mTOR-SREBP1 signaling axis with an HDAC inhibitor.","authors":"Huaxin Zhao, Yanling Wu, Soo Mi Kim","doi":"10.4196/kjpp.24.274","DOIUrl":"https://doi.org/10.4196/kjpp.24.274","url":null,"abstract":"<p><p>Colorectal cancer ranks third in global incidence and is the second leading cause of cancer-related mortality. Doxorubicin, an anthracycline chemotherapeutic drug, is integral to current cancer treatment protocols. However, toxicity and resistance to doxorubicin poses a significant challenge to effective therapy. Panobinostat has emerged as a critical agent in colorectal cancer treatment due to its potential to overcome doxorubicin resistance and enhance the efficacy of existing therapeutic protocols. This study aimed to evaluate the capability of panobinostat to surmount doxorubicin toxicity and resistance in colorectal cancer. Specifically, we assessed the efficacy of panobinostat in enhancing the therapeutic response to doxorubicin in colorectal cancer cells and explored the potential synergistic effects of their combined treatment. Our results demonstrate that the combination treatment significantly reduces cell viability and colony-forming ability in colorectal cancer cells compared to individual treatments. The combination induces significant apoptosis, as evidenced by increased levels of cleaved PARP and cleaved caspase-9, while also resulting in a greater reduction in p-Akt/p-GSK-3β/mTOR expression, along with substantial decreases in c-Myc and SREBP-1 levels, compared to monotherapies. Consistent with the <i>in vitro</i> experimental results, the combination treatment significantly inhibited tumor formation in colorectal cancer xenograft nude mice compared to the groups treated with either agent alone. In conclusion, our research suggests that the panobinostat effectively enhances the effect of doxorubicin and combination of two drugs significantly reduced colorectal cancer tumor growth by targeting the Akt/GSK-3β/mTOR signaling pathway, indicating a synergistic therapeutic potential of these two drugs in colorectal cancer treatment.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"29 3","pages":"321-335"},"PeriodicalIF":1.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12012316/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144050860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyaluronan-mediated motility receptor-mediated aerobic glycolysis enhances stem-like properties and chemoresistance in lung adenocarcinoma.","authors":"Wenwen Yu, Yubo Shi, Xiaoqiong Bao, Xiangxiang Chen, Yangyang Ni, Jincong Wang, Hua Ye","doi":"10.4196/kjpp.24.275","DOIUrl":"10.4196/kjpp.24.275","url":null,"abstract":"<p><p>Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan- mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"337-347"},"PeriodicalIF":1.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12012315/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143574618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of telomere-related diagnostic markers in osteoarthritis based on bioinformatics analysis and machine learning.","authors":"Sheng Xu, Jia Ye, Xiaochong Cai","doi":"10.4196/kjpp.24.322","DOIUrl":"https://doi.org/10.4196/kjpp.24.322","url":null,"abstract":"<p><p>Osteoarthritis (OA) is one of the most prevalent joint disorders, with aging considered a primary, irreversible factor contributing to its progression. Telomere-related cellular senescence may be a crucial factor influencing the OA process, yet biomarkers for OA based on telomere-related genes have not been clearly identified. The datasets GSE51588, GSE12021, and GSE55457 were retrieved from the Gene Expression Omnibus database. Initially, R software was utilized to identify differentially expressed genes between OA and normal samples. Subsequently, differentially expressed telomere-related genes (DETMRGs) were obtained, and their functional enrichment was analyzed. Feature genes for OA diagnosis were selected from DETMRGs using a combination of least absolute shrinkage and selection operator, support vector machine-recursive feature elimination, and Random Forest algorithms. The diagnostic value of these feature genes was then validated through receiver operating characteristic (ROC) curves and decision curve analysis. Additionally, CIBERSORT and xCell were employed to assess the infiltration of immune cells in OA tissues. Finally, potential drugs targeting candidate genes were predicted. Three telomere-related genes, <i>PGD</i>, <i>SLC7A5</i>, and <i>TKT</i>, have been identified as biomarkers for OA diagnosis and were confirmed through ROC diagnostic tests. The immune infiltration of mast cells, neutrophils, common lymphoid precursors, and eosinophils associated with <i>PGD</i>, <i>SLC7A5</i>, and <i>TKT</i> was reduced. Recognizing telomere-related genes <i>PGD</i>, <i>SLC7A5</i>, and <i>TKT</i> as potential diagnostic biomarkers for OA is significant, as it offers valuable insights into the role of telomere-related genes in OA. This discovery also provides valuable information for the diagnosis and treatment of OA.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"29 3","pages":"359-372"},"PeriodicalIF":1.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12012318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144026823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}