International Journal of Medical Sciences最新文献

{"title":"Development and Validation of Novel Senescence-TIME Biomarkers for Predicting the Prognosis and Immunotherapy Responsiveness of SKCM Patients.","authors":"Shiying Fan, Shuya Lu, Zilong Wu, Xu Li, Yisong Gao, Gan Mao, Mao Cai, Tianyu Song, Zuojie Peng, Chong Li, Kaixiong Tao, Wei Li","doi":"10.7150/ijms.127285","DOIUrl":"https://doi.org/10.7150/ijms.127285","url":null,"abstract":"<p><strong>Background: </strong>Increasing evidence indicates that tumor cellular senescence can impair antitumor immunity and promote skin cutaneous melanoma (SKCM) progression. However, effective methods for assessing tumor cellular senescent status and tumor immune microenvironment (TIME) status remain lacking. This study intends to establish a novel Senescence-TIME Risk Score (STIRS) based on senescence and TIME related genes to predict prognosis and immunotherapy responsiveness in SKCM patients, thereby providing new strategies for current clinical personalized treatment.</p><p><strong>Methods: </strong>We identified distinct senescent microenvironment patterns using t-distributed stochastic neighbor embedding (t-SNE) based on a set of senescence marker genes and predicted the TIME in SKCM using the estimation of stromal and immune cells in malignant tumor tissues using expression data (ESTIMATE) algorithm. Based on this, we divided the SKCM cohort into three groups: low-senescence & high-immunity, high-senescence & low-immunity, and mixed. We analyzed differentially expressed genes (DEGs) between the first two groups. Gene ontology (GO) enrichment analysis, kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis, gene set enrichment analysis (GSEA), and the construction of protein-protein interaction (PPI) network were used to investigate the functional relevance of DEGs. We screened DEGs using least absolute shrinkage and selection operation (LASSO) regression and random forest (RF) algorithm to construct the STIRS. Patients were grouped by the median of STIRS, and differences in expression of immune cells and immune checkpoints between groups were examined. The predictive capability of STIRS for immunotherapy was validated. Finally, we knocked down the core risk gene in the B16 cell line to validate its function.</p><p><strong>Results: </strong>We identified 994 DEGs predominantly enriched in TIME- and senescence-related pathways. The constructed STIRS comprises six signature genes. Patients in the high-STIRS group exhibited significantly poorer survival than those in the low-STIRS group, and STIRS negatively correlated with immune response and immunotherapy responsiveness. A nomogram integrating STIRS and clinical indicators demonstrated satisfactory predictive performance for SKCM patient prognosis. These findings validate the STIRS model as a reliable independent prognostic indicator. Additionally, knockdown of the core risk gene keratin 17 (KRT17) inhibited the invasion and proliferation of B16 cells, demonstrating the role of KRT17 in the progression of SKCM.</p><p><strong>Conclusion: </strong>This study proposed a novel STIRS model and selected the core risk gene KRT17 for functional validation, which had potential as a prognostic tool and a guide for creating personalized therapies for SKCM patients.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 4","pages":"1209-1224"},"PeriodicalIF":3.2,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13048859/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147622787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reviewing the Peripheral and Central Mechanisms of Visceral Hypersensitivity in Intestinal Disorders.","authors":"Wenhui Tang, Jiarui Wang, Wenlei Wang, Jiamiao Xue, Yuyan Wang, Fuhao Jiang, Dimkpa Christabel Kechiyerunda, Shengli Gao, Tao Yuan, Feifei Guo","doi":"10.7150/ijms.126361","DOIUrl":"10.7150/ijms.126361","url":null,"abstract":"<p><p>Visceral hypersensitivity (VH) is a condition where the internal organs have an enhanced sensitization to normal physiological stimuli or mild pathological stimuli, leading to chronic visceral pain or other discomforts, which is a typical characteristic of some intestinal disorders, such as irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD). VH might be caused by gene, psychological disorders, social stress factors, gut microbiota, and some other factors, but the exact mechanisms are not yet clear. This review focuses on recent developments in the effect of intestinal cells on sensitization of nociceptors, high excitability of brain nuclei regulating visceral pain, and the novel roles of gut microbiota in VH. It is hoped to synthesize research advancements to demonstrate the possible peripheral and intracerebral processes of hypersensitization. Additionally, more animal experiments and clinical studies are still needed to improve our understanding about VH to reduce the suffering of patients with IBS and IBD.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 3","pages":"1121-1143"},"PeriodicalIF":3.2,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12965073/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147377319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibitory effects of patchouli alcohol on hepatocellular carcinoma growth through accumulation of oxidative stress and inactivation of androgen receptor signaling.","authors":"Xiao-Fan Huang, Kai-Fu Chang, Nu-Man Tsai","doi":"10.7150/ijms.123787","DOIUrl":"https://doi.org/10.7150/ijms.123787","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is one of the most frequently diagnosed malignancies and exhibits a high mortality rate. Patchouli alcohol (PA) is a tricyclic sesquiterpene derived from <i>Pogostemon cablin</i>, and the present study evaluated the antihepatoma capacity of PA and described a potential strategy for its combination with sorafenib (SOR) <i>in vitro</i> and <i>in vivo</i>. The anticancer potential of PA against HCC was evaluated using the MTT assay, flow cytometry, western blotting, DCF-DA and JC-1 staining, TUNEL assay, immunofluorescence and immunohistochemistry staining, and migration and invasion assays. The results indicated that PA suppressed HCC growth by inducing reactive oxygen species (ROS) generation, mitochondrial membrane potential imbalance, and DNA damage, ultimately resulting in cell cycle arrest and apoptosis via the activation of p53/p21 and also extrinsic (Fas/FasL/caspase-8), intrinsic (Bax/Bcl2/caspase-9), and caspase-independent pathways. The combination of PA with SOR exhibited synergistic effects, exerted survival benefits, and improved the lifespan of mice at well-tolerated doses. Furthermore, PA targets the androgen receptor (AR) to inhibit dihydrotestosterone-induced (DHT)-induced cell proliferation, AR translocation to the nucleus, and downstream gene expression during HCC growth. On the whole, PA alone or in combination with SOR exhibited markedly improved therapeutic efficacy in HCC by blocking AR-mediated and multiple other signaling pathways. Therefore, this study provides an experimental basis for the evaluation of PA as an alternative drug (alone or in combination) for the treatment of HCC.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 4","pages":"1174-1189"},"PeriodicalIF":3.2,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13048856/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147622790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low-Intensity Extracorporeal Shock Wave Therapy Alleviates Detrusor Muscle Apoptosis and Extracellular Matrix Dysregulation in the Bladder of Diabetic Rats.","authors":"Yau-Hsuan Tsau, Hsun-Shuan Wang, I-Hsuan Tsai, Miao-Yi Wu, Chia-Chu Liu, Tusty-Jiuan Hsieh, Yung-Chin Lee","doi":"10.7150/ijms.121078","DOIUrl":"10.7150/ijms.121078","url":null,"abstract":"<p><p>Diabetic bladder dysfunction (DBD) affects 80% of diabetic patients, especially women. Yet, the management of DBD remains inconclusive. Building on our previous findings in animal models, low-intensity extracorporeal shock wave therapy (Li-ESWT) seems to be a promising potential therapy for DBD. However, the molecular mechanisms underlying the therapeutic effect of Li-ESWT on DBD still need to be clarified. To elucidate the molecular pathways involved in the therapeutic effect of Li-ESWT on DBD, a diabetic rat model was established using a high-fat diet in combination with streptozotocin (STZ) induction. Female Sprague-Dawley rats were randomly assigned to three groups: control, diabetes mellitus (DM), and DM treated with Li-ESWT for four weeks. To induce diabetes, the rats received a high-fat diet followed by two intraperitoneal injections of STZ (30 mg/kg), administered one week apart. Li-ESWT was delivered once weekly for four weeks, using an energy flux density of 0.03 mJ/mm², 500 shocks per session, at a frequency of 3 Hz. Our findings indicate that Li-ESWT significantly ameliorates pathological bladder changes, including muscle atrophy, apoptosis, and fibrosis, in diabetic rats. The expression of α-smooth muscle actin, a key component of the smooth muscle cytoskeleton, was markedly reduced in diabetic bladders but was partially restored following Li-ESWT treatment. Additionally, elevated levels of cleaved caspase-3, transforming growth factor-β1, and collagen I observed in diabetic bladders were attenuated by Li-ESWT. In summary, Li-ESWT exerts restorative effects on the detrusor smooth muscle, suggesting its potential to reverse structural and functional abnormalities in diabetic bladder dysfunction.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 3","pages":"1161-1173"},"PeriodicalIF":3.2,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12965066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147377431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Artemisia argyi</i>-enhanced Mesenchymal Stem Cell Exosomes Alleviates Inflammation in C28/I2 Chondrocytes by inhibiting NF-κB.","authors":"Shih-Wen Kao, Yu-Ting Hsu, Wei-Wen Kuo, Tai-Lung Huang, Kuan-Ho Lin, Chia-Hua Kuo, Dennis Jine-Yuan Hsieh, Tsung-Jung Ho, Shinn-Zong Lin, Chih-Yang Huang","doi":"10.7150/ijms.126119","DOIUrl":"10.7150/ijms.126119","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a degenerative joint disease with chronic inflammation, causing joint damage and function loss. Current treatments relieve symptoms but don't halt disease progression, highlighting the need for new therapies. Research shows mesenchymal stem cells (MSCs) can repair joints and reduce inflammation, but direct MSC injection may cause immune rejection, making MSC-derived exosomes a promising alternative. <i>Artemisia argyi</i> (AA) has antioxidant, anti-inflammatory, and anti-ageing effects that enhance stem cell function and cellular stability, making it a potential therapy for OA. This study explores whether AA extract can enhance exosomes from Wharton's jelly stem cells (WJSCs) for OA treatment. Results revealed that AA promoted WJSCs proliferation and increased both the yield and size of exosomes. Furthermore, AA-enhanced exosomes significantly suppressed NF-κB pathway related proteins (p-IKKα/β and p-NF-κB) and the matrix degrading protein MMP13 while increasing the expression of the cartilage extracellular matrix protein COL2A1, resulting in a greater reduction of NF-κB signaling proteins and MMP13 expression, along with increased COL2A1 levels. Additionally, these exosomes effectively reversed H₂O₂-induced ROS accumulation, with antioxidant effects surpassing those of untreated exosomes. Further studies using NF-κB activators confirmed that the therapeutic effects of these exosomes were primarily mediated by inhibition of the NF-κB signalling pathway. In conclusion, AA-enhanced WJSCs exosomes improved the proliferation, anti-inflammatory, and antioxidant capacities of C28/I2 chondrocytes under oxidative stress. These findings highlight their potential to reduce ROS levels, regulate pro-inflammatory proteins, and inhibit the NF-κB pathway, offering a promising strategy for protecting cartilage against damage caused by inflammatory joint diseases.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 3","pages":"1092-1104"},"PeriodicalIF":3.2,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12965070/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147377442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Visnagin Protects Against Lipopolysaccharide-Induced Acute Kidney Injury by Inhibiting Oxidative Stress and Reducing Ferroptosis.","authors":"Sheng-Wen Wu, Chen-Yu Chiang, Chien-Ying Lee, Shiuan-Shinn Lee, Wen-Ying Chen, Chun-Jung Chen, Ching-Chi Tseng, Yin-Che Lu, Yu-Hsiang Kuan","doi":"10.7150/ijms.125642","DOIUrl":"10.7150/ijms.125642","url":null,"abstract":"<p><strong>Background and objective: </strong>Sepsis-associated acute kidney injury (SA-AKI) is a life-threatening condition driven by oxidative stress, ferroptosis, and inflammation, yet effective treatments remain unavailable. Visnagin has antioxidant and anti-inflammatory properties and has been traditionally used for cardiovascular and renal disorders, but its role in modulating ferroptosis and redox imbalance in SA-AKI remains unclear. Thus, the study investigated the renoprotective effects of visnagin in a murine lipopolysaccharide (LPS)-induced AKI model, focusing on oxidative stress and ferroptosis.</p><p><strong>Methods: </strong>A systems pharmacology approach integrating network-based target prediction and molecular docking identified candidate targets. In vivo and in vitro validations in LPS-induced AKI mice and HK-2 cells assessed histopathology, oxidative biomarkers, ferroptosis mediators, and key signaling pathways.</p><p><strong>Results: </strong>Visnagin demonstrated affinity binding to <i>AKT1</i>, <i>NFE2L2</i>, <i>ACSL4</i>, and <i>TFRC</i>, indicating a potential role in modulating oxidative stress and ferroptosis. In vivo, visnagin alleviated renal injury, reduced lipid peroxidation, and downregulated ACSL4 and TfR1 expression, with this accompanied by reduction in renal Fe²⁺ levels. Although visnagin reduced the protein abundance of SOD, catalase, and GSH-Px, it markedly enhanced their enzymatic activities, likely due to decreased oxidative burden and preservation of enzyme functionality under LPS-induced stress. Additionally, visnagin inhibited p-Akt and p-Nrf2, suggesting suppression of upstream signaling pathways. In vitro, visnagin reduced intracellular ROS levels in HK-2 cells and exhibited scavenging activity against various radical species.</p><p><strong>Conclusions: </strong>Visnagin exerts protective actions through both modulation of Akt/Nrf2 signaling ACSL4/TfR1 signaling and direct free radical scavenging. These findings underscore visnagin's potential as a multitarget therapeutic agent for SA-AKI.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 3","pages":"1105-1120"},"PeriodicalIF":3.2,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12965074/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147377366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LIPUS as a potential strategy for anti-inflammation and repair: A review of the mechanisms.","authors":"Gaocheng Wang, Jianping Zhao, Jiaxuan Li, Zhanguo Zhang, Wanguang Zhang, Qian Chen, Jingjing Wang","doi":"10.7150/ijms.124996","DOIUrl":"10.7150/ijms.124996","url":null,"abstract":"<p><p>Hundreds of millions of people worldwide endure continuous suffering and significant economic burdens due to inflammatory diseases. Various acute and chronic inflammatory diseases and the natural aging of the human body are common causes of organ damage. Therefore, how to reasonably regulate inflammation, tissue repair and regeneration after organ damage has been of great concern, especially the pathological repair caused by inflammation will lead to the destruction of the original structure and function of tissues and organs. Low-intensity pulsed ultrasound (LIPUS) is a promising non-invasive physical therapy that can produce different biological effects on organs, tissues and cells. Certain clinical trials have demonstrated the outstanding capacity of LIPUS in anti-inflammation and repair. Many <i>in vivo</i> and <i>in vitro</i> basic studies have also reported the molecular effect mechanisms by which LIPUS exerts capacity of anti-inflammation and repair. This review focuses on the molecular mechanism of LIPUS anti-inflammation and repair and emphasizes the crucial role of LIPUS in various diseases. In addition, we compile clinical trials to provide readers with a more thorough understanding of the current potential of LIPUS in inflammation control and organ function restoration.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 3","pages":"1144-1160"},"PeriodicalIF":3.2,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12965064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147377450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated analysis uncovers <i>KCMF1</i> genetic susceptibility and the <i>SNRPD2</i> axis in renal cell carcinoma.","authors":"Jiunn-Bey Pao, Yu-Mei Hsueh, Pei-Ling Chen, Tzu-Hao Huang, Chia-Yang Li, Jiun-Hung Geng, Te-Ling Lu, Chao-Yuan Huang, Shu-Pin Huang, Bo-Ying Bao","doi":"10.7150/ijms.129880","DOIUrl":"https://doi.org/10.7150/ijms.129880","url":null,"abstract":"<p><p>The ZZ-type zinc-finger family has emerged as an important regulator of tumorigenesis; however, its roles in renal cell carcinoma (RCC) susceptibility and prognosis are largely unexplored. This study aimed to systematically evaluate the genetic variants within this gene family to identify novel risk drivers and elucidate their downstream pathogenic networks. A total of 148 single-nucleotide polymorphisms (SNPs) were genotyped across 17 ZZ-type zinc finger genes in a cohort of 630 Taiwanese participants (312 patients with RCC and 318 healthy controls). The results were validated using pooled transcriptomic analysis of 18 independent datasets. Weighted gene co-expression network analysis (WGCNA) was used to construct tumor-specific networks and identify key driver genes. The Asian-specific variant of <i>KCMF1</i> rs146409312 emerged as a significant susceptibility locus. The minor A allele conferred a 3.38-fold increased risk of RCC (adjusted odds ratio = 3.22, 95% confidence interval = 1.57-6.58, <i>p</i> = 0.001). <i>KCMF1</i> was consistently upregulated in tumor tissues and was associated with poor patient survival. WGCNA identified a clinically relevant <i>KCMF1</i>-associated gene module enriched in ribosomal biogenesis and MYC target signaling. Within this network, <i>SNRPD2</i> was identified as a critical hub gene, and its overexpression was strongly correlated with advanced tumor grade, stage, and reduced overall survival (<i>p</i> < 0.001). In conclusion, <i>KCMF1</i> rs146409312 was identified as a potent, population-specific risk factor for RCC. A pathogenic <i>KCMF1</i>-driven network converging on <i>SNRPD2</i> was delineated, offering novel insights into RCC etiology and highlighting potential biomarkers for prognostic stratification.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 4","pages":"1198-1208"},"PeriodicalIF":3.2,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13048855/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147622830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fermented <i>Clostridium butyricum</i> GKB7 Inhibits Osteoarthritis Induced by Anterior Cruciate Ligament Transection in a Preclinical Model.","authors":"Wei-Cheng Chen, Li-Chai Chen, You-Shan Tsai, Yen-Po Chen, Yen-Lien Chen, Chin-Chu Chen, Yen-You Lin, Tzu-Ching Chang, Chen-Ming Su, Chih-Hsin Tang","doi":"10.7150/ijms.126850","DOIUrl":"https://doi.org/10.7150/ijms.126850","url":null,"abstract":"<p><p>Aging-related osteoarthritis (OA) affects joints and causes functional impairment. Probiotics are recognized safe for consumption and numerous exhibit beneficial bioactivity for human health conditions. <i>Clostridium butyricum</i>, frequently found in the environment and reported to colonize the stomachs of adults and newborns, exhibits anti-inflammatory properties. This study investigated whether fermented <i>Clostridium butyricum</i> GKB7 is effective at preventing the advancement of OA. Fermented GKB7 reduces bone pain and the development of OA associated with anterior cruciate ligament transaction. Through the reduction of pro-inflammatory cytokines IL-1β and TNF-α, as well as the chondrolytic factors MMP-3, MMP-13, and ADAMTS5, fermented GKB7 inhibited the degradation of aggrecan and COL2A1. Bone loss and cartilage degradation were blocked as a result of this activity. According to our findings, fermented GKB7 enhances the prevention of OA development.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 4","pages":"1190-1197"},"PeriodicalIF":3.2,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13048858/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147622761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gene Mutations and Related Molecular Events in Distant Metastasis of Cervical Cancer: A Review.","authors":"Yinghua Guo, Shilong Li, Tingting Liu, Xiaolong Chang, Peiyan Qin, Nan Wang, Yingxiao Jiang, Na Lv, Niannian Li, Furong Hao","doi":"10.7150/ijms.123727","DOIUrl":"10.7150/ijms.123727","url":null,"abstract":"<p><p>Cervical cancer, a serious gynecological malignancy, often leads to poor patient prognosis due to distant metastasis. The metastasis mechanism is not fully understood. This study explores the link between gene mutations and distant metastasis in cervical cancer. <i>PDGFRA</i>, <i>TP53</i>, and <i>PIK3CA</i> mutations significantly influence metastasis. Despite its low incidence, <i>PDGFRA</i> mutation is closely tied to lymph node and distant metastasis. <i>TP53</i> mutation disrupts p53 protein function, promoting tumor cell proliferation, inhibiting apoptosis, and enhancing metastasis. <i>PIK3CA</i> mutation activates the PI3K/Akt pathway, stimulating cell proliferation and migration. Detecting these mutations is crucial for diagnosing distant metastasis. It helps identify high-risk patients early, improving diagnostic accuracy and specificity, and guiding clinical treatment decisions. Targeted therapies for <i>PDGFRA</i> and <i>PIK3CA</i> mutations can control tumor growth and metastasis but face challenges like drug resistance and high costs. This study offers a new theoretical basis and treatment strategy for cervical cancer, pointing to future research directions. Gene mutation detection enhances early identification of high-risk patients, improving diagnostic accuracy. Targeted therapies for <i>PDGFRA</i> and <i>PIK3CA</i> mutations control tumor growth but face drug resistance and cost issues. This study provides a new theoretical basis and treatment strategy for cervical cancer, guiding future research.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 3","pages":"1015-1032"},"PeriodicalIF":3.2,"publicationDate":"2026-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12964585/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147377425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}