{"title":"Research Progress of Epigenetic Modifications in Myopia.","authors":"Yinqiao Zhang, Zhaohui Yang, Miao Zhang, Yuanting Yang, Zhongyu Ma, Mengke Wu, Hongsheng Bi, Dadong Guo","doi":"10.7150/ijms.110640","DOIUrl":"10.7150/ijms.110640","url":null,"abstract":"<p><p>Myopia, also known as nearsightedness, refers to a refractive error of the eye that causes parallel rays of light to focus in front of the retina, affecting distance vision. High myopia significantly increases the risk of pathological myopia, leading to severe complications and an increased likelihood of myopia-related eye diseases. In recent decades, the incidence of myopia has continued to rise, posing significant social and human health issues. The complex interplay between genetic and environmental variables affects the development of myopia. Gene control depends to a large extent on epigenetic changes, which are reversible, inheritable, and sensitive to ecological shifts. Therefore, the pathophysiology and development of myopia are tightly linked to gene regulation mediated by epigenetic changes. To explore epigenetic modifications related to myopia, a PubMed search was conducted using keywords such as epigenetic modification, epigenetics, DNA methylation, RNA methylation, non-coding RNA, long non-coding RNA, short interfering RNA, microRNA, ribosomal RNA, circular RNA, transfer RNA, histone modification, histone methylation, and histone acetylation. This review presents the current understanding of these epigenetic modifications in myopia to provide new insights for advancing myopia research.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 12","pages":"3084-3100"},"PeriodicalIF":3.2,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12243994/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626273","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":"Niclosamide-Modulated Apoptosis and Autophagy in Breast Cancer Cells via Phosphorylated JNK as a Common Regulator.","authors":"Ming-Shan Chen, Tsung-Yi Chen, Shu-Hsin Chen, Shew-Meei Sheu","doi":"10.7150/ijms.106429","DOIUrl":"10.7150/ijms.106429","url":null,"abstract":"<p><p>Autophagy plays critical pro-survival and pro-apoptotic roles in regulating breast cancer death. Niclosamide is a U.S. FDA-approved drug that is used for parasite treatment. Exposure to niclosamide causes apoptosis in several different types of cancer cells, whereas its ability to regulate autophagy remains limited, especially in breast cancer. In this study, we evaluated the relative mechanism by which niclosamide regulates apoptosis and autophagy in breast cancer cells. We found that niclosamide induced G0/G1 cell cycle arrest and apoptosis in MCF-7 and T-47D cells. It also caused the turnover of microtubule-associated protein 1 light chain 3 (LC3-II), an autophagy marker, and arrested autophagosome maturation. Niclosamide-induced apoptosis was inhibited by an autophagy initiator (3-methyladenine) but significantly enhanced by chloroquine, an autophagy blocker. Both Jun-amino-terminal kinase (JNK) and reactive oxygen species (ROS) inhibitors decreased LC3-II accumulation and niclosamide-induced apoptosis. However, the ROS inhibitor reduced the expression of niclosamide-activated p-JNK in MCF-7 cells but not in T-47D cells. In conclusion, blocking autophagy is cytotoxic and promotes niclosamide-induced apoptosis. Phosphorylated JNK is identified for the first time as a common regulator of niclosamide-induced autophagy and apoptosis, acting through ROS-dependent or ROS-independent pathways.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 12","pages":"3120-3131"},"PeriodicalIF":3.2,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12243963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626269","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}
Xinrui Yao, Sitong Dong, Xiao Li, Ouxuan Liu, Yuexin Hu, Yuxuan Wang, Xiangcheng Fan, Bei Lin
{"title":"Causal Relationship between Gut Microbiota and Endometrial Cancer: A Two-Sample Mendelian Randomization Study.","authors":"Xinrui Yao, Sitong Dong, Xiao Li, Ouxuan Liu, Yuexin Hu, Yuxuan Wang, Xiangcheng Fan, Bei Lin","doi":"10.7150/ijms.112922","DOIUrl":"10.7150/ijms.112922","url":null,"abstract":"<p><p>Several relevant reports have shown that changes in the composition of the gut microbiota are related to the pathogenesis of endometrial cancer (EC). However, the causal effect of the gut microbiota on EC remains unknown. A two-sample Mendelian randomization (MR) study was used to assess the causal effects of the gut microbiota on EC, EC with endometrioid histologies and EC with non-endometrioid histologies. The genetic statistics of the gut microbiota, including 18,340 participants, were acquired from the MiBioGen database. The summary statistics of EC, EC with endometrioid histologies and EC with non-endometrioid histologies were obtained from the publicly available Genome-wide Association Study (GWAS) database. Suitable single nucleotide polymorphisms (SNPs) were selected as instrumental variables (IVs) (<i>P</i> < 5×10<sup>-8</sup>, r<sup>2</sup> < 0.001). The causal effects were evaluated via the MR-Egger regression method, the inverse-variance weighted (IVW) method, the weighted median test, the weighted mode test, and the simple mode test. The IVW analysis suggested that <i>Ruminococcusgnavusgroup</i> (OR=0.82, 95%CI=0.78-0.85, <i>P</i>=1.29×10<sup>-17</sup>), <i>Euryarchaeota</i> (OR=0.90, 95%CI=0.87-0.94, <i>P</i>=3.78×10<sup>-6</sup>), and <i>CandidatusSoleaferrea</i> (OR=0.92, 95%CI=0.87-0.98, <i>P</i>=0.01) had protective effects on EC and its subtypes. <i>Gammaproteobacteria</i> (OR=1.29, 95%CI=1.19-1.39, <i>P</i>=2.32×10<sup>-10</sup>) served as a risk factor for EC, and <i>Intestinimonas</i> (OR=1.33, 95%CI=1.10-1.62, <i>P</i>=3.68×10<sup>-3</sup>) had detrimental effects on EC with non-endometrioid histologies. The causal relationship between the gut microbiota and EC was explored through two-sample MR analysis, which is helpful for further understanding the gut microbiota-mediated development mechanism underlying EC.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 12","pages":"3142-3153"},"PeriodicalIF":3.2,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12244081/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626210","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":"Novel Genetic Variants in <i>PATL</i>2 Corresponding to Different Clinical Phenotypes of Female Infertility.","authors":"Xiaotao Yang, Xiangrui Shi, Jing Wang, Jingying Guo, Yinhu Huang, Pan Tang, Yu Zhao, Yanxi Li, Wei Liu, Qinghua Zhang","doi":"10.7150/ijms.109085","DOIUrl":"10.7150/ijms.109085","url":null,"abstract":"<p><p>PATL2, an RNA-binding protein and a translational repressor, plays a crucial role in maintaining mRNA homeostasis during female gametogenesis and early development of embryos. Rare pathogenic variants of its encoding gene have been implicated as causative factors for oocyte, zygote, and embryo maturation arrest (OZEMA), which results in female primary infertility and failed IVF or ICSI attempts. In this study, we identified multiple <i>PATL</i>2 variants carried by three patients from two unrelated families: compound heterozygous missense variants comprising novel c.1373T>C (p.I458T), and reported c.877G>T (p.D293Y); unprecedented homozygous missense variants of recurrent c.839G>A (p.R280Q). Molecular dynamics simulations revealed that variants I458T and D293Y severely damaged structural integrity of the PATL2 protein, strongly suggesting a more pronounced functional impairment than the other variant, R280Q. These computational results are in a good consistency with the corresponding clinical phenotypes and offer a plausible explanation for previously observed decrease of protein abundancy associated with the reported variants in <i>PATL</i>2. Our findings provide more insights into the significant impacts of both novel and recurrent <i>PATL</i>2 variants on female infertility and failed assisted reproduction.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 12","pages":"3132-3141"},"PeriodicalIF":3.2,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12243965/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626270","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}
Eun Ji Han, Ji Won Moon, Ji Min Son, Mihai Oltean, Mats Hellström, Francesco Boccardo, Min Jong Song
{"title":"Predicting the Outcome of Lymphovenous Anastomosis for Lower Extremity Lymphedema through Lymphoscintigraphy.","authors":"Eun Ji Han, Ji Won Moon, Ji Min Son, Mihai Oltean, Mats Hellström, Francesco Boccardo, Min Jong Song","doi":"10.7150/ijms.111506","DOIUrl":"10.7150/ijms.111506","url":null,"abstract":"<p><p><b>Background:</b> Lymphovenous anastomosis (LVA) is an effective treatment for restoring lymphatic function in patients with lymphedema. This study aimed to assess the predictive value of preoperative lymphoscintigraphy in female patients undergoing LVA for lower extremity lymphedema (LEL). <b>Methods:</b> Female patients with unilateral LEL who underwent preoperative lymphoscintigraphy followed by LVA were retrospectively examined. In the lymphoscintigraphy, the transport index (TI) was calculated based on five visual interpretation criteria: lymphatic transport kinetics, dermal backflow pattern, time to appearance of lymph nodes, visualization of lymph nodes, and visualization of vessels. For volume assessment, the LEL index (LELI) was calculated as the sum of circumferences at five predefined sites of the lower extremity, divided by body mass index. LELI was measured before and after LVA at 1, 3, and 6 months. Postoperative changes in LELI were compared with preoperative variables, including TI. <b>Results:</b> The study included 45 female patients (mean age 56 ± 10 years) with unilateral LEL, of whom 78% had clinical stage 3 lymphedema. The mean TI of the affected lower extremities at 240 and 120 min was 25.5 ± 11.0 and 26.5 ± 11.1, respectively. TI was significantly associated with clinical stage and preoperative volume excess. Postoperatively, the mean LELI reduction was 7 ± 5% at 1 month, 8 ± 5% at 3 months, and 6 ± 7% at 6 months. Significant negative correlations were found between the TI at both 240 and 120 min and postoperative LELI changes at 3 and 6 months (p < 0.05). <b>Conclusions:</b> Preoperative lymphoscintigraphy, specifically the TI, is valuable for assessing the severity of lymphedema and predicting short-term outcomes of LVA in female patients with LEL. The TI can be calculated from lymphoscintigraphy performed up to 2 h.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 13","pages":"3174-3181"},"PeriodicalIF":3.2,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788968","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":"Identification of IGF2BP3 for the Expression and Prognosis in Gastrointestinal Cancers.","authors":"Fengfeng Han, Chen He, Chen Qian, Yujie Wang, Mingge Zhou, Ruirui Yang, Zhou Zhang","doi":"10.7150/ijms.114411","DOIUrl":"10.7150/ijms.114411","url":null,"abstract":"<p><p><b>Purpose</b>: This study investigates the expression, diagnostic, and prognostic significance of IGF2BP3 in gastrointestinal cancers, providing new insights for clinical management and patient care. <b>Methods</b>: An integrated approach was used to analyze the expression and mutation of IGF2BP3 across various cancers, utilizing multiple online analytical tools. Data from the TCGA database were examined to identify differentially expressed genes (DEGs) in four types of gastrointestinal cancers and to assess the specific expression of IGF2BP3. Further validation was carried out through western blotting (WB), quantitative real-time PCR (qRT-PCR), and immunohistochemistry (IHC). Protein-protein interaction (PPI) network was also employed to investigate the relationships between IGF2BP3 and its associated genes. Additionally, bioinformatics databases were used to investigate the impact of IGF2BP3 on the diagnosis and prognosis of these cancers. <b>Results</b>: High expression of IGF2BP3 is a notable feature across these four gastrointestinal cancers, as demonstrated in public databases. Confirmation in cancer cells and tissues support this observation. Clinicopathological analysis reveals significant associations between IGF2BP3 expression and cancer stages in gastric cancer, and with cancer grades in liver cancer. The diagnostic accuracy of IGF2BP3 is found to be highest for esophageal cancer. Moreover, elevated IGF2BP3 levels correlate with poorer overall survival (OS) and progression-free survival (PFS) in liver cancer patients. <b>Conclusions</b>: This study underscores the significant expression of IGF2BP3 in gastrointestinal cancers and its potential value in both diagnostic and prognostic assessments. These findings could enhance diagnostic accuracy and support the development of targeted therapeutic strategies.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 13","pages":"3191-3201"},"PeriodicalIF":3.2,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320697/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788965","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>IL1A</i> regulates MSU-induced apoptosis and inflammatory response through TLR4/MyD88/NF-κB signaling pathway.","authors":"Fei Pan, Yun Zhang, Min Li, Mei Liu","doi":"10.7150/ijms.112102","DOIUrl":"10.7150/ijms.112102","url":null,"abstract":"<p><p><b>Background:</b> The increased inflammation associated with interleukin-1α (<i>IL-1A</i>) induced by monosodium urate (MSU) crystal-induced gouty arthritis is mediated through the NLRP3 inflammasome and NF-κB signaling pathways. This study investigated the role of <i>IL1A</i> in MSU-mediated inflammation and its therapeutic potential. <b>Methods:</b> MSU crystals were applied to THP-1 macrophages and human vascular endothelial cells (HUVECs) with or without <i>IL1A</i> knockdown. Quantitative reverse transcription polymerase chain reaction (qRT-PCR), western blotting (WB), cell counting kit-8 (CCK-8), flow cytometry, and enzyme-linked immunosorbent assay (ELISA) were used to assess <i>IL1A</i> expression, cell viability, apoptosis, and the generation of inflammatory cytokines. The activation of the NLRP3 inflammasome and TLR4/MyD88/NF-κB pathways was evaluated, with TAK-242 used to assess synergistic effects. <b>Results:</b> MSU increased <i>IL1A</i> expression, induced apoptosis, and reduced cell viability in HUVECs, effects reversed by <i>IL1A</i> knockdown. <i>IL1A</i> knockdown media mitigated apoptosis in HUVECs exposed to conditioned media from MSU-stimulated THP-1 macrophages. <i>IL1A</i> knockdown reduced MSU-induced proinflammatory cytokines and NLRP3 activation in THP-1 cells. TAK-242 showed synergistic effects, while <i>IL1A</i> knockdown inhibited TLR4/MyD88/NF-κB activation. <b>Conclusions:</b> <i>IL1A</i> promotes cell death and inflammation in MSU-induced gout. Knockdown of <i>IL1A</i> mitigates these effects, suggesting it may be a potential therapeutic target for MSU-induced inflammation.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 12","pages":"3070-3083"},"PeriodicalIF":3.2,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12244086/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626262","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}
Alberto Vilar Tabanera, Manuel Díez Alonso, Yousef Allaoua, Lucas Casalduero, Fernando Mendoza Moreno, Félix Mañes, Belén Matías, Lucía Diego, Cristina Vera Mansilla, Laura Castellá Bataller, Raúl Diaz-Pedrero, Miguel A Ortega, Melchor Álvarez de Mon, Alberto Gutiérrez
{"title":"Tumor Deposits in Non-Metastatic Colorectal Cancer as a Risk Factor of Peritoneal Metastasis.","authors":"Alberto Vilar Tabanera, Manuel Díez Alonso, Yousef Allaoua, Lucas Casalduero, Fernando Mendoza Moreno, Félix Mañes, Belén Matías, Lucía Diego, Cristina Vera Mansilla, Laura Castellá Bataller, Raúl Diaz-Pedrero, Miguel A Ortega, Melchor Álvarez de Mon, Alberto Gutiérrez","doi":"10.7150/ijms.113099","DOIUrl":"10.7150/ijms.113099","url":null,"abstract":"<p><p><b>Background:</b> Although tumor deposits (TD) have been known for almost a century, their origin and mode of spread remain controversial. The main objective is to analyze the prognostic value of tumor deposits in non-metastatic colorectal cancer as a risk factor of global recurrence, locoregional recurrence, liver and lung metastasis and specially for peritoneal metastasis (PM). <b>Methods</b>: This study analyzed 1,425 non-metastatic colorectal cancer patients. Four groups were built, according to the presence or absence of Lymph Node Metastasis (LNM) or TD. <b>Results</b>: The global recurrence rate in patients with TDs was significantly higher than those without TDs (17.8% vs 60.8%; p<0.001). Patients with TDs had a lower survival and suffered higher rates of liver metastasis (8.6% vs 26.7%; p<0.001); OR of 4.244 (95% CI: 3.004-5.994) and lung metastasis (7.4% vs 19.3%; p<0.001); (OR 3.585;95% CI: 2.397-5.362). However, the main differences were found in PM (4.7 % vs 26.1 %; p<0.001); (OR: 7.511 (95% CI:5.092-11.079). Distribution by groups shows that patients with TD and LNM had a higher rate of PM. Patients with TD without any LMN had higher PM rate than those with LNM without TD. In stage III, patients with TD suffered higher rates of PM, (26.1% vs 10.9%); p< 0.001). OR: 3.075 (95% CI: 1.969-4.803). <b>Conclusions</b>: The presence of TD increases the risk of peritoneal metastasis. Patients with TD without LNM had higher rate of peritoneal metastasis than those with LNM without TD. TD have independent prognostic value and provide complementary information. Prognostic value of TDs is underestimated in the current TNM system.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 13","pages":"3162-3173"},"PeriodicalIF":3.2,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320696/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788988","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":"Ginsenoside Rh7 affects β-catenin nuclear translocation by inhibiting <i>SHCBP1</i> expression, thereby inhibiting epithelial-mesenchymal transition in gastric cancer cells.","authors":"Xiaohong Zhang, Yanqing Mo, Li Feng","doi":"10.7150/ijms.112622","DOIUrl":"10.7150/ijms.112622","url":null,"abstract":"<p><p><b>Background:</b> Ginsenoside Rh7 is a bioactive compound with anticancer properties. This investigation was conducted to analyze the anticancer effects of ginsenoside Rh7 and its underlying molecular mechanisms in gastric cancer (GC) cells. <b>Methods:</b> The key gene module associated with GC was identified through weighted gene co-expression network analysis (WGCNA) of the GSE118897 dataset. Differentially expressed genes (DEGs) were examined in The Cancer Genome Atlas-Stomach Adenocarcinoma (TCGA-STAD) and the GSE118897 datasets. The central genes of this study were subsequently identified by intersection analysis and protein-protein interaction (PPI) network. Transcriptome sequencing evaluated the changes in <i>SHCBP1</i> expression in GC cells treated with Rh7. Immunoprecipitation (IP) was employed to analyze the relationship between β-catenin and <i>SHCBP1</i>. Functional assays, including Transwell, cell counting kit-8 (CCK-8), colony assays, and <i>in vivo</i> tumor models, evaluated the effects of Rh7 and <i>SHCBP1</i> on GC cell behaviors. <b>Results:</b> <i>SHCBP1</i> was upregulated in tumor samples in GSE118897 and TCGA-STAD. Ginsenoside Rh7 inhibited GC cell invasion, migration, and proliferation dose-dependently by downregulating <i>SHCBP1</i> expression. Transcriptome analysis confirmed Rh7-mediated <i>SHCBP1</i> inhibition. Rh7 promoted β-catenin nuclear translocation by reducing <i>SHCBP1</i> expression. Rescue experiments demonstrated that the overexpression of <i>SHCBP1</i> partially counterbalanced the impacts of Rh7 on epithelial-mesenchymal transition (EMT) regulation and GC cell growth <i>in vitro</i> and <i>in vivo</i>. <b>Conclusion:</b> Ginsenoside Rh7 suppresses GC progression by regulating SHCBP1-mediated β-catenin nuclear translocation, thereby inhibiting EMT, proliferation, migration, and invasion. This highlights its potential as a GC therapeutic drug and deserves further study of its mechanism of action.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 12","pages":"3053-3069"},"PeriodicalIF":3.2,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12244034/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626265","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}
Juan Tian, Xiaoyu Ding, Xiaoying Ren, Guang Wang, Wei Wang, Jia Liu
{"title":"Association between Magnesium Depletion Score and Advanced Cardiovascular-Kidney-Metabolic Syndrome Stages in US Adults.","authors":"Juan Tian, Xiaoyu Ding, Xiaoying Ren, Guang Wang, Wei Wang, Jia Liu","doi":"10.7150/ijms.115217","DOIUrl":"10.7150/ijms.115217","url":null,"abstract":"<p><p><b>Background:</b> Cardiovascular-kidney-metabolic (CKM) syndrome is highly prevalent. Advanced CKM stages have the potential for multiorgan disease, premature mortality, and excess morbidity. Magnesium deficiency has a prominent impact on the components of CKM syndrome. However, the relationship between magnesium depletion score (MgDS) and the risk of developing advanced stages of CKM syndrome is still unclear. <b>Methods:</b> We used data from the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2018. To investigate the relationship between MgDS categories and advanced CKM stages, we employed weighted multivariable logistic regression. Stratified and interaction analysis was conducted to find whether some demographics and lifestyle factors modified the association. Restricted cubic spline (RCS) analysis was implemented to investigate the dose-response relationships. Additionally, receiver operating characteristic (ROC) curve was plotted to assess the diagnostic accuracy of MgDS for advanced CKM stages. <b>Results</b>: The study population comprised 18,038 participants aged 20 to 79 years. The multivariable logistic regression suggested that high MgDS levels (MgDS = 2 and ≥ 3) were associated with higher odds of having advanced CKM stages compared with low MgDS level (MgDS = 0) in all adjusted models (<i>P</i> < 0.05). Stratified and interaction analysis indicated that PIR had significant effects on the association (<i>P</i> for interaction < 0.05). The RCS regression analyses demonstrated a positive linear association between MgDS and the incidence of advanced CKM stages (P for overall = 0.0003, P for nonlinear = 0.1374). The MgDS predicted the area of the ROC curve of 0.7577 (<i>P</i> < 0.05) and the optimal cutoff value was 2. <b>Conclusions:</b> Magnesium-depleted state as quantified by MgDS (MgDS ≥ 2) is a significant risk factor for advanced CKM stages, which suggests that identifying magnesium deficiency and improving the nutritional status of magnesium might mitigate the risk of advanced CKM stages.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 12","pages":"3101-3111"},"PeriodicalIF":3.2,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12244043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626207","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}