International Journal of Medical Sciences最新文献

{"title":"HK2-mediated Glycolysis Inhibits Mineralization of Cementoblasts Under Compression by Suppressing the Piezo1/Wnt Signaling.","authors":"Zhilong Huang, Hengyu Hu, Ye Meng, Houxuan Li, Lang Lei","doi":"10.7150/ijms.109287","DOIUrl":"10.7150/ijms.109287","url":null,"abstract":"<p><p><b>Background:</b> Orthodontically induced inflammatory root resorption (OIIRR) is a prevalent and severe complication during orthodontic tooth movement (OTM). Glycolysis plays a crucial role in the inflammatory responses. This study aimed to improve the cell compression model and investigate whether Hexokinase 2 (HK2)-mediated glycolysis regulates cementoblasts' mineralization through the mechanosensitive Piezo1/Wnt signaling under compressive force. <b>Methods:</b> Mouse cementoblasts (OCCM-30) were cultured under compressive force with different buffer membranes to mimic the periodontal membrane. The flow cytometry and CCK-8 assay were utilized to evaluate cell apoptosis and viability. Piezo1 and HK2 were knocked down by small interfering RNA (siRNA). The level of Wnt/β-catenin signaling was detected by qRT-PCR and Western blotting, and the cellular localization of β-catenin was detected by immunofluorescence staining. <b>Results:</b> The viability and apoptosis of cementoblasts showed no significant change under compression at 2.0 g/cm² for 12 hours with Polytetrafluoroethylene (PTFE) buffer membrane. HK2-mediated glycolysis was increased in compressed cementoblasts with elevated ratio of the receptor activator of nuclear factor kappa-B ligand/osteoprotegerin (RANKL/OPG) and decreased expression of Piezo1 and mineralization-related markers. The Piezo1 activated Wnt signaling by increasing the nuclear translocation of β-catenin, which increased the levels of mineral-related markers. Whereas, knockdown of Piezo1 showed the opposite trend. Knockdown of HK2 to inhibit glycolysis partially reversed the compression-induced decline in Piezo1 and mineralization-related markers, as well as the rise in the RANKL/OPG ratio. <b>Conclusions:</b> The cell compression model with PTFE buffer membrane effectively reduced cell damage. HK2-mediated glycolysis inhibited mineralization and enhanced osteoclast induction in cementoblasts under compression by suppressing the mechanosensitive Piezo1/Wnt signaling.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 13","pages":"3316-3328"},"PeriodicalIF":3.2,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320793/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788963","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":"Cardiovascular and brain effects of liraglutide in transthyretin amyloidosis (ATTR) mice models.","authors":"Mengqing Zhang, Zonglin Li, Xiaoling Cai, Fang Lv, Xin Wen, Chengcheng Guo, Chu Lin, Linong Ji","doi":"10.7150/ijms.112264","DOIUrl":"10.7150/ijms.112264","url":null,"abstract":"<p><p><b>Aim</b>: The effects of glucagon-like peptide-1 receptor agonists (GLP-1RAs) in hereditary transthyretin amyloidosis (ATTRv) remain uncertain. This study aims to investigate whether liraglutide interacts with transthyretin protein (TTR) and thereby exerts therapeutic effects for ATTRv. <b>Methods</b>: High throughput screening was conducted to characterize the drug targets of liraglutide, and microscale thermophoresis was used to observe direct binding of liraglutide to TTR. Humanized RBP4/TTR (normal)and RBP4/TTR^Val50Met (ATTRv) mice were constructed, and treated with liraglutide (0.3mg/kg/d) or placebo for 28 days. Fasting plasma glucose, intraperitoneal glucose tolerance test (IPGTT), and plasma brain natriuretic peptide (BNP) were measured. Brain and cardiac tissues were processed with western blot, enzyme-linked immunosorbent assay (ELISA), real-time quantitative polymerase chain reaction (PCR), and pathological staining to evaluate the lesion status in corresponding organs. <b>Results:</b> Liraglutide exhibited high affinity and direct combination ability to TTR. In ATTRv mice, liraglutide significantly decreased the contents of TTR protein in brain compared with placebo. However, the cardiovascular prognosis measurements including heart failure (plasma BNP concentrations), cardiac fibrosis (the relative expression levels of <i>Cola1</i> and <i>TGFβ1</i> in cardiac tissues), and pathological changes (right ventricular collagen percentage, ventricular septum thickness, left ventricular wall thickness, and left ventricular internal diameter) were statistically comparable between mice receiving liraglutide and placebo treatment. <b>Conclusion:</b> Liraglutide could decrease the deposition of TTR in brain tissues, while it did not improve cardiovascular outcomes in ATTRv mice compared to placebo. More researches regarding the mechanisms and therapeutic effects of GLP-1RAs to ATTRv are still required.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 13","pages":"3229-3241"},"PeriodicalIF":3.2,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320650/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788958","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":"Primary cilia and their role in preeclampsia.","authors":"Lingyun Liao, Rong Zhou, Min Liu","doi":"10.7150/ijms.114433","DOIUrl":"10.7150/ijms.114433","url":null,"abstract":"<p><p>Preeclampsia is a hypertensive disorder of pregnancy characterized by chronic placental ischemia and systemic maternal organ damage. The placenta is rich in blood vessels containing various types of cells, and preeclampsia is now widely accepted as a placenta-derived disease. Although the primary cilium regulates many diseases, its role in preeclampsia has not been comprehensively studied. Therefore, we conducted a review to provide valuable insights into the current understanding of the pathogenesis of preeclampsia, especially as related to the primary cilium, and to provide direction for new research objectives. Primary cilia are sensory microtubule-based organelles that translate extracellular clues into intracellular signals for molecular and cellular responses. They are crucial for the regulation of vascular development and have various mechanisms, such as epithelial-to-mesenchymal transition, reaction to mechanical stress, and mediation of signal transduction. Dysfunction of the primary cilia contributes to aberrant fluid sensing or signal transduction, resulting in vascular disorders. Here, we summarize that angiogenic factors or inflammatory cytokines change the biological behaviors and functions of placental cells in preeclampsia by altering the length or signaling function of primary cilia. We further outline the role of the primary cilia in vascular endothelial function and other female reproductive disorders. Further research is needed to understand the underlying mechanisms and clinical treatment of primary ciliary deficiency in preeclampsia.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 13","pages":"3260-3267"},"PeriodicalIF":3.2,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788969","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":"Single-Gene Mutations in Hepatocellular Carcinoma: Applications and Challenges in Precision Medicine.","authors":"Haiyang Yu, Xiangxiang Wu, Yiting Liu, Congling Xin, Yu Zhou, Xiaoyi Ding","doi":"10.7150/ijms.117603","DOIUrl":"10.7150/ijms.117603","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a genetically heterogeneous malignancy in which single-gene mutations serve as critical drivers of tumor initiation, progression, and therapeutic resistance. Advances in high-throughput genomics and liquid biopsy technologies have highlighted the clinical utility of mutations in genes such as TP53, CTNNB1, and TERT as diagnostic, prognostic, and predictive biomarkers. These mutations disrupt key oncogenic pathways, modulate the tumor immune microenvironment, and contribute to intratumoral heterogeneity, complicating disease management. Mutation-guided precision medicine, including telomerase inhibitors, Wnt/β-catenin pathway modulators, and immune checkpoint blockade, offers promising avenues for individualized treatment in HCC. However, challenges persist in translating these findings into clinical practice due to mutation complexity, resistance mechanisms, and limitations in biomarker standardization. Emerging strategies such as multi-omics integration, artificial intelligence, and gene editing technologies hold potential to overcome these barriers and facilitate the development of personalized therapeutic regimens. This review summarizes the molecular mechanisms, clinical applications, and translational challenges of single-gene mutations in HCC, with the aim of guiding future research and precision oncology.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 13","pages":"3268-3276"},"PeriodicalIF":3.2,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320797/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788985","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":"Association of long noncoding RNA MEG3 genetic variants with the risk of diabetic neuropathy.","authors":"Ying-Chi Fan, Po-Jen Yang, Yu-Fan Liu, Lun-Ching Chang, Shih-Chi Su, Shun-Fa Yang","doi":"10.7150/ijms.112883","DOIUrl":"10.7150/ijms.112883","url":null,"abstract":"<p><p>Diabetic neuropathy (DN), known to result from an interplay of acquired and genetic factors, is a common comorbidity of diabetes characterized by various forms of nerve damage. Maternally expressed gene 3 (MEG3) is an imprinted, non-coding RNA gene originally identified as a tumor suppressor. Recently, dysregulation of MEG3 levels was also observed in various neurodegenerative diseases. In this study, we aimed to investigate the potential association of <i>MEG3</i> gene polymorphisms with the risk for DN through genotyping five single-nucleotide polymorphisms (SNPs) of <i>MEG3</i> gene (rs4081134, rs10144253, rs7158663, rs3087918, and rs11160608) between 712 DN patients and 820 controls (diabetic individuals without neuropathic conditions). Our survey revealed a gender-specific association of rs7158663 with DN. We found that rs7158663 of <i>MEG3</i> gene was associated with an increased risk for DN in diabetic women (GA vs GG, AOR=1.604, <i>p</i>=0.005; GA+AA vs GG, AOR=1.547, <i>p</i>=0.007). Nevertheless, such genetic association was particularly seen in women but not detected in diabetic males. Moreover, a higher level of LDL-cholesterol was noted in female DN patients who carry homozygous major allele of rs7158663 (GG) than in those bearing at least one minor allele (GA+AA) (<i>p</i>=0.016), suggesting an effect of rs7158663 on modulating lipoprotein levels. Taken together, our results demonstrate a link of <i>MEG3</i> gene variants with dyslipidemia and neuropathic conditions in diabetic patients in a gender-specific manner.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 13","pages":"3242-3249"},"PeriodicalIF":3.2,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320800/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788957","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":"Research Progress of Combining High Tibial Osteotomy with Platelet-rich Plasma for Osteoarthritis Therapy.","authors":"Xiangdong Wen, Yichen Zhang, Xingchen Wei, Yang Su, Jinquan Cui, Senbo An, Shui Sun","doi":"10.7150/ijms.114227","DOIUrl":"10.7150/ijms.114227","url":null,"abstract":"<p><p>High tibial osteotomy (HTO) has been widely applied in clinical practice to treat unilateral knee osteoarthritis (OA). In order to improve the effectiveness of surgical treatment, researchers attempted to use a combination of platelet-rich plasma (PRP) and HTO therapy. We summarized the clinical outcomes of engaging HTO and PRP and found promising clinical advantages in improving postoperative pain and function, promoting cartilage repair, and increasing bone cartilage structure in patients. Further studies are needed to provide more convincing evidence of the efficacy of the combined therapy.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 13","pages":"3250-3259"},"PeriodicalIF":3.2,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320795/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788983","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":"Soluble endoglin reflects endothelial dysfunction in myocardial infarction patients: a retrospective observational study.","authors":"J Urbankova Rathouska, J Mrazkova, C Andrys, K Jankovicova, K Tripska, P Fikrova, I Nemeckova, S Eissazadeh, P Wohlfahrt, J Pitha, P Nachtigal","doi":"10.7150/ijms.115222","DOIUrl":"10.7150/ijms.115222","url":null,"abstract":"<p><p>Acute manifestations of ischemic heart disease are among the most serious and fatal consequences of atherosclerotic processes. In this study, we hypothesized that a soluble proprotein convertase subtilisin/kexin type 9 (PCSK9), soluble bone morphogenetic protein 4 (BMP-4), soluble E-selectin (sE-selectin), soluble endoglin (sENG) and soluble endocan (Endocan) would differ from healthy controls in myocardial infarction (MI) patients admitted to the hospital without any previous history of cardiovascular disease and with no cardioprotective drugs taken before admission. The study was conducted using a cross-sectional design. We analyzed data from 79 patients (mean age 54.1 ± 8.9, 18% of women) admitted for the first manifestation of MI and with no history of cardioprotective treatment use before the event. As a control group, we analyzed 17 age-matched healthy volunteers (mean age 51.5 ± 8.6, 47% of women). In addition to routinely obtaining clinical and laboratory data, we analyzed plasma concentrations of the aforementioned biomarkers using ELISA and Luminex analyses. Patients with MI did not differ from healthy controls in total cholesterol, LDL, non-HDL, and triglyceride levels. PCSK9, BMP-4, and sE-selectin levels did not differ significantly between the MI and the control group. Patients with MI had significantly higher sENG and Endocan levels than the control group. In addition, levels of sENG were significantly higher in patients with higher body mass index (BMI) and in smokers. We demonstrated that sENG could serve as a biomarker reflecting endothelial dysfunction in MI patients without prior treatment for cardiovascular risk factors.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 13","pages":"3220-3228"},"PeriodicalIF":3.2,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320647/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788986","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":"Role of Iron Metabolic Disturbances and Inflammatory Iron Biomarkers in Liver Transplant Prognosis.","authors":"Lu Yu, Jun Xu, Ting Que, Zhezhi Miao, Yifeng Zhou, Shuping Que, Shusen Zheng, Zhengtao Liu","doi":"10.7150/ijms.113479","DOIUrl":"10.7150/ijms.113479","url":null,"abstract":"<p><p>Iron metabolism plays a pivotal role in liver transplantation, significantly impacting outcomes for both donors and recipients. The liver, central to iron homeostasis, is often impaired in chronic liver diseases leading to metabolic disorders that exacerbate liver damage. Liver transplantation (LT) is a critical treatment for end-stage liver diseases, with iron status in both donors and recipients influencing post-transplant outcomes. Studies indicate that pre-transplant iron overload in recipients is associated with poor liver function recovery, increased graft rejection risk, and reduced patient survival. The iron metabolic state of donors also affects the functionality of the transplanted liver, impacting transplant success and patient prognosis. Biomarkers such as hepcidin, serum ferritin, and total iron-binding capacity are significant predictors of LT prognosis, yet their specific roles and impacts remain inconclusive. This review systematically assesses how variations in iron metabolic levels of donors and recipients affect patient outcomes following LT, aiming to optimize iron metabolism regulation in clinical management to enhance transplant success, reduce postoperative complications, and improve long-term patient quality of life. Future research should focus on developing personalized iron metabolism management protocols to refine these approaches and enhance transplant care.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 13","pages":"3202-3219"},"PeriodicalIF":3.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320645/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788984","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":"Efficacy and safety of direct oral anticoagulants in patients with venous thrombosis and inherited thrombophilia.","authors":"Amir Warwar, Iren Zargari, Nili Stein, Ibrahim Zoubi, Emad Muhammad, Shoshan Perek, Marwa Naamneh, Meir Preis, Walid Saliba","doi":"10.7150/ijms.108258","DOIUrl":"10.7150/ijms.108258","url":null,"abstract":"<p><p><b>Introduction:</b> Inherited thrombophilia screening is widely performed in patients with venous thromboembolism (VTE). Although recent studies suggest that direct oral anticoagulants (DOACs) may provide comparable efficacy and safety to Vitamin K antagonists (VKAs) in this population, robust evidence to support their extensive use is still lacking. We aimed to evaluate the rates of VTE recurrence and overall bleeding in patients with inherited thrombophilia treated with DOACs versus VKAs, with particular interest in those with severe thrombophilia. <b>Methods:</b> Using the electronic database of the largest healthcare provider in Israel, we conducted a retrospective search for patients with a recorded VTE between 2012 and 2021 (the index event). Patients aged 18 or older at the time of diagnosis were included if they began treatment with either a DOAC or a VKA within 30 days of the index event, provided they had laboratory evidence of inherited thrombophilia. Patients were followed up for two independent outcomes (VTE recurrence and overall bleeding) until December 31, 2022 or until termination of follow-up due to death, switching from one oral anticoagulation class to another, or discontinuation of oral anticoagulation. Rates of VTE recurrence and overall bleeding were compared using Cox regression and reported as hazard ratios (HRs) with 95% confidence intervals (CIs). <b>Results:</b> A total of 398 patients (median age 50.9±17.8, males 51.8%, severe thrombophilia 24.9%) were included. Among these, 230 patients (57.8%) were prescribed DOACs, while 168 patients (42.2%) received VKAs. The median follow-up for VTE recurrence and overall bleeding was 21.1 months and 20 months, respectively. Using the VKAs group as a reference, the hazard ratio for VTE recurrence on DOACs was 1.25 (95% CI, 0.23-6.7), and the hazard ratio for overall bleeding on DOACs was 0.33 (95% CI, 0.03-3.7). Restricting the analysis to 99 patients with severe thrombophilia (46 on DOACs, 53 on VKAs) showed no substantial differences in both efficacy and safety. <b>Conclusions:</b> Among patients with inherited thrombophilia treated with DOACs or VKAs, this study found no significant difference in the risk of recurrent VTE and observed a non-significant trend toward a lower risk of bleeding with DOACs.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 13","pages":"3182-3190"},"PeriodicalIF":3.2,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320646/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788961","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":"Investigation of the Relationship Between University Students' Nomophobia and Psychological Distress: A Cross-sectional Study.","authors":"Rakesh Kumar, Aisha Osman Yousif, Mohammed Ismail Humaida","doi":"10.7150/ijms.112738","DOIUrl":"10.7150/ijms.112738","url":null,"abstract":"<p><p><b>Background:</b> This study investigated the relationship between nomophobia, psychological distress, and demographic factors among students. <b>Methods:</b> This cross-sectional study used a convenience sampling approach to collect data from 723 respondents. The study participants were university students from the University of Ha'il. Distress factors were measured as dependent variables using the Depression Anxiety Stress Scale (DASS)-21, while nomophobia was the independent variable measured using the Nomophobia Questionnaire (NMP-Q). The relationships were assessed using Pearson's correlation, whereas the relationship power of these factors was assessed using hierarchical regression. <b>Results:</b> The study results revealed that four dimensions of nomophobia were significantly correlated with depression, anxiety, stress, and overall DASS-21 scores (p < 0.01). Additionally, nomophobia was significantly associated with distress factors (depression: β = 0.11, p-value < 0.01, anxiety: β = 0.11, p-value < 0.01, stress: β = 0.08, p-value < 0.01). Mobile usage was also significantly associated with the same distress factors (depression: β = 1.67, p-value < 0.01, anxiety: β = 1.65, p-value < 0.01, stress: β = 1.65, p-value < 0.01). Additionally, gender was associated with anxiety (β = 2.75, p-value < 0.01,). <b>Conclusion:</b> Nomophobia significantly exacerbates distress and is a leading cause of stress, anxiety, and depression. The study found that high mobile phone use significantly contributes to psychological distress, which leads to low academic performance, which-in turn-further increases distress.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 12","pages":"3154-3161"},"PeriodicalIF":3.2,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12244064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626267","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}