International Journal of Medical Sciences最新文献

{"title":"Risks of cardiovascular disease and cerebrovascular disease following kidney transplantation: A nationwide, population-based cohort study.","authors":"Tung-Han Tsai, Kuang-Hua Huang, Hsin Chen, Shuo-Yan Gau, Kun-Yu Su, Min-Ling Tsai, Chien-Ying Lee","doi":"10.7150/ijms.108744","DOIUrl":"https://doi.org/10.7150/ijms.108744","url":null,"abstract":"<p><p><b>Background:</b> Kidney transplant recipients (KTRs) have an increased risk for cardiovascular disease (CVD) and cerebrovascular disease (CBD). This study investigated the risks of CVD and CBD following kidney transplantation. <b>Materials and methods:</b> This retrospective cohort study enrolled 3596 KTRs between 2003 and 2017. Propensity Score Matching (PSM) was performed to select patients without a kidney transplant, who were assigned to the control group. Each KTR was matched with five patients without a kidney transplant by sex, age, insured salary, urbanization level, Charlson comorbidity index (CCI), and year of inclusion in the study. A Cox proportional hazards model was employed to investigate the risks of incident CVD and CBD in KTRs after adjusting for relevant variables. Furthermore, we analyzed for CVD and CBD risk 6 months and 1, 3, and 5 years after transplantation. <b>Results:</b> Among KTRs, the CVD incidence rate per 1,000 person-years was 33.98, which was significantly higher than that among patients without a kidney transplant. After adjusting for confounding variables, KTRs had a significantly higher risk of CVD (adjusted hazard ratio [aHR], 1.74; 95% confidence interval [CI], 1.58-1.93) than did patients without a kidney transplant. Regarding cumulative incidence, the risk of CVD increased over time. Among the four follow-up periods we assessed, the 5-year follow-up period had the highest CVD risk (aHR, 1.35; 95% CI, 1.17-1.56), followed by the 3-year follow-up period (aHR, 1.34; 95% CI, 1.13-1.59). KTRs also had a significantly higher risk of CBD (aHR, 1.43; 95% CI, 1.23-1.68) than did patients without a kidney transplant. <b>Conclusion:</b> CVD risk is higher among KTRs than among those without a kidney transplant, and this risk increases over time. CBD risk was also higher among KTRs. Large, randomized controlled prospective studies are needed to thoroughly evaluate the relationship between kidney transplantation and the risks of CVD and CBD.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2237-2246"},"PeriodicalIF":3.2,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035839/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144022386","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":"Comprehensive Characterization of the Oxidative Stress Profiles in Neonatal Necrotizing Enterocolitis.","authors":"Xiaofeng Xiong, Luyao Wu, Xin Liu, Jing Wang, Jun Xiao, Ke Chen, Didi Zhuansun, Xinyao Meng, Jiexiong Feng, Xuyong Chen","doi":"10.7150/ijms.109008","DOIUrl":"https://doi.org/10.7150/ijms.109008","url":null,"abstract":"<p><p><b>Objective:</b> This study aims to portray the characteristics of oxidative stress (OS) in cases of Necrotizing enterocolitis (NEC), identify the hub genes and associated mechanisms involved, and explore potential drugs for NEC. <b>Methods:</b> We performed a comprehensive analysis integrating bulk-RNA sequencing and single-cell RNA sequencing datasets, coupled with various techniques including differential analysis, gene set enrichment analysis, and immune infiltration analysis. We aimed to systematically elucidate the variations in functions related to OS among distinct cell populations within both NEC and non-NEC tissues. Additionally, we depicted the longitudinal changes in immune cells, with a particular focus on macrophages, throughout the progression of NEC. NEC mice model was established and RT-qPCR was performed to validate the expression of the hub genes. <b>Results:</b> In total, 465 OS related genes were found, and 53 of them were significantly differentially expressed. These genes were mainly involved in several signaling pathways, such as TNF signaling pathway, IL-17 signaling pathway, FOXO signaling pathway, inflammatory bowel disease. The top 10 hub genes were <i>MMP2</i>, <i>IL1A</i>, <i>MMP3</i>, <i>HGF</i>, <i>HP</i>, <i>IL10</i>, <i>PPARGC1A</i>, <i>TLR4</i>, <i>MMP9</i> and <i>HMOX1</i>. Ten kinds of drug were discovered as the potential treatment for NEC. Four specific macrophages subtypes and relative function were identified in NEC. RT-qPCR and immunofluorescence staining confirmed the expression of the hub genes in NEC model. <b>Conclusions:</b> This investigation yielded innovative insights into the immune environment and therapeutic methodologies directed at oxidative stress in the pathogenesis of NEC.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2139-2154"},"PeriodicalIF":3.2,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035842/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028250","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 insights into the role of ferroptosis in temporomandibular joint osteoarthritis and knee osteoarthritis.","authors":"Yuxin Zhang, Dahe Zhang, Xiaoyu Liao, Qingyu Xu, Lingtong Bu, Jisi Zheng, Pei Shen, Chi Yang","doi":"10.7150/ijms.107057","DOIUrl":"https://doi.org/10.7150/ijms.107057","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by pain, limited movement, and joint stiffness, significantly impacting the quality of life and imposing substantial economic burdens. This review paper delves into the novel insights of ferroptosis, an iron-dependent form of cell death associated with lipid peroxidation, in the context of temporomandibular joint osteoarthritis (TMJ OA) and knee osteoarthritis (KOA). We explore the pathogenic characteristics of OA, including synovitis, chondrocyte death, and extracellular matrix (ECM) degradation, and discuss the limitations of current therapeutic interventions. Emerging evidence suggests a significant relationship between ferroptosis and OA, with iron accumulation and lipid peroxidation observed in osteoarthritic cartilage. This review highlights the role of ferroptosis in chondrocyte malfunction and apoptosis, inflammation, and extracellular matrix breakdown, which are central to OA pathogenesis. We also discuss potential therapeutic targets, such as Transient Receptor Potential Vanilloid 1 (TRPV1), Glutathione Peroxidase 4 (GPX4), and Nuclear Factor Erythroid 2-Related Factor 2 (NRF2), which modulate ferroptosis and OA progression. The paper consolidates studies on ferroptosis in OA, offering a comprehensive understanding of its role and the development of innovative therapies targeting this cell death mechanism to improve treatment outcomes for OA patients.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2119-2131"},"PeriodicalIF":3.2,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035841/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143999724","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":"Heterogeneity of Renal Endothelial Cells, Interact with Neighboring Cells, and Endothelial Injury in Chronic Kidney Disease: Mechanisms and Therapeutic Implications.","authors":"Meiyu Zhang, Wu Liu, Haoran Dai, Hanxue Jiang, Qihan Zhao, Wenbin Liu, Hongliang Rui, Baoli Liu","doi":"10.7150/ijms.108299","DOIUrl":"https://doi.org/10.7150/ijms.108299","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) is closely associated with endothelial dysfunction, leading to symptoms such as albuminuria, edema, and coagulopathy. Recent advancements in single-cell sequencing have deepened our understanding of the heterogeneity of renal endothelial cells, which is significantly influenced by their microenvironment. Understanding the influence of neighboring cells on endothelial heterogeneity is essential for elucidating the mechanisms underlying vascular dysfunction and CKD progression. This review explores the latest research on renal endothelial cell heterogeneity and their interactions with neighboring cells. We further discuss the mechanisms of endothelial injury in CKD, including alterations to the endothelial glycocalyx, inflammation, oxidative stress, and dysfunction of the glomerular filtration barrier. Renal endothelial injury contributes to complications, including cardiovascular disease, diabetic nephropathy, and impaired vascular function. Therapeutic strategies encompass antihypertensive, hypoglycemic, and lipid-lowering treatments, supplemented by emerging approaches such as anti-inflammatory therapies, gene therapy, and lifestyle modifications. Through reviewing the relationship between endothelial injury and CKD progression, we emphasize potential strategies to enhance prognosis and mitigate disease progression.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2103-2118"},"PeriodicalIF":3.2,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144012664","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":"Application and research progress of artificial intelligence in allergic diseases.","authors":"Hong Tan, Xuehua Zhou, Huajie Wu, Min Wang, Han Zhou, Yue Qin, Yun Zhang, Qiuhong Li, Jianfeng Luo, Hui Su, Xin Sun","doi":"10.7150/ijms.105422","DOIUrl":"https://doi.org/10.7150/ijms.105422","url":null,"abstract":"<p><p>Artificial intelligence (AI), as a new technology that can assist or even replace some human functions, can collect and analyse large amounts of textual, visual and auditory data through techniques such as Reinforcement Learning, Machine Learning, Deep Learning and Natural Language Processing to establish complex, non-linear relationships and construct models. These can support doctors in disease prediction, diagnosis, treatment and management, and play a significant role in clinical risk prediction, improving the accuracy of disease diagnosis, assisting in the development of new drugs, and enabling precision treatment and personalised management. In recent years, AI has been used in the prediction, diagnosis, treatment and management of allergic diseases. Allergic diseases are a type of chronic non-communicable disease that have the potential to affect a number of different systems and organs, seriously impacting people's mental health and quality of life. In this paper, we focus on asthma and summarise the application and research progress of AI in asthma, atopic dermatitis, food allergies, allergic rhinitis and urticaria, from the perspectives of disease prediction, diagnosis, treatment and management. We also briefly analyse the advantages and limitations of various intelligent assistance methods, in order to provide a reference for research teams and medical staff.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2088-2102"},"PeriodicalIF":3.2,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035833/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144014492","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":"Reduced risk of diabetic retinopathy in osteoarthritis patients undergoing joint replacement surgery.","authors":"Chin-Te Huang, Yat-Yin Law, Kai Wang, Chia-Yi Lee, Jing-Yang Huang, Shun-Fa Yang, Hsiang-Wen Chien","doi":"10.7150/ijms.109689","DOIUrl":"https://doi.org/10.7150/ijms.109689","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a progressive joint disorder frequently associated with multiple comorbidities. Emerging research suggests a potential link between OA and diabetic retinopathy, a microvascular complication of diabetes mellitus. This study investigates whether joint replacement surgery influences the risk of developing diabetic retinopathy in individuals with OA. Using data from the TriNetX database, we conducted a retrospective cohort study, categorizing OA patients into two groups based on whether they had undergone joint replacement surgery, with each group comprising 164,653 individuals. The primary outcome was the incidence of diabetic retinopathy, analyzed using Cox proportional hazards regression. Among patients who underwent joint replacement surgery, 844 developed diabetic retinopathy, compared to 1,336 cases in the non-surgery group. The incidence of diabetic retinopathy was significantly lower in the surgery group (P < 0.001). Additionally, cumulative incidence analysis confirmed a reduced risk in the surgery group (P < 0.001). Subgroup analyses further demonstrated a consistently lower risk across most demographic subgroups. In conclusion, our findings suggest that joint replacement surgery in OA patients is associated with a reduced risk of developing diabetic retinopathy. Further research is warranted to explore the underlying mechanisms and potential clinical implications.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2132-2138"},"PeriodicalIF":3.2,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143964475","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":"Cordycepin ameliorates morphine tolerance by inhibiting spinal cord ferroptosis and inflammation via targeting SIRT1.","authors":"Zheng Li, Jie Liu, Jie Ju, Xiaoling Peng, Wei Zhao, Jihao Ren, Xiaoqian Jia, Jihong Wang, Feng Gao","doi":"10.7150/ijms.108518","DOIUrl":"https://doi.org/10.7150/ijms.108518","url":null,"abstract":"<p><p>Morphine tolerance caused by long-term use of morphine is a major medical problem. Neuroinflammation plays an important role in morphine tolerance, and currently no drugs have been found for clinical use to alleviate neuroinflammation during morphine tolerance. Cordycepin is the main active component of fungus cordycepin militaris, has been demonstrated to have anti-oxidative stress and anti-inflammatory properties in various diseases. In this study, we established a rat model of morphine tolerance, examined the effect of cordycepin on the development of morphine tolerance, and evaluated its potential regulatory mechanisms. We found that cordycepin treatment ameliorated the development of morphine tolerance, improved mitochondrial damage associated with ferroptosis, by reducing the levels of reactive oxygen species (ROS), malondialdehyde (MDA) and Fe²⁺, increasing superoxide dismutase (SOD) and glutathione (GSH) levels, and decreasing the secretion of pro-inflammatory factors (IL-1β, IL-6, and TNF-α). Besides, cordycepin upregulated the expression of SIRT1, SLC7A11 and GPX4. Further research found that the above effects of cordycepin on morphine-tolerant rats were abolished by SIRT1 selective inhibitor EX-527. Thus, these findings indicated that cordycepin could ameliorate the development of morphine tolerance by inhibiting spinal cord ferroptosis and inflammation via targeting SIRT1. Collectively, these results demonstrated the protective effects of cordycepin and highlighted its therapeutic potential as a drug component for morphine tolerance treatment and prevention.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2059-2074"},"PeriodicalIF":3.2,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035829/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143999582","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":"Modulation of Chemotherapy Sensitivity of Breast Cancer Cells through Transforming Growth Factor-beta Pathway-mediated Alterations in DNA Damage Response.","authors":"Abdullah S Alhamed, Mohammad S El-Wetidy, Mervat M Abdelwahed, Sabry M Attia, Abdulrahman M Alabkka, Saleh A Alaraj, Khalid Alhazzani, Ahmed Z Alanazi, Faris Almutairi, Ibrahem A Alotibi, Mohammed Alqinyah","doi":"10.7150/ijms.111217","DOIUrl":"https://doi.org/10.7150/ijms.111217","url":null,"abstract":"<p><p>Chemotherapeutic drugs, like cisplatin, function by damaging genomic DNA, thus inducing cell apoptosis. Cancer cells can enhance their DNA repair capacity, leading to chemotherapeutic resistance. Nucleotide excision repair (NER) involves repairing DNA adducts and crosslinks caused by chemotherapeutic agents. Transforming growth factor-beta (TGF-β) pathway contributes to carcinogenesis, DNA repair alteration, and chemoresistance. However, the connection between TGF-β pathway, NER function alteration, and resistance to cisplatin therapy remains elusive. Therefore, the objective of current study was to fill this gap by assessing the impact of TGF-β inhibition and activation on cisplatin-induced antiproliferation, apoptosis, and DNA damage using the MTT assay, flow cytometry analysis, and COMET assay, respectively. Four NER genes, XPA, XPB, XPC, and XPF, were measured using Real-time Polymerase Chain Reaction (qPCR). MDA-MB-231 cell line was utilized as a model of breast cancer. Blockade of the TGF-β pathway strengthened cisplatin cytotoxicity, whereas induction of the TGF-β pathway suppressed cisplatin cytotoxicity. In cisplatin-treated breast cancer cells, DNA damage significantly increased upon the TGF-β pathway inhibition. Conversely, cisplatin-induced DNA damage decreased significantly upon TGF-β pathway stimulation. Finally, cisplatin caused an overexpression of the four NER genes which was curtailed and augmented by TGF-β inhibition and stimulation, respectively. Overall, this study presented evidence of the impact exerted by TGF-β pathway on NER and cisplatin sensitivity of breast cancer cells.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2031-2039"},"PeriodicalIF":3.2,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035844/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144063719","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":"Emodin: an alveolar macrophage protector in acute pancreatitis induced lung injury.","authors":"Zhe Chen, Xuanchi Dong, Yongwei Song, Bowen Lan, Yalan Luo, Haiyun Wen, Hailong Chen","doi":"10.7150/ijms.105965","DOIUrl":"https://doi.org/10.7150/ijms.105965","url":null,"abstract":"<p><p><b>Background:</b> Emodin (EMO), an anthraquinone derivative from roots and leaves of various plants, has been widely used in many inflammatory diseases. Alveolar macrophages (AMs) play a critical role in maintaining alveolar homeostasis in the lung. However, the comprehensive mechanisms of EMO therapy on AMs during acute pancreatitis-associated lung injury (AP-ALI) have not been reported. <b>Methods:</b> Both in vivo [caerulein/ lipopolysaccharides (LPS)-induced AP-ALI in mice] and in vitro MH-S models were generated to assess the protective features of EMO on mitochondrial damage and mitophagy dysfunction of AMs during AP-ALI progression. <b>Results:</b> First, in vivo, the relative quantity of AMs was significantly decreased with time in AP-ALI mice; however, the mitochondrial flux presented earlier changes than the relative quantity of AMs in our experimental system. EMO pretreatment significantly alleviated the severity of lung injury and improved the damaged alveolar structure, reversing mitochondrial impairment in AMs. Secondly, in vitro, EMO significantly enhanced mitophagy and alleviated mitochondrial damage. Furthermore, the results following mitophagy inhibition by 3-methyladenine (3-MA) demonstrated that the protective effects of EMO were partially achieved by manipulating the mitophagy-mitochondria-alveolar macrophage axis. <b>Conclusion:</b> These data enabled a more comprehensive understanding of the therapeutic effects of EMO in AP-ALI.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2075-2087"},"PeriodicalIF":3.2,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035834/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144011435","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":"Malignant features related PRDX1 associated with osimertinib sensitivity of EGFR-mutant lung adenocarcinoma.","authors":"Wenying Jiang, Maonan Wang, Xiaoqian Yu, Guoqian Liu, Xiaoyun He, Cheng Mei, Chunlin Ou","doi":"10.7150/ijms.107255","DOIUrl":"https://doi.org/10.7150/ijms.107255","url":null,"abstract":"<p><p>The peroxiredoxin (PRDX) family, also known as the peroxidase family, consists of six members that participate in a variety of essential bio-processes in carcinogenesis. However, their molecular role in lung adenocarcinoma (LUAD) has not been systematically explored. Using bioinformatic tools, we systematically analyzed the expression, prognostic value and drug sensitivity of the PRDX gene family members in LUAD. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to verify the expression of PRDX1 in both LUAD tissues and cells. Cell Counting Kit-8 (CCK-8) assay was applied to detect the half-maximal inhibitory concentration (IC₅₀) of osimertinib in LUAD. A series of cellular drug assays, including 5-Ethynyl-2'-deoxyuridine (EdU), colony formation, and apoptosis assays, were performed to explore the correlation of PRDX1 with epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) sensitivity by using EGFR-mutant and wild-type LUAD cell lines. Among all the PRDX family members, PRDX1 has a promising prognostic value and is associated with EGFR mutations, as verified by experiments conducted on collected LUAD specimens. In addition, pathway enrichment analysis suggested that PRDX1 expression positively correlated with DNA repair, which is often considered to be inextricably linked to drug resistance in tumor cells. Thus, we validated the correlation between PRDX1 and EGFR-TKI sensitivity through a series of <i>in vitro</i> experiments and found that PRDX1 inhibition along with osimertinib treatment resulted in synergistic inhibition of tumor growth. Moreover, we found that PRDX1 was negatively correlated with the immune infiltration of dendritic cells (DCs) in the tumor microenvironment (TME) of LUAD, further suggesting an oncogenic role of PRDX1. This study demonstrates that high PRDX1 expression could be a potential diagnostic and prognostic marker of LUAD, and the strategy of PRDX1 knockdown provides new insights into improving the therapeutic sensitivity of EGFR-TKI in patients with LUAD.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2040-2058"},"PeriodicalIF":3.2,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035832/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144011438","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}