International journal of molecular medicine最新文献

{"title":"PSAT1 regulated by STAT4 enhances the proliferation, invasion and migration of ovarian cancer cells via the PI3K/AKT pathway.","authors":"Xiao Li, Shuang Wang, Xin Nie, Yuexin Hu, Ouxuan Liu, Yuxuan Wang, Bei Lin","doi":"10.3892/ijmm.2025.5529","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5529","url":null,"abstract":"<p><p>Epithelial ovarian cancer, the most prevalent form of ovarian cancer, is a health concern worldwide. Phosphoserine aminotransferase 1 (PSAT1), as the rate‑limiting enzyme in serine synthesis, is key in the conversion of 3‑phosphoglycerate to serine. The present study explored the role of PSAT1 expression in epithelial ovarian tumors. Gene Expression Profiling Interactive Analysis was used for gene expression and survival analyses. The effects of PSAT1 overexpression and knockdown on invasion, migration, proliferation and cell cycle progression of ovarian cancer cell lines were investigated both <i>in vitro</i> and <i>in vivo</i>. Western blotting was conducted to assess alterations in PI3K/AKT signalling pathway proteins. Database and tissue sample data confirmed that PSAT1 was significantly upregulated in ovarian cancer. Preliminary functional investigations indicated that PSAT1 was involved in modulation of invasion and migration, demonstrating the capacity of PSAT1 to enhance expression of the PI3K/AKT signalling pathway. These findings suggested that PSAT1 served a critical role in the onset and progression of ovarian cancer, thereby offering a theoretical basis for early detection and therapeutic strategies.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 6","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12005366/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144063765","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":"The function of chloride channels in digestive system disease (Review).","authors":"Yanxia Hu, Biguang Tuo","doi":"10.3892/ijmm.2025.5540","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5540","url":null,"abstract":"<p><p>Cation channels have been extensively studied in the context of digestive disorders, but comparatively little attention has been given to anions and their associated channels. Chloride ions, the most abundant anions in the human body, act as signaling molecules, modulating cellular behavior and playing a key role in regulating multiorgan physiological and pathophysiological mechanisms. The intra‑ and extracellular distributions of chloride ions are primarily controlled by various chloride channels and transporters. Currently, these chloride channels are classified into several groups: The chloride channels family, cystic fibrosis transmembrane conductance regulator, calcium‑activated chloride channels, volume‑regulated anion channels, proton‑activated chloride channels and ligand‑gated anion channels. This review aims to summarize the roles of chloride ion channels and transporter proteins in digestive system diseases, providing a theoretical basis for future research and offering potential new strategies for disease treatment.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 6","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12045473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144022318","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":"Current updates regarding biogenesis, functions and dysregulation of microRNAs in cancer: Innovative approaches for detection using CRISPR/Cas13‑based platforms (Review).","authors":"Abdulaziz A Aloliqi, Abdullah M Alnuqaydan, Aqel Albutti, Basmah F Alharbi, Arshad Husain Rahmani, Amjad Ali Khan","doi":"10.3892/ijmm.2025.5531","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5531","url":null,"abstract":"<p><p>MicroRNAs (miRNAs) are short non‑coding RNAs, which perform a key role in cellular differentiation and development. Most human diseases, particularly cancer, are linked to miRNA functional dysregulation implicated in the expression of tumor‑suppressive or oncogenic targets. Cancer hallmarks such as continued proliferative signaling, dodging growth suppressors, invasion and metastasis, triggering angiogenesis, and avoiding cell death have all been demonstrated to be affected by dysregulated miRNAs. Thus, for the treatment of different cancer types, the detection and quantification of this type of RNA is significant. The classical and current methods of RNA detection, including northern blotting, reverse transcription‑quantitative PCR, rolling circle amplification and next‑generation sequencing, may be effective but differ in efficiency and accuracy. Furthermore, these approaches are expensive, and require special instrumentation and expertise. Thus, researchers are constantly looking for more innovative approaches for miRNA detection, which can be advantageous in all aspects. In this regard, an RNA manipulation tool known as the CRISPR and CRISPR‑associated sequence 13 (CRISPR/Cas13) system has been found to be more advantageous in miRNA detection. The Cas13‑based miRNA detection approach is cost effective and requires no special instrumentation or expertise. However, more research and validation are required to confirm the growing body of CRISPR/Cas13‑based research that has identified miRNAs as possible cancer biomarkers for diagnosis and prognosis, and as targets for treatment. In the present review, current updates regarding miRNA biogenesis, structural and functional aspects, and miRNA dysregulation during cancer are described. In addition, novel approaches using the CRISPR/Cas13 system as a next‑generation tool for miRNA detection are discussed. Furthermore, challenges and prospects of CRISPR/Cas13‑based miRNA detection approaches are described.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 6","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12021393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144022339","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 in myocardial function and diseases related to muscarinic acetylcholine receptor (Review).","authors":"Chuqiao Shen, Qiang Zuo, Zhengbin Shao, Yixuan Lin, Shuo Chen","doi":"10.3892/ijmm.2025.5527","DOIUrl":"10.3892/ijmm.2025.5527","url":null,"abstract":"<p><p>Muscarinic acetylcholine (ACh) receptors (also known as M receptors) are widely distributed in all organs and tissues of the body, mainly playing a role in cholinergic nerve conduction. There are five known subtypes of muscarinic ACh receptors, but their pharmacological mechanisms of action on myocardial function have remained to be clearly defined. Functional myocardial diseases and myocardial injuries, such as arrhythmia, myocardial ischemia, myocarditis and myocardial fibrosis, may be affected by muscarinic ACh receptors. This article reviews the research progress of the regulation of myocardial function by muscarinic ACh receptors and related diseases, with the aim of developing better strategies and providing references for further revealing and clarifying the signal transduction and mechanisms of muscarinic ACh receptors in cardiomyocytes, and finding potential myocardial protective drugs that act on muscarinic ACh receptors.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 6","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12005369/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143779921","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":"Epigenetic regulation of ferroptosis in gastrointestinal cancers (Review).","authors":"Linqiang Gong, Linlin Wu, Shiyuan Zhao, Shuai Xiao, Xue Chu, Yazhou Zhang, Fengfeng Li, Shuhui Li, Hui Yang, Pei Jiang","doi":"10.3892/ijmm.2025.5534","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5534","url":null,"abstract":"<p><p>Ferroptosis is a type of iron‑dependent cell death characterized by excessive lipid peroxidation and may serve as a potential therapeutic target in cancer treatment. While the mechanisms governing ferroptosis continue to be explored and elucidated, an increasing body of research highlights the significant impact of epigenetic modifications on the sensitivity of cancer cells to ferroptosis. Epigenetic processes, such as DNA methylation, histone modifications and non‑coding RNAs, have been identified as key regulators that modulate the expression of ferroptosis‑related genes. These alterations can either enhance or inhibit the sensitivity of gastrointestinal cancer (GIC) cells to ferroptosis, thereby affecting the fate of GICs. Drugs that target epigenetic markers for advanced‑stage cancer have shown promising results in enhancing ferroptosis and inhibiting tumor growth. This review explores the intricate relationship between epigenetic regulation and ferroptosis in GICs. Additionally, the potential of leveraging epigenetic modifications to trigger ferroptosis in GICs is investigated. This review highlights the importance of further research to elucidate the specific mechanisms underlying epigenetic control of ferroptosis and to advance the development of novel therapeutic approaches.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 6","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12045471/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143982562","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":"Honokiol ameliorates pyroptosis in intestinal ischemia‑reperfusion injury by regulating the SIRT3‑mediated NLRP3 inflammasome.","authors":"Ke Wu, Qiuling Wang, Zhengyu Zhang, Wei Luo, Jing Peng, Xin Ma, Li Wang, Chunguang Xie, Wubin Guo","doi":"10.3892/ijmm.2025.5537","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5537","url":null,"abstract":"<p><p>Intestinal ischemia‑reperfusion (IIR) injury is caused by the restoration of blood supply after a period of ischemia. It occurs in numerous clinical pathologies, such as intestinal obstruction, incarcerated hernia and septic shock, with mortality rates of 50‑80%. Honokiol (HKL), isolated from the herb <i>Magnolia officinalis</i>, is a biphenolic natural product with antioxidative, antibacterial, antitumor and anti‑inflammatory properties. Additionally, HKL has protective effects in ischemia‑reperfusion injuries, but its role and specific mechanisms in IIR injury are yet to be elucidated. In the present study, the superior mesenteric artery was ligated in rats to establish an IIR model. Hematoxylin and eosin staining and ELISA revealed that HKL administration ameliorated IIR‑induced injury in rats, which was demonstrated by a reduced destruction to the intestinal mucosa, as well as a reduced serum intestinal fatty acid‑binding protein concentration and Chiu's score in 10 mg/kg HKL treated IIR‑induced rats compared with those without HKL treatment. Additionally, immunohistochemical (IHC) staining and western blotting revealed that the occludin and tight junction protein 1 protein levels were increased in the 10 mg/kg HKL treated IIR‑induced rats compared with those without HKL treatment. Furthermore, an in vitro hypoxia/reoxygenation (H/R) cell model was established using IEC‑6 cells. Cell Counting Kit‑8 and lactate dehydrogenase (LDH) assays indicated that HKL mitigated the H/R‑inhibited cell viability and decreased the LDH levels in cell supernatants. Mechanistically, immunofluorescent (IF) staining and western blotting revealed that HKL inhibited H/R‑triggered pyroptosis. Furthermore, Mito‑Tracker, mitochondrial membrane potential and MitoSOX staining as well as western blotting revealed that reducing mitochondrial reactive oxygen species (ROS) inhibited the H/R‑induced pyroptosis by mitigating mitochondrial dysfunction. In the present H/R cell model, HKL improved the mitochondrial function by increasing the expression of sirtuin 3 (SIRT3), while IF staining and western blotting indicated that silencing SIRT3 notably reduced the beneficial effect of HKL on pyroptosis. In addition, IHC staining and western blotting revealed that HKL treatment mitigated the IIR‑induced pyroptosis in rats. Therefore, HKL treatment may mitigate IIR‑induced mitochondrial dysfunction and reduce mitochondrial ROS production by increasing the expression of SIRT3 protein, potentially resulting in an inhibition of pyroptosis during IIR.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 6","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12045469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143994263","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":"ABCG8‑mediated sterol efflux increases cancer cell progression via the LRP6/Wnt/β‑catenin signaling pathway in radiotherapy‑resistant MDA‑MB‑231 triple‑negative breast cancer cells.","authors":"Young Shin Ko, Ju Yeong Won, Hana Jin, Nam Binh Nguyen, Yaeram Won, Vedaste Nsanzimana, Seung Pil Yun, Sang Won Park, Hye Jung Kim","doi":"10.3892/ijmm.2025.5521","DOIUrl":"10.3892/ijmm.2025.5521","url":null,"abstract":"<p><p>Expression levels of ATP‑binding cassette (ABC) transporters are known to be increased in various tumor cells, including in breast cancer, and they are responsible for mediating drug resistance, leading to treatment failure. In the present study, gene expression array analysis revealed that among ABC transporter subtypes, ABC subfamily G member 8 (ABCG8) was one of the most increased in radiotherapy‑resistant triple‑negative breast cancer (RT‑R‑TNBC) cells compared with in TNBC cells. ABCG8 is involved in sterol efflux; however, its role in cancer is not well known. Therefore, the present study investigated the effect of ABCG8 on tumor progression in RT‑R‑TNBC cells. Gene expression profiling was conducted using the QuantiSeq 3' mRNA‑Seq Service, followed by western blotting to confirm protein levels. Loss‑of‑function assays using small interfering RNA (si) transfection were performed to assess the roles of ABCG8 and its regulatory signaling pathways. RT‑R‑MDA‑MB‑231 cells exhibited increased cholesterol levels in both cells and the surrounding media via induction of sterol regulatory element binding protein 1 (mature form) and fatty acid synthase. siABCG8 transfection increased intracellular cholesterol levels but decreased cholesterol levels in the media, indicating an accumulation of cholesterol inside cells. Additionally, RT‑R‑MDA‑MB‑231 cells exhibited increased levels of β‑catenin compared with MDA‑MB‑231 cells, which was significantly reduced by ABCG8 knockdown. Furthermore, ABCG8 knockdown led to cell cycle arrest in the G2/M phase in RT‑R‑MDA‑MB‑231 cells by reducing Polo‑like kinase 1 (PLK1) and Cyclin B1 expression. RT‑R‑MDA‑MB‑231 cells also exhibited increased phosphorylated‑low‑density lipoprotein (LDL) receptor‑related protein 6 (LRP6) levels compared with MDA‑MB‑231 cells, and these were decreased by siABCG8 transfection. LRP6 siRNA transfection decreased β‑catenin, PLK1 and Cyclin B1 expression. In addition, feedback mechanisms such as liver X receptor and inducible degrader of LDL were decreased in RT‑R‑MDA‑MB‑231 cells under normal conditions compared with in MDA‑MB‑231 cells. To the best of our knowledge, the present study was the first to suggest that the cholesterol exported by ABCG8, not inside the cells, may affect cancer progression via the LRP6/Wnt/β‑catenin signaling pathway in RT‑R‑TNBC. The regulation of this pathway may offer a potential therapeutic strategy for the treatment of RT‑R‑TNBC.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 5","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11964413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669773","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":"Oxidative stress in endometriosis: Sources, mechanisms and therapeutic potential of antioxidants (Review).","authors":"Li Huang, Ling Shi, Maoya Li, Xiaolan Yin, Xiaoli Ji","doi":"10.3892/ijmm.2025.5513","DOIUrl":"10.3892/ijmm.2025.5513","url":null,"abstract":"<p><p>Endometriosis affects ~15% of women of reproductive age worldwide, impacting ~190 million individuals. Despite its high prevalence, the precise pathogenesis of endometriosis remains unclear. Emerging evidence has highlighted oxidative stress as a pivotal factor in the initiation and progression of this disease. The present review comprehensively summarizes the sources of oxidative stress in endometriosis, including redox imbalance characterized by increased oxidative markers and diminished antioxidant defenses, mitochondrial dysfunction leading to excessive production of reactive oxygen species (ROS), and aberrant iron metabolism that further amplifies ROS generation. The accumulation of ROS disrupts cellular redox homeostasis, thereby exacerbating oxidative stress and activating key cell proliferation signaling pathways, such as the Raf/MEK/ERK and mTOR pathways. Activation of these pathways promotes the survival and proliferation of ectopic endometrial cells, contributing to lesion development and disease progression. The present review also discusses how oxidative stress induces epigenetic modifications that may further drive the pathological features of endometriosis. Finally, the recent advances in the application of antioxidants as therapeutic agents for endometriosis are highlighted, underscoring their potential to mitigate oxidative stress and ameliorate disease symptoms. Understanding the intricate relationship between oxidative stress and endometriosis may pave the way for novel diagnostic and therapeutic strategies aimed at improving patient outcomes.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 5","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hesperetin induces apoptosis in lung squamous carcinoma cells via G₂/M cycle arrest, inhibition of the Notch1 pathway and activation of endoplasmic reticulum stress.","authors":"Qianlong Xie, Ziming He, Lingfang Tan, Min Li, Min Zhuang, Chen Liu, Sunhui Chen, Long Jin, Yuxia Sui","doi":"10.3892/ijmm.2025.5518","DOIUrl":"10.3892/ijmm.2025.5518","url":null,"abstract":"<p><p>Hesperetin (HST), a natural flavonoid, has potent antitumor effects on lung adenocarcinoma; however, its effects on lung squamous cell carcinoma (LUSC) are currently unknown. The present study aimed to investigate the anticancer effects of HST on LUSC cells. The influence of 37.5, 75 and 150 <i>µ</i>M HST on the H1703 cell line, and of 75, 150 and 300 <i>µ</i>M HST on the H226 cell line was determined using the Cell Counting Kit‑8 method, cell cycle assay, JC‑1 mitochondrial membrane potential assay and Annexin V‑FITC/PI staining. DMSO‑treated cells were used as the control group. Western blotting was performed to detect the protein expression levels of cyclin B1, CDK1, Bcl‑2, Bax, caspase‑3, cleaved caspase‑3, phosphorylated‑eIF2α, eIF2α, glucose‑regulated protein 78, CHOP, Notch1 and Hes‑1. The relationship between endoplasmic reticulum stress (ERS), Notch1 signaling and apoptosis was examined using the ERS‑inhibitor 4‑phenylbutyric acid (4‑PBA; 500 <i>µ</i>M) and the Notch1 signaling activator Jagged‑1 (4 <i>µ</i>M). <i>In vivo</i>, mice were divided into control, HST (30, 60 and 90 mg/kg/q2d) and cisplatin (2 mg/kg/q2d) groups to evaluate the anti‑LUSC effects of HST. The results revealed that HST inhibited the viability of H226 and H1703 cells, leading to cell cycle arrest at the G₂/M phase and the induction of cell apoptosis. In addition, HST downregulated the Notch1 signaling pathway and increased ERS. In H1703 cells, 4‑PBA and Jagged‑1 reduced the expression of apoptosis‑related proteins, and Jagged‑1 also reduced the expression of ERS‑related proteins. <i>In vivo</i>, HST reduced tumor growth without any apparent toxic side effects. In conclusion, HST may exert its antitumor effects by inducing G₂/M cell cycle arrest and inhibiting the Notch1 signaling pathway to activate ERS‑induced apoptosis, making it a promising agent for treating LUSC.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 5","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11936485/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624460","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":"[Retracted] Genotoxicity of chloroacetamide herbicides and their metabolites <i>in vitro</i> and <i>in vivo</i>.","authors":"Xinyan Ma, Ying Zhang, Mingyang Guan, Weidong Zhang, Huifang Tian, Caixiao Jiang, Xiaoxin Tan, Weijun Kang","doi":"10.3892/ijmm.2025.5511","DOIUrl":"10.3892/ijmm.2025.5511","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that certain of the JNK and phosphorylated (pho)‑JNK western blotting data shown in Fig. 8 on p. 7 were strikingly similar to data featured in a pair of other articles written by different authors at different research institutes, one of which (submitted to the journal <i>Molecular Medicine Reports</i>) has been subsequently retracted, whereas the other (submitted to the journal Renal Failure) was received at that journal prior to the receipt of the above article at International Journal of Molecular Medicine. In view of the fact that the abovementioned data had already apparently been submitted elsewhere prior to the receipt of this paper at <i>International Journal of Molecular Medicine</i>, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 47: 103, 2021; DOI: 10.3892/ijmm.2021.4936].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 5","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11913432/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573018","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}