International journal of molecular medicine最新文献

{"title":"Research status and future perspectives of IL‑27 in the treatment of stroke (Review).","authors":"Weiqin Liu, Zhenyou Zou, Wenyang Li, Guang Yang, Jie Zhang, Zhenyu Zhang, Hua Yao","doi":"10.3892/ijmm.2025.5557","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5557","url":null,"abstract":"<p><p>Stroke is a life‑threatening cerebrovascular disorder categorized into two major subtypes: Ischemic and hemorrhagic. Characterized by high morbidity and mortality rates, its clinical management remains challenging due to limited therapeutic options. Interleukin (IL)‑27, a pleiotropic cytokine with demonstrated neuroprotective potential, has emerged as a promising candidate for stroke intervention. IL‑27 exerts immunomodulatory effects within the central nervous system, including suppression of proinflammatory T‑cell proliferation and induction of regulatory T‑cell differentiation. These mechanisms collectively attenuate neuroinflammation, mitigate neuronal apoptosis and prevent neurodegenerative processes. The efficacy of IL‑27 in reducing cerebral damage in both ischemic and hemorrhagic stroke models has been validated, although clinical translation remains to be achieved. The present review summarizes: i) The epidemiology of stroke; ii) the immunoregulatory functions of IL‑27 and its neuroprotective mechanisms across stroke subtypes; iii) innovative brain‑targeted delivery approaches; iv) IL‑27 clinical applicability with supporting evidence; and v) possible risks and solutions in clinical applications. By collating the current knowledge, the present study provides a translational framework for advancing IL‑27‑based therapies in stroke management.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144179893","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":"Epigenetic roles of chromatin remodeling complexes in bone biology and the pathogenesis of bone‑related disease (Review).","authors":"Wenxiao Wu, Yinxing Cui, Yuqi Wu, Yan Ni, Chunling Zhao, Weichao Sun, Qian Yi","doi":"10.3892/ijmm.2025.5556","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5556","url":null,"abstract":"<p><p>Chromatin remodeling complexes are essential regulators of chromatin architecture, facilitating critical processes such as nucleosome sliding, eviction, histone exchange and post‑translational modifications. By providing an additional layer of epigenetic regulation beyond the canonical genetic code, these complexes significantly influence bone biology and health. Epigenetic regulation through chromatin remodeling complexes is crucial in modulating gene expression and cellular behavior in bone cells. However, alterations in the activity of chromatin remodeling complexes can also contribute to the progression of various bone diseases. Emerging evidence suggests that specific chromatin remodeling factors may serve as potential biomarkers for diagnosing bone‑related conditions and as therapeutic targets for intervention. The present review aims to elucidate the intricate relationship between chromatin remodeling complexes and bone‑related diseases, including osteoporosis, osteoarthritis and osteosarcoma. The present review discusses the diverse subunits of these complexes and their multifaceted roles in regulating key cellular processes such as stemness, differentiation, proliferation, senescence and apoptosis in bone cells. Notably, the present review provides a comprehensive overview of the roles of various chromatin remodeling subunits, such as BRG1, BAF47 and chromodomain‑helicase‑DNA binding 7 (CHD7), in bone metabolism, highlighting their disease‑specific mechanisms, including bromodomain‑containing protein (BRD)9‑mediated pyroptosis in intervertebral disc degeneration and CHD7‑driven bone‑fat imbalance. Furthermore, the present review highlights the therapeutic potential of targeting dysfunctional subunits (such as BRD7 in osteosarcoma and SS18 in synovial sarcoma) and propose AI‑driven structural biology approaches to design chemical modulators. The understudied impact of aging on chromatin remodeling activity in bone homeostasis is also underscored, advocating for longitudinal studies to address this gap. Finally, the distinct functions of each chromatin remodeling complex and its specific subunits in the context of bone‑related diseases were also explored, providing a comprehensive understanding of their contributions to both normal bone physiology and pathological conditions.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144180502","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":"[Corrigendum] Morin exerts cytoprotective effects against oxidative stress in C2C12 myoblasts via the upregulation of Nrf2‑dependent HO‑1 expression and the activation of the ERK pathway.","authors":"Moon Hee Lee, Min Ho Han, Dae-Sung Lee, Cheol Park, Su-Hyun Hong, Gi-Young Kim, Sang Hoon Hong, Kyoung Seob Song, Il-Whan Choi, Hee-Jae Cha, Yung Hyun Choi","doi":"10.3892/ijmm.2025.5555","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5555","url":null,"abstract":"<p><p>Following the publication of the above article, an interested reader drew to the authors' attention that the β‑actin blots in Figs. 4B and 5B were apparently the same, even though different experimental conditions were reported for these figure parts; moreover, the data shown as the Lamin B blot in Fig. 5A had also been incorporated as the Akt data in Fig. 5C of a different paper submitted by the same group and published in the journal <i>Oncology Reports</i>. However, the authors were able to re‑examine their data, and realized how these errors had occurred. Upon repeating the experiments relating to the affected figure parts, which resulted in the generation of similar results, revised versions of Figs. 4 and 5, now including replacement data for Fig. 4A and Fig. 5A and B, are shown on the next page. Note that the errors made with the assembly of the data in these figures did not affect the overall conclusions reported in the paper. The authors are grateful to have been given the opportunity to publish this corrigendum, and all the authors agree with its publication; furthermore, they apologize to the Editor of <i>International Journal of Molecular Medicine</i> and to the readership for any inconvenience caused. [International Journal of Molecular Medicine 39: 399‑406, 2017; DOI: 10.3892/ijmm.2016.2837].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144181525","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":"[Corrigendum] Predictive DNA damage signaling for low‑dose ionizing radiation.","authors":"Jeong-In Park, Seung-Youn Jung, Kyung-Hee Song, Dong-Hyeon Lee, Jiyeon Ahn, Sang-Gu Hwang, In-Su Jung, Dae-Seog Lim, Jie-Young Song","doi":"10.3892/ijmm.2025.5553","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5553","url":null,"abstract":"<p><p>Following the publication of the above article, the authors drew to the Editor's attention that two pairs of the data panels shown for the flow cytometric experiments in Fig. 3B on p. 7 had inadvertently been duplicated in the figure, such that these data were derived from the same original source, even though they were intended to have shown the results from different experiments. The authors were able to consult their original data, however, and the revised version of Fig. 3, now containing the correctly assembled flow cytometric plots in Fig. 3B, is shown on the next page. Note that the errors made in assembling these figures did not affect the overall conclusions reported in the paper. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of <i>International Journal of Molecular Medicine</i> for granting them the opportunity to publish this. Furthermore, they apologize to the readership for any inconvenience caused. [International Journal of Molecular Medicine 53: 56, 2024; DOI: 10.3892/ijmm.2024.5380].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142150","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":"miR‑34a induces apoptosis and pyroptosis in D‑Galactose‑induced aging cochlear hair cells via inhibiting TFAM and promoting mitochondrial dysfunction <i>in vitro</i> and <i>in vivo</i>.","authors":"Yilan Wang, Ming Yang, Guihua Wang, Weimin Liu, Bin Deng, Xiaoran Yang, Xuzhao Li","doi":"10.3892/ijmm.2025.5541","DOIUrl":"10.3892/ijmm.2025.5541","url":null,"abstract":"<p><p>Aging of the auditory system causes progressive hearing deficit and affects millions of people; however, the underlying mechanism remains largely unknown. D‑galactose (D‑gal)‑induced aging models were established <i>in vitro</i> using HEI‑OC1 cells and <i>in vivo</i> using C57BL/6 mice to investigate the role of miR‑34a in age‑related hearing loss (ARHL). HEI‑OC1 cells were treated with D‑gal for, while mice received daily intraperitoneal injections of D‑gal for six weeks. Molecular and functional analyses, including reverse transcription‑quantitative PCR, Western blot, flow cytometry, immunofluorescence, and dual‑luciferase reporter assays, were performed to evaluate oxidative stress, mitochondrial dysfunction, apoptosis, and pyroptosis, with miR‑34a inhibitor and DRP1 inhibitor (Mdivi‑1) used to assess their regulatory effects. D‑gal induced hair cell loss by apoptosis and pyroptosis, which was modulated by microRNA (miR)‑34a via mitochondrial dysfunction <i>in vitro</i> and <i>in vivo</i>. Inhibition of mitochondrial transcription factor A (TFAM), which is the target gene of miR‑34a, was involved in the underlying molecular mechanism. miR‑34a mediated apoptosis and pyroptosis in D‑gal‑induced cochlear hair cells via inhibiting TFAM and promoting mitochondrial dysfunction <i>in vitro</i> and <i>in vivo</i> and may serve as a new potential target for future ARHL treatment.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081035/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143980825","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":"Developments in the connection between epithelial‑mesenchymal transition and endoplasmic reticulum stress (Review).","authors":"Hongyu Chai, Shun Yao, Ya Gao, Qian Hu, Wei Su","doi":"10.3892/ijmm.2025.5543","DOIUrl":"10.3892/ijmm.2025.5543","url":null,"abstract":"<p><p>Endoplasmic reticulum stress (ERS) and epithelial‑mesenchymal transition (EMT) have important roles in fibrosis and tumour development. Moderate ERS activates cellular defence mechanisms in response to noxious stimuli; however, sustained or overly strong ERS induces apoptosis. In this disease process, EMT induces epithelial cells to acquire the ability to migrate and invade. Reportedly, ERS directly or indirectly regulates EMT processes through multiple mechanisms (such as key transcription factors, signalling pathways, ferroptosis, autophagy and oxidative stress), and both processes form a complex network of interactions. Given the critical roles of ERS and EMT in disease, targeted intervention of these two processes has emerged as a potential therapeutic strategy. In the present study, the molecular interaction mechanism of ERS and EMT was systematically explored, research progress in fibrotic and neoplastic diseases was reviewed and the potential application prospects of related targeted therapies were examined, which may provide new ideas for the development of drugs to reverse fibrosis and treat tumours.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081031/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143993352","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":"Precision oncolytic viral therapy in colorectal cancer: Genetic targeting and immune modulation for personalized treatment (Review).","authors":"Muhammad Haris Sultan, Qi Zhan, Yigang Wang, Yulong Xia, Xiaoyuan Jia","doi":"10.3892/ijmm.2025.5545","DOIUrl":"10.3892/ijmm.2025.5545","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is a leading health issue and treatments to eradicate it, such as conventional chemotherapy, are non‑selective and come with a number of complications. The present review focuses on the relatively new area of precision oncolytic viral therapy (OVT), with genetic targeting and immune modifications that offer a new future for CRC treatment. In the present review, an overview of the selection factors that are considered optimal for an oncolytic virus, mechanisms of oncolysis and immunomodulation applied to the OVT, as well as new strategies to improve the efficacy of this method are described. Additionally, cause‑and‑effect relationships are examined for OVT efficacy, mediated by the tumor microenvironment, and directions for genetic manipulation of viral specificity are explored. The possibility of synergy between OVT and immune checkpoint inhibitors and other treatment approaches are demonstrated. Incorporating the details of the present review, biomarker‑guided combination therapies in precision OVT for individualized CRC care, significant issues and future trends in this required area of medicine are highlighted. Increasingly, OVT is leaving the experimental stage and may become routine practice; it provides a new perspective on overcoming CRC and highlights the importance of further research and clinical work.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081034/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143999498","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 of liquid biopsy in differentiating lung cancer from benign pulmonary nodules (Review).","authors":"Mingcheng Peng, Jun Gong, Taixue An, Hongbing Cheng, Liangji Chen, Mengyang Cai, Jinhua Lan, Yueting Tang","doi":"10.3892/ijmm.2025.5547","DOIUrl":"10.3892/ijmm.2025.5547","url":null,"abstract":"<p><p>The diagnosis of malignant and benign pulmonary nodules has always been a prominent research topic. Accurately distinguishing between these types of lesions, particularly small or ground glass nodules, is crucial for the early detection and proactive treatment of lung cancer, ultimately leading to improved patient survival. Although various imaging methods and tissue biopsies have advanced the diagnostic efficacy of pulmonary nodules, each approach possesses inherent limitations. In recent years, there has been a growing interest in liquid biopsy as a non‑invasive and easily obtainable alternative. Furthermore, in‑depth investigations into the mechanisms underlying tumor initiation and progression have contributed to the development of circulating biomarkers for monitoring treatment response and efficacy in lung cancer. This review provides a comprehensive overview of the current landscape of pulmonary nodule diagnosis while highlighting the latest advancements in liquid biopsy techniques, such as extracellular vesicles, tumor‑educated platelets, non‑coding RNA, circulating tumor DNA and circulating antibodies.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101102/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143993337","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":"Curcumenol inhibits malignant progression and promotes ferroptosis via the SLC7A11/NF‑κB/TGF‑β pathway in triple‑negative breast cancer.","authors":"Feifei Li, Qin Qi, Yu Qiao, Yan Huang, Yuan Lu, Kan Gu, Huirong Liu, Chunfang Gao, Sheng Liu, Huangan Wu","doi":"10.3892/ijmm.2025.5552","DOIUrl":"10.3892/ijmm.2025.5552","url":null,"abstract":"<p><p>Triple‑negative breast cancer (TNBC) exhibits a high degree of malignancy and a propensity for metastasis, ultimately resulting in unfavorable patient outcomes. <i>Curcuma phaeocaulis</i> Valeton is a common herb used in traditional Chinese medicine to treat TNBC. Curcumenol (Cur) is a natural compound derived from <i>C. phaeocaulis</i> Valeton, the effects of which on breast cancer remain under‑reported. The present study elucidated that Cur could effectively inhibit the survival ability of TNBC cells and enhance their sensitivity to paclitaxel. Western blotting (WB) further revealed that Cur modulated apoptosis and epithelial‑mesenchymal transition (EMT) in TNBC. Findings from animal experiments further validated these observations. In the established TNBC mouse model, Cur was shown to exert an inhibitory effect on tumor growth, effectively attenuate EMT and substantially reduce the incidence of lung metastasis. Integrated analyses using RNA sequencing, WB and reverse transcription‑quantitative polymerase chain reaction demonstrated that Cur markedly downregulated the expression levels of solute carrier family 7 member 11 (SLC7A11), phosphorylated‑NF‑κB and TGF‑β. Molecular docking studies further validated that Cur can establish stable interactions with SLC7A11. In‑depth bioinformatics analysis revealed a positive association between high SLC7A11 expression and reduced disease‑free survival in patients with breast cancer. Additionally, in TNBC cells, Cur was revealed to reduce the mitochondrial membrane potential and promote the accumulation of lipid reactive oxygen species. Subsequent experimental investigations demonstrated that Cur can counteract the inhibitory influence of ferrostatin‑1 on ferroptosis. These findings strongly implied a potential underlying mechanism, suggesting that Cur may impede the malignant progression of TNBC via the modulation of ferroptosis. In conclusion, the findings of the present study underscore the marked efficacy of Cur in hampering the progression of TNBC by suppressing the SLC7A11/NF‑κB/TGF‑β signaling pathway.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077039","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":"Farnesoid X receptor‑driven metabolic plasticity: Bridging physiological adaptation and malignant transformation in lipid handling (Review).","authors":"Yanning Sun, Kai Sun, Hongju Ling, Qinghua Xia","doi":"10.3892/ijmm.2025.5551","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5551","url":null,"abstract":"<p><p>Metabolic reprogramming represents a hallmark of malignant tumors, manifested through progressive alterations in nutrient utilization patterns during oncogenesis. As fundamental constituents of biological membranes, essential components of signaling pathways, and critical energy substrates, lipids undergo comprehensive metabolic restructuring in neoplastic cells. This lipid remodeling confers enhanced adaptability to sustain uncontrolled proliferation while promoting aggressive migratory phenotypes. Farnesoid X receptor (FXR), a ligand‑activated nuclear receptor responsive to bile acid (BA) derivatives and cholesterol metabolites, orchestrates key aspects of lipid homeostasis. Its regulatory network encompasses cholesterol/BA metabolism, fatty acid (FA) metabolism and plasma lipoprotein trafficking pathways. Emerging evidence positions FXR as a pleiotropic modulator in oncogenesis, with dysregulated expression patterns documented across multiple tumor lineages and premalignant lesions. This mechanistic understanding has propelled FXR‑targeted therapeutics into the forefront of precision oncology development. The present review critically examines the FXR‑lipid axis in lipid‑enriched malignancies, with particular emphasis on its regulatory circuitry governing BA flux and FA turnover.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077714","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}