International journal of molecular medicine最新文献

{"title":"Salidroside attenuates myocardial ischemia‑reperfusion‑induced oxidative stress and ferroptosis by promoting USP11‑mediated  deubiquitination of PRDX2.","authors":"Zhi-Cong Qiu, Jian-Nan Li, Yi-Zhou Li, Zi-Ming Wu, Xu-Dong Luo, Rui-Yuan Zeng, Song-Qing Lai, Shi-Tao Zhao, Li Wan","doi":"10.3892/ijmm.2026.6000","DOIUrl":"10.3892/ijmm.2026.6000","url":null,"abstract":"<p><p>Myocardial ischemia/reperfusion (I/R) injury is closely associated with excessive oxidative stress and ferroptosis. <i>Salidroside</i> (Sal), a major active component of Rhodiola, has demonstrated cardioprotective properties, yet its precise mechanisms in regulating ferroptosis remain unclear. The present study investigated whether Sal attenuates myocardial I/R injury by modulating ubiquitin‑specific protease 11 (USP11)‑mediated deubiquitination and stabilization of peroxiredoxin 2 (PRDX2). An <i>in vitro</i> H9c2 anoxia/reoxygenation (A/R) model and an <i>in vivo</i> rat I/R model were established. Sal significantly improved the viability of A/R‑injured H9c2 cells and reduced reactive oxygen species accumulation, ferrous iron overload and lipid peroxidation. Mechanistically, Sal upregulated the expression levels of USP11, glutathione peroxidase 4 and PRDX2 while suppressing prostaglandin‑endoperoxide synthase 2; notably, these effects were attenuated by USP11 silencing. Molecular docking and cellular thermal shift assay analyses suggested that USP11 may represent a potential molecular target involved in Sal‑mediated cardioprotection, thereby increasing its thermal stability and strengthening the USP11‑PRDX2 interaction. This may facilitate the USP11‑mediated stabilization of PRDX2, prolonging its half‑life and preserving cellular redox homeostasis. <i>In vivo</i> experiments further demonstrated that Sal pretreatment markedly reduced myocardial infarct size and improved cardiac contractile function, which was associated with the concurrent upregulation of the USP11‑PRDX2 axis. Collectively, these findings indicate that Sal confers robust cardioprotection against I/R injury by engaging USP11 and promoting the stabilization of PRDX2, thereby suppressing oxidative stress and ferroptosis. USP11 represents a promising therapeutic target for mitigating myocardial I/R injury.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13637566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038542","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] Downregulation of LINC00707 promotes osteogenic differentiation of human bone marrow‑derived mesenchymal stem cells by regulating DKK1 via targeting miR‑103a‑3p.","authors":"Jun Liu, Minfei Wu, Guang Feng, Rui Li, Yang Wang, Jianhang Jiao","doi":"10.3892/ijmm.2026.5965","DOIUrl":"10.3892/ijmm.2026.5965","url":null,"abstract":"<p><p>Following the publication of the above paper, the authors contacted the Editorial Office to explain that they had incorrectly assembled certain of the data included in the western blots featured in Fig. 2D on p. 1033, and wished to issue a corrigendum. Upon performing an independent analysis of the data in this paper in the Editorial Office, however, it came to light that the data in question were strikingly similar to data which had already been submitted to the same journal (<i>International Journal of Molecular Medicine</i>) in a paper written by different authors at a different research institute. Upon asking the authors for an explanation concerning these data, the authors presented to the office a series of blots related to the same experiments, including the purported integral blots associated with the published data. However, owing to a number of remaining uncertainties concerning the blots provided resulting from an additional assessment of the raw underlying data made using the software analysis program, the Editor of <i>International Journal of Molecular Medicine</i> has decided that this paper should be retracted from the Journal on account of a lack of confidence in the originally presented data. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine  46: 1029‑1038, 2020; DOI: 10.3892/ijmm.2020.4672].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13541271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148840029","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":"[Corrigendum] Alteration of the Wnt/GSK3β/β‑catenin signalling pathway by rapamycin ameliorates pathology in an Alzheimer's disease model.","authors":"Jingfei Chen, Zhimin Long, Yanzhen Li, Min Luo, Shifang Luo, Guiqiong He","doi":"10.3892/ijmm.2026.6003","DOIUrl":"https://doi.org/10.3892/ijmm.2026.6003","url":null,"abstract":"<p><p>Following the publication of the above article, a concerned author drew to the authors' attention that they had apparently used an inappropriate antibody in their study: In the Materials and methods section, the authors had reported the use of Abcam's recombinant antibody against plant homeodomain (PHD) finger protein 1 (a.k.a. PHF1; cat. no. ab184951) to probe for the unrelated protein, tau paired helical filaments (PHFs). Based on their search of previous literature, the authors acknowledged that they had made a methodological error in selecting the incorrect antibody; therefore, the western blot assay results shown in Fig. 4A on p. 317 for protein PHF1 should be considered to be invalid. Given that this issue has come to light, the authors have now purchased the correct and specific antibody targeting phosphorylated tau (p‑tau‑S404) from ABclonal Viotech Co., Ltd (cat. no. AP1378) and completely repeated the relevant experiments, in strict accordance with the original experimental protocols and conditions. In addition, the authors provided the Editorial Office with the raw data from the repeated experiments, and also proof of purchase of the correct antibody. The corrected version of Fig. 4, now showing the revised data for the PHF1 blots in Fig. 4A together with re‑quantified bar charts for these data shown in Fig. 4B, is featured on the next page. Additional changes to the text should also be noted: The text in the Materials and methods section, '<i>Western blot analysis</i>' subsection, on p. 315 (left-hand column, lines 14-15), should read as follows (changes highlighted in <b>bold</b>): '...rabbit anti insulin degrading enzyme (IDE) antibody (ab133561), <b>rabbit anti‑PHF‑1 antibody (ab184951)</b>, mouse anti‑GSK3β antibody (ab93926)...'. In addition, revisions have also been made to the legend for Fig. 4. The authors confirm that the error made in performing these experiments has not had a significant impact on either the results or the conclusions reported in this study, and all the authors agree with the publication of this Corrigendum. The authors are grateful to the Editor of <i>International Journal of Molecular Medicine</i> for allowing them the opportunity to publish this Corrigendum; furthermore, they apologize to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 44: 313‑323, 2019; DOI: 10.3892/ijmm.2019.4198].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13637568/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149109248","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":"Neutrophil extracellular traps in cardiovascular disease: Mechanisms and therapeutic implications (Review).","authors":"Zhao Wang, Mingde Chang, Wenyu Shang, Yunfeng Jia, Xiaoyu Shan, Xinnong Chen, Yingxi Yang, Junping Zhang","doi":"10.3892/ijmm.2026.5994","DOIUrl":"10.3892/ijmm.2026.5994","url":null,"abstract":"<p><p>Neutrophil extracellular traps (NETs) are web‑like structures composed of decondensed chromatin and granular proteins. Initially identified as an antimicrobial defense mechanism, NETs have now been demonstrated to be profoundly involved in the processes of sterile inflammation, thrombosis and fibrosis in cardiovascular diseases. The present review systematically delineated the interaction networks between NETs and macrophages, monocytes, endothelial cells, fibroblasts and platelets, untangling NETs as a central hub that integrates the pathological triad of inflammation, thrombosis and fibrosis. Building on this foundation, the specific mechanisms of NETs in cardiac diseases, including acute myocardial infarction, atrial fibrillation and heart failure and in vascular diseases, such as atherosclerosis, hypertension and abdominal aortic aneurysm, are elaborated. Finally, from four dimensions, NETs degradation, targeting of NETs components, inhibition of NETosis formation and indirect intervention through inflammatory metabolic pathways, the preclinical evidence and translational bottlenecks of strategies such as DNase I, histone‑neutralizing agents and PAD4 inhibitors were systematically evaluated. The present review aimed to promote the transition of NETs from a fundamental pathological hub into a targetable node for cardiovascular therapy.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13600330/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038527","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":"Breaking the cycle of fibrosis: Ferroptosis as a therapeutic target (Review).","authors":"Xincheng Feng, Jue Zhang, Qinghong Ma, Chao Sun","doi":"10.3892/ijmm.2026.5969","DOIUrl":"10.3892/ijmm.2026.5969","url":null,"abstract":"<p><p>Fibrosis, characterized by abnormal deposition of extracellular matrix, is a chronic disease that progressively remodels tissues, leading to organ failure, earning it the moniker the 'silent killer' of organ function. Recently, ferroptosis, a novel form of regulated cell death, has garnered attention in research; its molecular mechanisms, including the lipid peroxidation cascade, dysregulation of glutathione metabolism and imbalance in iron ion homeostasis, have been closely linked to the progression of fibrosis. The present review systematically elaborates on the process of fibrosis, the main mechanisms of ferroptosis and the role of ferroptosis in fibrosis. The review also discusses intervention strategies targeting the key signaling nodes of ferroptosis during the inflammatory initiation and cell proliferation stages. In addition, it also elaborates on innovative therapeutic strategies based on regulating the ferroptosis pathway, including engineered exosome‑mediated gene delivery systems and iron chelators encapsulated by multifunctional nanoparticles. Through a summary of current evidence, the present review provides a mechanistic rationale and new perspectives for the development of precision anti‑fibrotic therapies targeting ferroptosis.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13541276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148840120","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":"[Corrigendum] Inactivation of von Hippel‑Lindau increases ovarian cancer cell aggressiveness through the HIF1α/miR‑210/VMP1 signaling pathway.","authors":"Ting Liu, Le Zhao, Wei Chen, Zhen Li, Huilian Hou, Lu Ding, Xu Li","doi":"10.3892/ijmm.2026.5983","DOIUrl":"10.3892/ijmm.2026.5983","url":null,"abstract":"<p><p>Following the publication of the above paper, a concerned reader drew the Editor's attention to the fact that a number of data panels shown for the cell migration assay data in Fig. 1C on p. 1238 and Fig. 3A on p. 1240 appeared to contain overlapping sections, such that data which were intended to show the results of differently performed experiments were apparently derived from a much smaller number of original sources. The authors were contacted by the Editorial Office to offer an explanation for these apparent anomalies in the presentation of the data in this paper, and they have replied to confirm that Figs. 1 and 3 were assembled incorrectly; moreover, although the overlapping images appeared to represent different fields of view, the authors suspected that the errors may have occurred when misfiled images were inserted from the wrong folder during figure preparation. In addition to the issues with Figs. 1 and 3, and even though there were no obvious issues of data mishandling present, the authors also declared that they were unable to retrieve the original experimental data relating to the cell migration assay experiments shown in Fig. 4. The authors requested that the cell migration experiments pertaining to Figs. 1, 3 and 4 be repeated, and the Editor agreed to the authors' request. The revised versions of Figs. 1, 3 and 4, now showing new data for Figs. 1C, 3A and 4B, together with new histograms that have been prepared for the re‑quantification of the new data, are shown on the next two pages. Note that the results obtained from the newly performed experiments were broadly similar to the originally published results, and therefore the revisions made to these three figures have not grossly affected either the results or the conclusions reported in this study. All the authors agree with the publication of this Corrigendum, and they are grateful to the Editor of <i>International Journal of Molecular Medicine</i> for granting them the opportunity to publish this Corrigendum; furthermore, they apologize to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 33: 1236‑1242, 2014; DOI: 10.3892/ijmm.2014.1661].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13592808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944599","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":"[Corrigendum] Integrative transcriptomic analysis unveils FXR as a key regulator of intestinal stemness and inflammation in ulcerative colitis.","authors":"Hao Lin, Xinran Cheng, Yangyang Ren, Yongmei Zhang, Weixu Chen, Qingyan Lu, Yiqing Tian","doi":"10.3892/ijmm.2026.5985","DOIUrl":"10.3892/ijmm.2026.5985","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Following the publication of the above article, an interested reader raised several comments on the study that required clarification on the part of the authors in order to confirm the reporting of certain of the results, and to make the paper fully comprehensible. First, in the Materials and methods section, the single‑cell RNA sequencing (RNA‑seq) source did not appear to match the presented groups for the scRNA‑seq data that were obtained from the GSE116222 dataset, specifically using 'three human UC samples', where three distinct groups, namely the 'Normal', 'Non‑inflamed' and 'Inflamed' groups, were shown in various of the figures (for example, Fig. 1D and Fig. 6K). Secondly, the description of the Weighted Gene Co‑expression Network Analysis (WGCNA) in the Materials and methods section did not tally with the findings reported in the Results section. It was stated in the '&lt;i&gt;Construction of co‑expression network&lt;/i&gt;' subsection of the Methods that WGCNA was performed 'based on the GSE116222 dataset, specifically exploring the association between FXR and CD133 in intestinal cells'; however, all the WGCNA results shown (in Figs. 4D and 5A) were based on the bulk transcriptome dataset GSE87466, not on single‑cell data; no WGCNA output from GSE116222 was presented in the paper. Thirdly, some confusion between human and mouse data appeared in the reporting of the experiments in Fig. 1E. The figure part showed macroscopic photographs of whole large intestines and spleens labeled 'Control' and 'UC groups', and these images must have been derived from the DSS‑treated mouse model. The figure legend did not specify that these are mouse data, and the labeling of the 'UC group' was misleading.  Finally, a typographical error in the reporting of the human control group sex distribution was contained in the '&lt;i&gt;Human sample collection and processing&lt;/i&gt;' subsection: 'the control group consisted of 8 men and 2 men' was presumably intended to have read as '8 men and 2 women'. The authors have considered these points, and acknowledge that clarifications of all of them are necessary in the published paper; therefore, the following changes and edits to the text are required (all highlighted in &lt;b&gt;bold&lt;/b&gt;). First, in the 'Materials and methods' section, in the '&lt;i&gt;Single‑cell RNA sequencing (scRNA‑seq)&lt;/i&gt;' subsection, the text which read as 'scRNA‑seq data from three human UC samples were downloaded from the Gene Expression Omnibus (GEO) database...' has now been changed to 'scRNA‑seq data from &lt;b&gt;9 samples (3 healthy, 3 non‑inflamed, and 3 UC)&lt;/b&gt; were downloaded from the Gene Expression Omnibus (GEO) database...' In response to the second of the reader's queries, in the '&lt;i&gt;Construction of co‑expression network&lt;/i&gt;' subsection of the Methods, the text which read: 'In the present study, the 'WGCNA' package in R was employed to construct a co‑expression network based on the GSE116222 dataset, specifically exploring the association between FXR and CD133 ","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13592805/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148989942","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":"[Corrigendum] Adjudin delays cellular senescence through Sirt3‑mediated attenuation of ROS production.","authors":"Keyi Geng, Ningzhen Fu, Xiao Yang, Weiliang Xia","doi":"10.3892/ijmm.2026.6001","DOIUrl":"10.3892/ijmm.2026.6001","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Following the publication of the above article, a concerned reader drew to the authors' attention that, regarding the images of the mouse embryo fibroblast (MEF) cells with senescence‑associated β‑galactosidase (SA‑β‑gal) staining shown in Fig. 1B on p. 3254, the panels on the far left and the far right on the bottom row of data [showing treatments with 0 µM and 40 µM adjudin respectively in the presence of hydroxyurea (HU)] contained an overlapping section of data (albeit after turning the right‑hand panel through 90°), such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original source. In addition, the reader also observed that one of the antibodies the authors had used in their study was apparently selected inappropriately: The antibody (cat. no. ab51243) that the authors reported to have used is specific for the protein known as p16‑ARC (or ARPC5), not the apoptosis‑associated protein p16‑INK4a, as was intended. After re‑examining their original data, the authors have realized that the data in Fig. 1B were assembled incorrectly. A revised version of Fig. 1 is shown on the next page, now featuring data for all the panels in Fig. 1B from one of the repeated sets of experiments. Concerning the potential selection of an inappropriate antibody to probe for p16 protein, the authors expressed their regret that they had not retained their original receipt for the purchase of this antibody, and were not in a position to prove whether or not the antibody had been chosen legitimately for the affected experiments; however, an increased abundance of p16‑INK4a was used as an indicator of cellular senescence in combination with the abundance of p21 and the fraction of cells that contained a SA‑β‑gal signal. In view of this, the authors considered that removing the p16 data from the paper would not compromise the conclusions drawn in this study.  After considering this appeal, the Editor has approved the authors' request that the p16 data be omitted from this study. Therefore, all references to 'p16' in this study (as were featured in the Abstract, and the Materials and methods, Results and Discussion sections) should be considered to be eliminated from this paper; the revised version of Fig. 1 that has been provided to take account of the new data in Fig. 1B also no longer includes the p16 data, and a new version of Fig. 3 has also been provided (on the third page of this corrigendum), again with the p16 data excluded. Note that the revisions made to these figures, and the omission of the data relating to p16, do not affect the overall conclusions reported in the paper. The authors express their gratitude to the Editor of &lt;i&gt;International Journal of Molecular Medicine&lt;/i&gt; for allowing them the opportunity to publish this corrigendum, and apologize to the readership for any inconvenience caused. [International Journal of Molecular Medicine 42: 3522‑3529, 2018; DOI: 10.","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13637567/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038529","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":"lncRNA <i>TUG1</i> mediates palmitic acid‑induced neuronal lipotoxic injury via the miR‑449a‑5p/caspase‑3 and Akt/GSK‑3β axes.","authors":"Ya-Dong Wei, Peng-Quan Chen, Xin Zheng, Le-Qi Wu, Xin-Yi Wang, Xin-Ran Gao, Jin-Fang Ge","doi":"10.3892/ijmm.2026.5966","DOIUrl":"10.3892/ijmm.2026.5966","url":null,"abstract":"<p><p>A close relationship exists between excessive lipids and structural and functional brain dysfunction, with the long non‑coding (lncRNA)‑microRNA (miR)‑mRNA network having an emerging role. Given the increasingly recognized role of the lncRNA taurine upregulated gene 1 (<i>TUG1</i>) in metabolic and neurodegenerative diseases, the present study investigated its function and mechanism in palmitic acid (PA)‑induced neuronal injury. Results showed that lncRNA <i>TUG1</i> expression was elevated in PA‑treated HT‑22 and SH‑SY5Y cells. Moreover, cell‑based <i>in vitro</i> detection including reverse transcription‑quantitative polymerase chain reaction, western blotting and lactate dehydrogenase cytotoxicity assays demonstrated a positive association between lncRNA <i>TUG1</i> expression and lactate dehydrogenase release and cleaved caspase‑3 levels, whereas a negative association was observed with the expression levels of Bcl‑2 and synaptic proteins (synapsin‑1, synaptotagmin‑1 and brain‑derived neurotrophic factor) and the ratios of phosphorylated (p‑)Akt/Akt and p‑GSK‑3β/GSK‑3β. The downregulation of lncRNA <i>TUG1</i> reversed PA‑induced damage in HT‑22 cells. Bioinformatics and dual‑luciferase assays identified miR‑449a‑5p as the direct target of lncRNA <i>TUG1</i>. Rescue experiments revealed that miR‑449a‑5p mediated the effects of lncRNA <i>TUG1</i> by targeting caspase‑3 via the Akt/GSK‑3β pathway. Collectively, these findings establish a causal axis in which lncRNA <i>TUG1</i> derepresses caspase‑3 and suppresses Akt/GSK‑3β signaling by sponging miR‑449a‑5p, thereby driving neuronal lipotoxic injury.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13541273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148840153","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":"Interferon regulatory factors orchestrate CD8⁺ T cell function (Review).","authors":"Fa-Xi Wang, Chun-Liang Yang, Shan-Jie Rong, Qi-Jie Chen, Xiong-Tao Yue, Fei Sun","doi":"10.3892/ijmm.2026.5982","DOIUrl":"10.3892/ijmm.2026.5982","url":null,"abstract":"<p><p>The fate of CD8⁺ T cells is dictated by epigenetic remodeling, metabolic rewiring and most critically, the transcriptional reprogramming that integrates diverse extracellular signaling pathways. Transcription factors (TFs) predetermine cell differentiation state and lineage‑specifying hub TFs are decisive for CD8⁺ T cell functional maturation. The present study aimed to summarize the indispensable roles of interferon regulatory factors (IRFs) in CD8⁺ T cell biology from early thymic development to the acquisition of distinct functional states. Alone or together with other TFs, IRFs are involved in the regulation of CD8⁺ T cell commitment, effector differentiation, memory maintenance and terminal exhaustion. In clinical practice, IRF family members hold potential as prognostic biomarkers and valuable therapeutic targets in CD8⁺ T cell‑associated immune disorders, such as tumors, transplant rejection, infection and autoinflammatory diseases.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13592810/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944741","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}