International journal of molecular medicine最新文献

{"title":"[Retracted] Endothelial cell‑derived exosomes protect SH‑SY5Y nerve cells against ischemia/reperfusion injury.","authors":"Bing Xiao, Yi Chai, Shigang Lv, Minhua Ye, Miaojing Wu, Liyuan Xie, Yanghua Fan, Xingen Zhu, Ziyun Gao","doi":"10.3892/ijmm.2025.5549","DOIUrl":"10.3892/ijmm.2025.5549","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the flow cytometric data shown in Figs. 3A and 5E, and certain of the EdU assay data shown in Fig. 5C were strikingly similar to data that had either already appeared in previously published articles that were written by different authors at different research institutes, or were featured in articles that were submitted for publication to different journals at around the same time, or have otherwise subsequently appeared in print elsewhere. Owing to the fact that the contentious data in the above article had already been published prior to its submission to <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 40: 1201‑1209, 2017; DOI: 10.3892/ijmm.2017.3106].</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/PMC12121983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077060","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] Effect of apelin on the cardiac hemodynamics in hypertensive rats with heart failure.","authors":"Hui Pang, Bing Han, Tao Yu, Zhenkun Zong","doi":"10.3892/ijmm.2025.5536","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5536","url":null,"abstract":"<p><p>Following the publication of the above article, a concerned reader drew to the authors' attention that, regarding the western blot data shown in Fig. 7B on p. 762, a number of the bands shown to represent phosphorylated (p)‑ERK‑1/2 bands were strikingly similar to bands that were showing the results from the total (t)‑ERK‑1/2 experiments; moreover, certain of the bands in question were non‑contiguous in terms of how they were positioned in the gels. Upon examining these data independently in the Editorial Office, the Editor of <i>International Journal of Molecular Medicine</i> has determined that this article should be retracted from the Journal on the basis of an overall lack of confidence in the presented data. 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 of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 34: 756‑764, 2014; DOI: 10.3892/ijmm.2014.1829].</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/PMC12045472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144007565","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] Hypoxia‑induced expression of CXCR4 favors trophoblast cell migration and invasion via the activation of HIF‑1α.","authors":"Zhan Zhang, Pengyun Li, Yan Wang, Huan Yan","doi":"10.3892/ijmm.2025.5528","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5528","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, regarding the Transwell migration and invasion assay experiments shown in Figs. 3A, 4C, 5C and G, a number of the individual panels contained overlapping sections of data, both within and across the figure parts, such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original sources. In view of the fact that these figures were assembled erroneously, 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 presented data. After having been in contact with the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 42: 1508‑1516, 2018; DOI: 10.3892/ijmm.2018.3701].</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/PMC12005362/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144006342","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] Paeonol induces the apoptosis of the SGC‑7901 gastric cancer cell line by downregulating ERBB2 and inhibiting the NF‑κB signaling pathway.","authors":"Jun Fu, Luhua Yu, Jie Luo, Rui Huo, Bing Zhu","doi":"10.3892/ijmm.2025.5532","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5532","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, regarding the flow cytometric plots shown in Fig. 7 on p. 1479, although the number of data points increased with an increasing concentration of paenol, the patterning of the dots were similar comparing across the panels, which would not have been anticipated as the result if these experiments had been performed discretely, suggesting a fundamental flaw in the way in which these experiments were performed. 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 presented data. 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 42: 1473‑1483, 2018; DOI: 10.3892/ijmm.2018.3704].</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/PMC12021388/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978978","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] Pharmacokinetics and antitumor efficacy of DSPE‑PEG2000 polymeric liposomes loaded with quercetin and temozolomide: Analysis of their effectiveness in enhancing the chemosensitization of drug‑resistant glioma cells.","authors":"Jun Hu, Junjie Wang, Gang Wang, Zhongjun Yao, Xiaoqian Dang","doi":"10.3892/ijmm.2025.5530","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5530","url":null,"abstract":"<p><p>Following the publication of the above article, an interested reader drew to the Editor's attention that data in certain of the figures appeared to be strikingly similar to that included in three other articles that had been contributed to other publications by the same research group. After having investigated the matter in the Editorial Office in conjunction with the authors, it transpired that certain of the flow cytometric (FCM) data featured in Fig. 4C on p. 697 had been placed erroneously in the published version of this figure, and were duplicates of data featured correctly/as intended in another one of this group's papers. Since the cell experiments in both studies were conducted simultaneously, the subsequent cell growth pictures were also taken at the same time, and the data were inadvertently mislabelled. Upon reviewing their data, the authors realized that the images of the QUE‑NLs (50 μM), QUE‑NLs (100 μM) and QUE‑NLs (200 μM) administration groups in Fig. 4C were the FCM plots that had been featured incorrectly in this figure (as indicated by the green labels in the corrected version of Fig. 4, which is shown on the next page). Furthermore, the cell growth images shown in Fig. 4B for the 'DMSO' and 'Control‑NLs' experiments had also been assembled incorrectly in this figure; the correct images for the 'DMSO' and 'Control‑NLs' data panels are also highlighted by the green labels in the corrected version of Fig. 4 on the next page.  The authors can confirm that the errors made in assembling this figure did not have any 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; furthermore, they apologize to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 37: 690‑702, 2016; DOI: 10.3892/ijmm.2016.2458].</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/PMC12005372/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143993544","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] miR‑217 inhibits the migration and invasion of HeLa cells through modulating MAPK1.","authors":"Lihong Zhu, Shumei Yang, Jianfeng Wang","doi":"10.3892/ijmm.2025.5525","DOIUrl":"10.3892/ijmm.2025.5525","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, regarding the Transwell invasion assay experiments shown in Figs. 2D and 5F, the 'Mimic control' panel in Fig. 2D appeared to contain an overlapping section of data with the 'Blank' data panel in Fig. 5F, 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 control western blot data (GAPDH protein bands) shown in the western blots in Figs. 3C and 5H were apparently the same, although the images had been inserted into these figures as mirror images of each other. In view of the fact that these figures were assembled erroneously, 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 presented data. 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 44: 1824‑1832, 2019; DOI: 10.3892/ijmm.2019.4328].</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/PMC12005373/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143779998","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":"Ceftriaxone affects ferroptosis and alleviates glial cell activation in Parkinson's disease.","authors":"Hui Zhi, Xiaoyu Wang, Yujia Chen, Zenglin Cai, Jingwei Li, Dongkai Guo","doi":"10.3892/ijmm.2025.5526","DOIUrl":"10.3892/ijmm.2025.5526","url":null,"abstract":"<p><p>Parkinson's disease (PD) is the second most common neurodegenerative disorder, which is characterized by the death of dopaminergic neurons. It has been reported that ceftriaxone (CEF) exerts promising effects on alleviating dopaminergic neuron death in PD models. However, the neuroprotective mechanisms of CEF in PD have not been well understood. In the present study, to investigate the neuroprotective effects of CEF through western blot and immunofluorescence assays, two <i>in vivo</i> models were established, namely the 1‑methyl‑4‑phenyl‑1,2,3,6‑tetrahydropyridine (MPTP)‑ and lipopolysaccharide (LPS)‑induced models. Additionally, three <i>in vitro</i> models were used to explore the neuroprotective mechanisms of CEF, namely the 1‑methyl‑4‑phenylpyridinium ion (MPP+)‑induced dopaminergic neuron injury, LPS‑induced microglia activation and TNFα‑induced astrocyte activation models, with key insights derived from western blot and qPCR experiments. The <i>in vivo</i> studies demonstrated that CEF exerted neuroprotective effects and reduced glial cell activation. Additionally, CEF reversed the reduction of tyrosine hydroxylase and suppressed the activation of microglia and astrocytes. Furthermore, the <i>in vitro</i> experiments revealed that CEF could display both direct and indirect neuroprotective effects and could directly alleviate MPP+‑induced neuronal toxicity and suppress the activation of microglia and astrocytes. In addition, CEF indirectly reduced neuronal injury caused by conditioned medium from activated microglia and astrocytes. Mechanistic studies revealed that CEF inhibited the ferroptosis pathway via regulating the expression of solute carrier family 7 member 11 and glutathione peroxidase 4 in a non‑cell‑specific manner. Via inhibiting ferroptosis, CEF could directly protect dopaminergic neurons and prevent glial cell activation, and indirectly impair neurons. In conclusion, the results of the current study highlighted the potential research and therapeutic value of CEF in regulating ferroptosis in PD.</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/PMC12005368/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780001","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":"Trim38 attenuates pressure overload‑induced cardiac hypertrophy by suppressing the TAK1/JNK/P38 signaling pathway.","authors":"Yanan Pang, Luyao Wu, Jiachun Xia, Xin Xu, Chenshan Gao, Lei Hou, Li Jiang","doi":"10.3892/ijmm.2025.5539","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5539","url":null,"abstract":"<p><p>Pathological cardiac hypertrophy is a major contributor to heart failure (HF), resulting in high mortality rates worldwide; therefore, identifying key molecules in pathological cardiac hypertrophy is of critical importance for preventing or reversing HF. Tripartite motif 38 (Trim38) is an E3 ubiquitin ligase that serves a pivotal role in various diseases. The present study aimed to elucidate the regulatory role of Trim38 in pressure overload‑induced pathological cardiac hypertrophy and to explore its underlying molecular mechanisms. The expression of Trim38 was decreased in hypertrophic heart tissues from a murine model of transverse aortic constriction (TAC) and in neonatal rat cardiomyocytes (NRCMs) treated with phenylephrine (PE). Furthermore, Trim38 knockout (Trim38‑KO) aggravated cardiac hypertrophy after TAC, and Trim38 knockdown in cardiomyocytes increased cell cross section area, and upregulated the expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) following treatment with PE. Ubiquitinomics analysis revealed that the MAPK signaling pathway was regulated by Trim38. Furthermore, western blotting confirmed that Trim38‑KO activated TAK1 and JNK/P38. By contrast, Trim38 overexpression in NRCMs suppressed the JNK/P38 signaling pathway and inhibited the phosphorylation of TAK1. Furthermore, Trim38 knockdown resulted in a marked enhancement of TAK1 phosphorylation, concomitant with an augmentation of cardiomyocyte area and a significant upregulation of the hypertrophic biomarkers ANP and BNP. By contrast, infection with an adenovirus containing dominant‑negative TAK1 inhibited TAK1 activity, which attenuated Trim38 knockdown‑induced cardiomyocyte hypertrophy, confirming that TAK1 is a key molecule involved in the protective effects of Trim38 on cardiomyocytes. In conclusion, to the best of our knowledge, the present study is the first to reveal that Trim38 confers protection against pathological cardiac hypertrophy by inhibiting the TAK1/JNK/P38 signaling pathway; therefore, Trim38 may be a promising target for treating cardiac hypertrophy.</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/PMC12045468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144016129","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":"Crosstalk between ferroptosis and endoplasmic reticulum stress: A potential target for ovarian cancer therapy (Review).","authors":"Jiaqi Yang, Yu Wang, Fangyuan Liu, Yizhong Zhang, Fengjuan Han","doi":"10.3892/ijmm.2025.5538","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5538","url":null,"abstract":"<p><p>Ferroptosis is a unique mode of cell death driven by iron‑dependent phospholipid peroxidation, and its mechanism primarily involves disturbances in iron metabolism, imbalances in the lipid antioxidant system and accumulation of lipid peroxides. Protein processing, modification and folding in the endoplasmic reticulum (ER) are closely related regulatory processes that determine cell function, fate and survival. The uncontrolled proliferative capacity of malignant cells generates an unfavorable microenvironment characterized by high metabolic demand, hypoxia, nutrient deprivation and acidosis, which promotes the accumulation of misfolded or unfolded proteins in the ER, leading to ER stress (ERS). Ferroptosis and ERS share common pathways in several diseases, and the two interact to affect cell survival and death. Additionally, cell death pathways are not linear signaling cascades, and different pathways of cell death may be interrelated at multiple levels. Ferroptosis and ERS in ovarian cancer (OC) have attracted increasing research interest; however, both are discussed separately regarding OC. The present review aims to summarize the associations and potential links between ferroptosis and ERS, aiming to provide research references for the development of therapeutic approaches for the management of OC.</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/PMC12045474/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144007381","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":"Harnessing multi‑omics to revolutionize understanding and management of osteosarcoma: A pathway to precision medicine (Review).","authors":"Xuesong Chen, Bin Tian, Yiqun Wang, Jiang Zheng, Xin Kang","doi":"10.3892/ijmm.2025.5533","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5533","url":null,"abstract":"<p><p>Osteosarcoma, the most prevalent primary bone malignancy in children and adolescents, poses significant challenges due to its aggressive nature and propensity for metastasis. Despite advances in treatment, survival rates for high‑risk patients remain unsatisfactory, underscoring the urgent need for innovative approaches. This review explores the vital role of multi‑omics‑integrating genomics, transcriptomics, proteomics and metabolomics‑in unraveling the complex biological landscapes of osteosarcoma. By providing comprehensive insights into tumor heterogeneity, signaling pathways and metabolic reprogramming, multi‑omics facilitates the identification of novel biomarkers and therapeutic targets. The objective of the present study was to highlight the transformative potential of multi‑omics in enhancing the understanding and management of osteosarcoma, ultimately paving the way for personalized treatment strategies and improved patient outcomes. Through this synthesis, the study calls for a concerted effort to integrate multi‑omics into clinical practice, fostering a more precise approach to osteosarcoma care.</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/PMC12021390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143996062","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}