Molecular medicine reports最新文献

{"title":"[Retracted] PPM1A as a key target of the application of Jiawei‑Maxing‑Shigan decoction for the attenuation of radiation‑induced epithelial‑mesenchymal transition in type II alveolar epithelial cells.","authors":"Jinhua Lu, Shengyou Lin, Zechen Lin, Xianlei Lin, Yuezhong Shen, Jingyang Su","doi":"10.3892/mmr.2026.13971","DOIUrl":"10.3892/mmr.2026.13971","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 western blot data featured in Figs. 2B, 4B, 5C and 6A had either already been submitted for publication, or were already published, in several articles in different journals written by different authors at different research institutes. A subsequent investigation of this paper underaken by the Editorial Office confirmed the authenticity of these findings. Owing to the fact that the contentious data in the above article had either already been submitted for publication, or were already published, prior to its submission to <i>Molecular Medicine Reports</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. [Molecular Medicine Reports 24: 825, 2021; DOI: 10.3892/mmr.2021.12465].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13439036/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148630846","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":"From oxidative stress to epigenetic regulation: Molecular mechanisms of preterm brain injury and neuroprotective strategies (Review).","authors":"Yuying Li, Ling Wei, Fang Sun, Huixia Wu, Xijun Sun, Yirong Gan, Xiaohua Kong","doi":"10.3892/mmr.2026.14005","DOIUrl":"10.3892/mmr.2026.14005","url":null,"abstract":"<p><p>Preterm brain injury remains a leading cause of long‑term neurodevelopmental impairment despite advances in neonatal care. Oxidative stress (OS), arising from mitochondrial dysfunction, nicotinamide adenine dinucleotide phosphate oxidase activation and iron‑mediated Fenton reactions, selectively damages the developing brain because of immature antioxidant defenses and vulnerable oligodendrocyte progenitor cells. Critically, OS triggers enduring epigenetic modifications including DNA methylation alterations, histone acetylation changes and microRNA dysregulation, thereby translating acute perinatal insults into sustained changes in gene expression. The complex cellular interplay involving microglia, astrocytes and the neurovascular unit determines injury progression and repair capacity. Emerging neuroprotective strategies include antioxidant therapies, pathway‑targeted agents and cell‑based approaches, while artificial intelligence applications show promise for early risk stratification and personalized monitoring, although these tools remain under prospective validation. The present review synthesized current evidence on the pathological cascade from OS to epigenetic dysregulation in preterm brain injury, evaluated the latest advances in neuroprotective interventions and aimed to inform the development of precision‑based, developmentally timed interventions that address the multifactorial nature of preterm brain injury and improve long‑term neurodevelopmental outcomes.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13573286/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891752","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":"Role of CMTM6 in disease pathogenesis and clinical translation potential (Review).","authors":"Rongtou Huang, Danning Mo, Huitian Huang, Minmin Zhang, Wenhong Yu, Buqing Cao","doi":"10.3892/mmr.2026.13977","DOIUrl":"10.3892/mmr.2026.13977","url":null,"abstract":"<p><p>The chemokine‑like factor (CKLF)‑like MARVEL transmembrane domain‑containing (CMTM) family belongs to the human CKLF gene superfamily, which comprises CKLF and CMTM1‑8. Among its members, CMTM6 encodes a protein exhibiting structural and functional characteristics that lie between classical chemokines and tetraspanins. CMTM6 is expressed in several normal tissues, including those of the immune, reproductive and nervous systems. Notably, its expression is frequently upregulated across a broad spectrum of tumors including, but not limited to, carcinomas of the lung, liver and gastrointestinal tract. CMTM6 contributes to tumor proliferation, invasion and metastasis by inhibiting immune responses, facilitating immune evasion and inducing epithelial‑mesenchymal transition, thereby influencing patient prognosis and survival outcomes. The present review systematically summarizes the molecular functions, mechanisms of action, disease‑related expression patterns and clinical translational applications of CMTM6, aiming to provide novel clinical insights and to guide the development of CMTM6‑targeted therapeutic strategies.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13454919/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148630888","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 on drugs targeting mitochondria‑associated membranes for the treatment of atherosclerosis (Review).","authors":"Shaoying An, Wenhui Sun, Lizhou Shi, Hai Chen, Zhongcheng Mo","doi":"10.3892/mmr.2026.13987","DOIUrl":"https://doi.org/10.3892/mmr.2026.13987","url":null,"abstract":"<p><p>Mitochondria‑associated membranes (MAMs) are specialized contact sites between the endoplasmic reticulum and mitochondria, and serve as the structural foundation for material exchange and signal transduction between these two organelles. MAMs serve critical roles in lipid metabolism, calcium homeostasis, mitochondrial dynamics, autophagy and inflammatory regulation, all of which are closely involved in the pathogenesis of atherosclerosis (AS). Dysregulation of MAM function can promote oxidative stress and chronic inflammation, thereby accelerating atherosclerotic progression. The present review focuses on the molecular mechanisms through which MAMs regulate key cellular processes and influence AS development. Advances in therapeutic agents that target MAMs are summarized, including metformin, statins, 4‑phenylbutyric acid and traditional Chinese medicine compounds, which exert anti‑atherosclerotic effects by restoring MAM integrity, modulating calcium signalling and inhibiting inflammasome activation. By integrating the current knowledge on MAM biology and pharmacology, the present review aims to provide novel strategies for the prevention and treatment of AS through targeted regulation of MAMs.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148765134","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] Human cytomegalovirus RL13 protein interacts with host NUDT14 protein affecting viral DNA replication.","authors":"Guili Wang, Gaowei Ren, Xin Cui, Zhitao Lu, Yanping Ma, Ying Qi, Yujing Huang, Zhongyang Liu, Zhengrong Sun, Qiang Ruan","doi":"10.3892/mmr.2026.14000","DOIUrl":"10.3892/mmr.2026.14000","url":null,"abstract":"<p><p>Following the publication of the above article, a concerned author drew to the Editor's attention that there appeared to be splicing events (and breaks in the continuity) of certain of the gels shown for the GST‑pulldown experiments in Fig. 1 on p. 2170, and the co‑immunoprecipitation experiments shown in Fig. 2 on p. 2171. After assessing their data, the authors have responded to the office to explain that they integrated data from repeated analyses into these figures, rather than the data all being generated from the same experiments. The authors also presented all their original data to the Editorial Office for our perusal, and wished to point out that the data in question were only intended to show qualitative results, and did not form part of the main analysis of the study; nor did the results from these experiments have a major impact on the reported conclusions. After volunteering to repeat these experiments, the authors were given authorization to do so by the Editor, and the revised versions of Figs. 1 and 2 (with revised figure legends) are shown opposite. The revised figures have both resolved the presentational difficulties associated with the original figures, and confirmed the original findings as presented in the published paper. All the authors approve of the publication of this corrigendum, and are grateful to the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this; furthermore, they apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 13: 2167-2174, 2016; DOI: 10.3892/mmr.2016.4778].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13543147/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148840798","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":"6'‑O‑Caffeoylarbutin attenuates experimental hyperuricemia by regulating renal and intestinal urate transport, intestinal barrier integrity, and gut microbiota.","authors":"Xuezhi Yu, Yang Zhang, Konchun Sun, Rui Yang, Xingde Li, Xiuzhen Chen, Tiantian Li, Xiaolei Yang, Ming Li, Lu Liu, Fei Li, Baochun Shen","doi":"10.3892/mmr.2026.13992","DOIUrl":"10.3892/mmr.2026.13992","url":null,"abstract":"<p><p>Hyperuricemia (HUA) is primarily attributed to insufficient uric acid (UA) excretion. 6'‑O‑Caffeoylarbutin (CA), the primary bioactive constituent of anti‑gout herbal tea (Que Zui tea), has demonstrated potential urate‑lowering effects; however, its underlying mechanisms require further elucidation. In the present study, a hypoxanthine (HX) and potassium oxonate (PO) induced hyperuricemia (HUA) mouse model was established to assess the effects of different doses of CA. Biochemical analyses, histopathological examination, western blotting and 16S rRNA gene sequencing were conducted to explore the underlying mechanisms. Notably, CA markedly reduced serum uric acid (SUA), serum creatinine (SCr) and blood urea nitrogen (BUN) levels and alleviated renal and intestinal histopathological damage. In the kidney, CA upregulated ATP‑binding cassette sub‑family G member 2 (ABCG2), and downregulated glucose transporter 9 (GLUT9) and urate transporter 1 expression (URAT1). In the intestine, CA increased ABCG2, PDZ domain containing 1 (PDZK1) and tight junction protein expression, while decreasing GLUT9, suggesting improved urate excretion and barrier integrity. 16S ribosomal RNA sequencing revealed that CA was associated with increased gut microbial diversity and reduced abundance of potentially harmful bacteria, including <i>Desulfovibrio</i>. Phylogenetic Investigation of Communities by Reconstruction of Unobserved States‑based prediction suggested accompanying shifts in microbial functions related to transport and metabolism. In conclusion, these findings suggested that CA may exert beneficial effects on HUA involving regulation of renal and intestinal urate transport, improvement of intestinal barrier function and favorable modulation of gut microbiota. CA may therefore serve as a potential candidate for functional food development or therapeutic strategies against HUA.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13504438/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795585","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":"TREM2 in glioma: Reprogramming the immune microenvironment from mechanistic understanding to clinical translation (Review).","authors":"Junqi Fan, Hongyan Shen, Dan Liu, Songbai Luo, Qingqing Huang, Yi Wen, Libang Yuan","doi":"10.3892/mmr.2026.13952","DOIUrl":"10.3892/mmr.2026.13952","url":null,"abstract":"<p><p>The poor prognosis of high‑grade gliomas, such as glioblastoma, is largely driven by a notably immunosuppressive tumor microenvironment (TME), wherein microglia and tumor‑associated macrophages play important roles. The present review summarizes the current evidence supporting triggering receptor expressed on myeloid cells 2 (TREM2) as a key immunoregulator in the glioma TME. The present review explores the context‑dependent dual role of TREM2, which can either be hijacked to promote immunosuppression and tumor progression or inhibit tumor progression through its notable functions in phagocytosis and antigen presentation. The present review also examines the clinical association of TREM2 expression with glioma grade and patient prognosis, evaluating its potential as a diagnostic and prognostic biomarker. Furthermore, the present review discusses the current landscape of TREM2‑targeted therapeutic strategies, from direct TREM2 inhibition and myeloid‑targeted immunocytokines to nano‑engineered drug delivery systems, and addresses the core translational challenges of these strategies. Looking forward, the importance of leveraging spatial multi‑omics and artificial intelligence to decipher the functional heterogeneity of TREM2 and to guide precision immunotherapy is highlighted. In conclusion, the present review provides a comprehensive framework for understanding the role of TREM2 in glioma; this receptor serves not only as a biomarker for glioma, but as an important signaling hub in the glioma TME. Therefore, the present review aims to support the development of novel therapeutic strategies targeting the immune microenvironment in glioma.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13351602/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148376072","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] Resistin aggravates the expression of proinflammatory cytokines in cerulein‑stimulated AR42J pancreatic acinar cells.","authors":"Chong-Yi Jiang, Wei Wang","doi":"10.3892/mmr.2026.13960","DOIUrl":"10.3892/mmr.2026.13960","url":null,"abstract":"<p><p>Following the publication of the above paper, the authors contacted the Editorial Office to explain that the western blots included in Fig. 3 on p. 504 had inadvertently been included in error. Given the time that has elapsed since the publication of this paper, the authors no longer had access to their original data, and so they have repeated these experiments, and the revised version of this figure is presented below. Note that the results obtained in these experiments are broadly similar to the published results, and the overall scientific conclusions reported in the article are not affected by repeating these experiments. The authors are grateful to the Editor of <i>Oncology Letters</i> for allowing them the opportunity to publish this Corrigendum, and all the authors agree with its publication. [Oncology Letters 15: 502‑506, 2017; DOI: 10.3892/mmr.2016.6027].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13376805/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148422627","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] Matrine‑induced apoptosis in Hep3B cells via the inhibition of MDM2.","authors":"Ning Zhou, Jiequn Li, Ting Li, Guangshun Chen, Zhongqiang Zhang, Zhongzhou Si","doi":"10.3892/mmr.2026.13963","DOIUrl":"10.3892/mmr.2026.13963","url":null,"abstract":"<p><p>Following the publication of the above paper, the following areas of concern associated with the western blot data featured in Figs. 3, 4 and 5 were drawn to the Editor's attention by a concerned reader, essentially involving the apparent incorrect assembly of blots within these figures and duplications of data: i) Control blots were shared between Figs. 3A and 5A, where the experimental conditions were reported to be different; ii) MDM2 blots may have been featured incorrectly in Figs. 4B and 5A, as the control blots/reported experimental conditions featured in these figure parts appeared to be the same; and iii) there was also the probable duplication of protein bands of interest comparing Fig. 5A and B. A subsequent analysis of the data in this paper performed by the Editorial Office also revealed the potential re‑use of data in a paper that was published a year later, also in the journal <i>Molecular Medicine Reports</i>, albeit no authors were held in common comparing these papers, and that paper has since been retracted on account of the re‑use of data with another article: Given the identification of the above problems associated with the assembly of data in three of the figures in this paper, the Editor has decided that it should be retracted from the Journal on account of a lack of confidence in the 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. [Molecular Medicine Reports 15: 442‑450, 2017; DOI: 10.3892/mmr.2016.5999].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13389622/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148472016","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":"A‑Raf: A serine/threonine protein kinase with important biological functions (Review).","authors":"Muhan Yang, Mengying Chen, Jinmei Wei, Yanling Li, Chen Long, Yan Lei, Yanhong Zhou","doi":"10.3892/mmr.2026.13959","DOIUrl":"10.3892/mmr.2026.13959","url":null,"abstract":"<p><p>A‑Raf is a serine/threonine protein kinase that belongs to the RAF kinase family. A‑Raf serves key roles in various physiological and pathological processes, including cell cycle regulation, apoptosis, material transport and metabolism, embryonic development, bone mass maintenance and tumor progression. As research has advanced, the functional mechanisms of the A‑Raf gene have attracted increasing attention. To systematically summarize its biological functions, the present review focuses on the effects of A‑Raf on the cell cycle, apoptosis and cell proliferation, its influence on cellular material transport and metabolic processes, its role in organismal development and bone mass maintenance, its impact on tumor progression, the effects of genetic variations on A‑Raf function and the regulation of A‑Raf by upstream factors. The present review therefore aimed to provide a novel perspective for the comprehensive understanding of the function of A‑Raf.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13376584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148422690","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}