Molecular medicine reports最新文献

{"title":"[Retracted] Resveratrol pretreatment attenuates traumatic brain injury in rats by suppressing NLRP3 inflammasome activation via SIRT1.","authors":"Peng Zou, Xiaoxiao Liu, Gang Li, Yangang Wang","doi":"10.3892/mmr.2026.13901","DOIUrl":"https://doi.org/10.3892/mmr.2026.13901","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, in addition to the apparent duplication of control GAPDH western blots comparing Figs. 1A and 2C, the SIRT1 western blot data featured in Fig. 5A on p. 3215 had already been published previously in an article written entirely by different authors in different departments of the same research institute in the journal <i>Mediators of Inflammation</i>. Owing to the fact that the contentious data in the above article had already been 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 17: 3212‑3217, 2018; DOI: 10.3892/mmr.2017.8241].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840206","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":"Gut microbiota and its metabolites: Key factors of drug resistance in the treatment of advanced prostate cancer (Review).","authors":"Jingheng Song, Hongguo Cui, Peisen Yang, Yankai Xu, Yuanyuan Liu, Gang Zhang, Yangyang Liu, Aimin Tian, Jizhong Che, Hui Sun, Zhengchao Zhang","doi":"10.3892/mmr.2026.13900","DOIUrl":"https://doi.org/10.3892/mmr.2026.13900","url":null,"abstract":"<p><p>Prostate cancer (PCa) is a leading cause of cancer‑related deaths among men, and its incidence is increasing worldwide. Current treatments include androgen deprivation therapy, surgery, radiotherapy, chemotherapy and immunotherapy, among others. Surgical treatment has a less effective therapeutic effect in patients with advanced PCa. However, drug‑based treatments often lead to the development of drug resistance, highlighting the need to adopt new treatment strategies. The present review summarizes the role of gut microbiota and its metabolites in the treatment resistance of advanced PCa, potential microbiome‑targeted therapies and future research directions, for developing novel therapeutic approaches to overcome drug resistance and improve prognosis.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840340","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":"Applications of humanized mice in <i>Mycobacterium tuberculosis</i> infections (Review).","authors":"Binghua Han, Fang Liu, Jinzhao Long, Jiongjiong Wang, Yange Cui, Haiyan Yang","doi":"10.3892/mmr.2026.13898","DOIUrl":"https://doi.org/10.3892/mmr.2026.13898","url":null,"abstract":"<p><p>Tuberculosis is an infectious disease caused by <i>Mycobacterium tuberculosis</i> (<i>M.tb</i>), which poses a notable threat to human health. The present review aims to explore the application of humanized mice in the study of <i>M.tb</i> infections. Due to differences in immune responses between mice and humans, humanized mice with human immune systems have been developed as models to characterize human immune responses to <i>M.tb</i>. The present review searched for research on humanized mice and tuberculosis in Web of Science and PubMed using the keywords 'humanized', 'mice' or 'mouse' and 'tuberculosis', and summarized the findings. Humanized non‑obese diabetic (NOD).Cg‑Rag1^tm1MoMIl2rg^tm1Wjl and NOD.Cg‑Prkdc^scidIl2rg^tm1Wjl mice have the potential to accelerate the screening of vaccine candidates, therapeutic regimens and the 'bench to bedside' translation process. New therapies, such as IgG1 P1AM25 in humanized Fcγ receptor mice and phage DS6A in humanized NOD.Cg‑Prkdc^scid Il2rg^tm1Wjl Tg(cytomegalovirus‑interleukin‑3, granulocyte‑macrophage colony‑stimulating factor and KIT ligand)1Eav/MloySzJ mice, may have potential for treating tuberculosis. The humanized bone marrow‑liver‑thymus and human leukocyte antigens transgenic mouse models are effective tools for studying the co‑infection of <i>M.tb</i> and human immunodeficiency virus (HIV). The present review highlights the key role of humanized mouse models in advancing the understanding of <i>M.tb</i> infection, including host‑pathogen interactions, immune evasion mechanisms, vaccine development, therapeutic interventions and co‑infection with HIV. In conclusion, humanized mice provide a powerful platform for bridging the gap between preclinical research and clinical tuberculosis therapeutics.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840247","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":"Multifaceted regulatory role of proline‑ and glutamine-rich splicing factor in tumors (Review).","authors":"Shilin Zhang, Zhenhua Li, Li Fu","doi":"10.3892/mmr.2026.13896","DOIUrl":"https://doi.org/10.3892/mmr.2026.13896","url":null,"abstract":"<p><p>Proline‑ and glutamine‑rich splicing factor (SFPQ) is an RNA‑binding protein that is predominantly localized in the nucleus and plays a multifaceted regulatory role in the process of gene expression. The functions of SFPQ include the promotion or inhibition of gene transcription, pre‑mRNA splicing, mRNA processing, transport and localization, and translation. The primary impact of SFPQ on cellular processes is the regulation of cell cycle progression and apoptosis. In addition, SFPQ represents an important element of paraspeckles, exerting a notable influence on gene expression within the nucleus. The expression of SFPQ is altered in tumors, promoting the development and drug resistance of tumors in various ways, notably altering the prognosis of patients. In the present review, the fundamental physiological functions of SFPQ and its particular effects on tumorigenesis and development are discussed.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840264","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":"[Retracted] Rosiglitazone exerts neuroprotective effects via the suppression of neuronal autophagy and apoptosis in the cortex following traumatic brain injury.","authors":"Junchao Yao, Kebin Zheng, Xiang Zhang","doi":"10.3892/mmr.2026.13894","DOIUrl":"10.3892/mmr.2026.13894","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 various of the western blot data featured in Fig. 2B appeared to have also been included in Figs. 4B and 8A; moreover, western blot data also appeared to have been duplicated comparing Figs. 3A and 8A, Figs. 4B and 5A, Figs. 3A and 5A, and Figs. 6A and 7A. In addition, western blot data featured in various of these figures also reappeared in two papers written by different authors at different research institutes that were submitted for publication at later dates to the journals <i>Experimental and Therapeutic Medicine</i> and <i>Molecular Medicine Reports</i>. In view of the fact that so many instances of the duplication of data within several of the figures in the above paper were identified, the Editor has decided that this paper 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 12: 6591‑6597, 2015; DOI: 10.3892/mmr.2015.4292].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13153862/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776573","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":"Effects of ALDH2 gene expression on the oxidative stress‑mediated NF‑κB/mTOR pathway in ketamine‑induced cystitis.","authors":"Xiao Jian Xi, Yong Yao, Peng Gu, Min Hao Zhang","doi":"10.3892/mmr.2026.13895","DOIUrl":"10.3892/mmr.2026.13895","url":null,"abstract":"<p><p>Aldehyde dehydrogenase 2 (ALDH2) serves an important role in regulating the development of organ injury. The present study aimed to investigate the effects of ALDH2 gene expression on the oxidative stress‑mediated NF‑κB/mTOR pathway in ketamine (Ket)‑induced cystitis (KIC). Primarily, human bladder epithelial cells of the SV‑HUC‑1 cell line were divided into groups for incubation with different concentrations of Ket: 0, 0.5, 1, 1.5 and 2 mM. ALDH2 protein expression was then detected after 48 h of incubation with Ket. Subsequently, SV‑HUC‑1 cells were separated into a number of treatment groups, including: i) Control groups, comprising negative control (NC), NC + mTOR activator MHY1485 (Act), NC + Ket and NC + Ket + Act groups; ii) ALDH2 knockdown groups that were transfected with siRNA sequences targeting ALDH2 (si‑ALDH2), including si‑ALDH2, si‑ALDH2 + Act, si‑ALDH2 + Ket and si‑ALDH2 + Ket + Act groups; and iii) ALDH2 overexpression (OE‑ALDH2) transfection groups, comprising OE‑ALDH2, OE‑ALDH2 + Act, OE‑ALDH2 + Ket and OE‑ALDH2 + Ket + Act groups. The levels of apoptosis, oxidative stress and inflammatory protein expression were assessed in each group. The results of the present study demonstrated that ALDH2 protein expression was significantly higher after treatment with Ket compared with the control group. Further analysis revealed that the si‑ALDH2 + Ket group demonstrated the highest levels of apoptosis, oxidative stress and inflammatory protein expression amongst all treatment groups. The levels of these indicators notably improved in the OE‑ALDH2 + Ket group compared with the NC + Ket group. Therefore, the results of the present study revealed that ALDH2 overexpression reduced Ket‑induced apoptosis, oxidative stress and inflammatory protein expression. Furthermore, co‑treatment with Act was shown to mitigate these factors. Additionally, ALDH2 may have modulated the inflammatory response by promoting mTOR activation and inhibiting NF‑κB phosphorylation. The present study concluded that ALDH2 may represent a novel target for KIC treatment.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13153863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840324","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 neutrophil extracellular traps in sepsis‑induced coagulopathy (Review).","authors":"Jiandong Hu, Mengli Jin, Zhihua Cao, Binbin Zheng, Yuan Zheng, Hao Shen","doi":"10.3892/mmr.2026.13897","DOIUrl":"https://doi.org/10.3892/mmr.2026.13897","url":null,"abstract":"<p><p>Sepsis affects an estimated 166 million individuals globally with 21.4 million annual deaths and represents a notable public health challenge. Sepsis‑induced coagulopathy (SIC) is a marked complication of sepsis, characterized by dysregulated hemostasis and microvascular thrombosis. Neutrophil extracellular traps (NETs) are pivotal mediators linking innate immunity to thrombo‑inflammation in this process. The present review systematically examined the epidemiology and pathogenesis of SIC, the molecular mechanisms of NET release (suicidal, vital, mitochondrial and non‑canonical pathways) and the mechanistic pathways by which NETs regulate SIC. NETs disrupt endothelial integrity, amplify platelet activation, propagate coagulation cascades and suppress fibrinolysis, thereby establishing a self‑amplifying cycle that accelerates progression to disseminated intravascular coagulation and multiple organ failure. Furthermore, the present review highlighted current therapeutic strategies targeting NETs, including inhibition of NET synthesis, acceleration of NET clearance and disruption of platelet‑neutrophil interactions. Elucidating the central role of NETs in SIC pathophysiology may facilitate the development of novel biomarkers and precision therapeutic interventions for this life‑threatening condition.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840330","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":"Cepharanthine inhibits lysosomes and induces apoptosis in triple‑negative breast cancer cells.","authors":"Juan Li, Siqin Zhou, Yu Wang, Guanghan Ou, Danli Yang, Liwen Shen","doi":"10.3892/mmr.2026.13899","DOIUrl":"https://doi.org/10.3892/mmr.2026.13899","url":null,"abstract":"<p><p>Triple‑negative breast cancer (TNBC) is an aggressive malignancy with limited treatment options and a poor prognosis. The present study investigated the anti‑TNBC effects and underlying mechanisms of cepharanthine (CEP), an isoquinoline alkaloid derived from <i>Stephania cephalantha</i>. The findings showed that CEP inhibited colony formation and induced apoptosis in TNBC cells. Mechanistic investigations revealed that CEP upregulated the pro‑apoptotic protein phorbol‑12‑myristate‑13‑acetate‑induced protein 1 (NOXA), downregulated the anti‑apoptotic protein Bcl‑2 and reduced the mitochondrial membrane potential (ΔΨm). Using quantitative proteomics and limited proteolysis‑coupled mass spectrometry, the present study demonstrated that CEP bound directly to the lysosomal enzymes cathepsin B and cathepsin D, thereby impairing their maturation and suppressing lysosomal degradation. This inhibition triggered the nuclear accumulation of transcription factor EB (TFEB), a factor that regulates the expression of Bcl‑2 family members. These findings indicated that CEP induced apoptosis by inhibiting lysosomal function and activating TFEB, leading to the upregulation of NOXA and downregulation of Bcl‑2. In conclusion, the present study demonstrated the pro‑apoptotic effect of CEP in TNBC cells and identified lysosomal enzymes as the direct target for its mechanism of action. These findings provided a foundation for further investigation of the pharmacological mechanisms of CEP.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840286","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":"[Expression of Concern] Electroacupuncture at GV20‑GB7 regulates mitophagy to protect against neurological deficits following intracerebral hemorrhage via inhibition of apoptosis.","authors":"Ruiqiao Guan, Zhihao Li, Xiaohong Dai, Wei Zou, Xueping Yu, Hao Liu, Qiuxin Chen, Wei Teng, Peng Liu, Xiaoying Liu, Shanshan Dong","doi":"10.3892/mmr.2026.13870","DOIUrl":"10.3892/mmr.2026.13870","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, in comparing the bar charts shown in Fig. 2D and F on p. 5 representing the quantification of the western blot data featured in Fig. 2C and E respectively, these bar charts were strikingly similar, suggesting that the same chart may have erroneously been included in this figure twice to represent the different experimental conditions. The authors have been contacted by the Editorial Office to offer an explanation for this apparent anomaly in the presentation of the data in this paper, and we are awaiting their response. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of these potential problems while the Editorial Office continues to investigate this matter further. [Molecular Medicine Reports 24: 492, 2021; DOI: 10.3892/mmr.2021.12131].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"33 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13088085/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147608850","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":"Urinary 8‑OHdG and MDA as rapid biodosimetry markers in the lethal/sublethal dose range.","authors":"Satoru Monzen, Kenji Terada, Yusuke Tawata, Takanori Sato, Nozomi Kousaka, Yasushi Mariya","doi":"10.3892/mmr.2026.13884","DOIUrl":"https://doi.org/10.3892/mmr.2026.13884","url":null,"abstract":"<p><p>Rapid and accurate assessment of ionizing radiation exposure is essential for effective triage in acute radiation syndrome. However, although several biodosimetry approaches are available (such as clinical signs, routine laboratory markers and cytogenetic assays), rapid and scalable dose stratification remains challenging in large‑scale emergencies. The present study evaluated two oxidative stress‑related urinary metabolites, 8‑hydroxy‑2'‑deoxyguanosine (8‑OHdG) and malondialdehyde (MDA), as candidate biomarkers in the high‑dose exposure range. Male C57BL/6NJcl mice (8 weeks) received whole‑body X‑irradiation (0‑10 Gy at 1.0 Gy/min). Urine samples were collected at 24 or 72 h postexposure. Urinary 8‑OHdG was quantified using a lateral flow immunochromatographic assay (with ELISA validation) and MDA levels were measured using a thiobarbituric acid‑reactive substances assay. Values were normalized to creatinine. Tissue distribution was assessed across multiple organs, and bone marrow cell cultures were used to examine extracellular release and to support tissue‑origin inference under controlled conditions. Bone marrow injury was evaluated by flow cytometry detection of apoptotic cells. Urinary 8‑OHdG and MDA levels increased dose‑dependently, with significant correlations (8‑OHdG: r=0.55 at 24 h, r=0.50 at 72 h; MDA: r=0.65 at 24 h, r=0.50 at 72 h; all P<0.05). A sharp rise occurred at ≥7 Gy, where 8‑OHdG levels rose 3.7‑fold and MDA levels rose 2.3‑fold relative to controls. Tissue analyses identified the bone marrow and spleen as primary sources. <i>In vitro</i> bone marrow cultures confirmed dose‑dependent release, while cell death profiling indicated a shift toward necrosis at high doses. Together, these findings supported the potential utility of urinary 8‑OHdG and MDA as rapid and noninvasive biomarkers for early risk stratification in radiation emergencies.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"33 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776637","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}