Molecular medicine reports最新文献

{"title":"Role of the NLRP3 inflammasome in diabetes and its complications (Review).","authors":"Xinyi Jiao, Guoqing Tian","doi":"10.3892/mmr.2025.13657","DOIUrl":"https://doi.org/10.3892/mmr.2025.13657","url":null,"abstract":"<p><p>Diabetes and its complications are systemic metabolic disorders triggered by chronic hyperglycemia, with the NOD‑like receptor family pyrin domain‑containing 3 (NLRP3) inflammasome carrying out a central role in disease progression. Activation of the NLRP3 inflammasome is involved not only in the onset of diabetes but also in its complications, including cardiovascular disease, nephropathy and retinopathy. The present review outlines the core mechanisms of the NLRP3 inflammasome and its specific contributions to diabetes and associated conditions. Additionally, emerging therapeutic strategies that target the NLRP3 inflammasome were explored, offering novel insights into the management of diabetes and its associated complications.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 5","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12395217/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961724","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":"Potential role of Fanconi anemia pathway in the pathogenesis of endometrial cancer (Review).","authors":"Mengmeng Yao, Chuqi Liu, Huiyu Ping, Kaidi Meng, Xinru Li, Qingxin Li, Yuanmin Qi, Ziming Zhu, Li Zhang, Aizhong Han","doi":"10.3892/mmr.2025.13660","DOIUrl":"10.3892/mmr.2025.13660","url":null,"abstract":"<p><p>Endometrial cancer (EC) is a common gynecologic malignancy that often exhibits molecular features such as extensive somatic copy number alterations, microsatellite instability and frequent <i>TP53</i> mutations, which considerably affect the physical and mental well‑being of women. The Fanconi anemia (FA) pathway is a DNA damage repair pathway involving multiple FA genes that play crucial roles in DNA damage repair as well as the maintenance of genome stability. Abnormalities in FA, such as deletions or mutations, may lead to defects in DNA damage repair, resulting in increased genomic instability and/or an abnormal cell cycle, ultimately leading to EC. This comprehensive review provides a systematic summary of EC‑related FA genes, elucidates the roles of various FA genes in EC and further speculates on their related mechanisms to facilitate the development of targeted therapies that specifically target key genes, leading to a more accurate and efficient treatment for EC. The present review searched PubMed and Google Scholar for articles published in English up to June 2025 using keywords such as Fanconi anemia pathway, 22 FA genes (<i>FANCA</i>, <i>FANCB</i>, <i>FANCC</i>, <i>FANCD1/BRCA2</i>, <i>FANCD2</i>, <i>FANCE</i>, <i>FANCF</i>, <i>FANCG</i>, <i>FANCI</i>, <i>FANCJ/BRIP1</i>, <i>FANCL</i>, <i>FANCM</i>, <i>FANCN/PALB2</i>, <i>FANCO/RAD51C</i>, <i>FANCP/SLX4</i>, <i>FANCQ/XPF</i>, <i>FANCR/RAD51</i>, <i>FANCS/BRCA1</i>, <i>FANCT/UBE2T</i>, <i>FANCU/XRCC2</i>, <i>FANCV/REV7</i>, <i>FANCW/RFWD3</i>), endometrial cancer (type I: Endometrioid adenocarcinoma; Type II Uterine serous carcinoma, clear‑cell carcinoma, carcinosarcoma), somatic copy number alterations, microsatellite instability, TP53 mutations, pathogenesis, genomic instability, target therapy.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 5","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12404022/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961748","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] Lidocaine inhibits the progression of retinoblastoma <i>in vitro</i> and <i>in vivo</i> by modulating the miR‑520a‑3p/EGFR axis.","authors":"Weiyi Xia, Libo Wang, Dongyi Yu, Xing Mu, Xin Zhou","doi":"10.3892/mmr.2025.13669","DOIUrl":"10.3892/mmr.2025.13669","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that flow cytometric (FCM) assay data featured in Figs. 2 and 7B were strikingly similar to FCM data which were ultimately published in a number of other papers in different journals that were written by different authors at different research institutes, including a paper that was submitted on an earlier date to the journal <i>Experimental and Therapeutic Medicine</i>.  Owing to the fact that the contentious data in the above article were found to be strikingly similar to data that have appeared elsewhere in other papers in the scientific literature, the Editor of <i>Molecular Medicine Reports</i> has decided that this paper should be retracted from the Journal. After contacting the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 20: 1333‑1342, 2019; DOI: 10.3892/mmr.2019.10363].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 5","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12426587/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000912","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":"Aberrant activation of the PI3K/AKT/HIF‑1α pathway promotes glycolysis and lenvatinib resistance in liver cancer.","authors":"Jinfeng Wang, Jianfei Shi, Lili Mi, Man Zhao, Guangjie Han, Fei Yin","doi":"10.3892/mmr.2025.13666","DOIUrl":"10.3892/mmr.2025.13666","url":null,"abstract":"<p><p>Lenvatinib, a multi‑target tyrosine kinase inhibitor, has been approved as the first‑line treatment for advanced liver cancer (LC). However, its efficacy is markedly hindered by the rapid emergence of drug resistance. The phosphatidylinositol 3 kinase/protein kinase B/hypoxia‑inducible factor‑1 α (PI3K/AKT/HIF‑1α) signaling axis represents a key oncogenic pathway that regulates diverse biological processes, including aerobic glycolysis, and is closely associated with tumor progression and therapeutic resistance. However, the specific contribution of the PI3K/AKT/HIF‑1α pathway and aerobic glycolysis to lenvatinib resistance in LC, as well as the potential mechanistic interplay between these processes, remains inadequately elucidated. In the present study, colony formation, flow cytometry and Transwell assays were performed to evaluate the proliferative, apoptotic and invasive capabilities of LC cells. Cell aerobic glycolysis was assessed by detecting glucose uptake, lactate production, intracellular ATP levels and the expression of key glucose metabolism‑related genes. Compared with their parental counterparts, lenvatinib‑resistant (LR) Huh7 and HepG2 cells exhibited an enhanced glycolytic phenotype, characterized by increased glucose uptake, elevated lactate production, higher intracellular ATP levels and upregulated expression of key glycolysis‑related genes. Notably, aberrant activation of the PI3K/AKT/HIF‑1α signaling pathway was observed in LR LC cells. LY294002, a specific PI3K inhibitor, effectively inhibited the PI3K/AKT/HIF‑1α pathway and glycolytic activity in LR cells. Co‑administration of LY294002 with lenvatinib markedly suppressed the PI3K/AKT/HIF‑1α pathway and attenuated the glycolytic activity of Huh7‑LR/HepG2‑LR cells. Moreover, this combination treatment inhibited proliferation and invasion while inducing apoptosis and G₀/G₁ phase cell cycle arrest in LR cells. This evidence indicated that inhibition of the PI3K/AKT/HIF‑1α signaling pathway effectively restored the sensitivity of LR cells to lenvatinib. The findings in the present study demonstrate that aberrant activation of the PI3K/AKT/HIF‑1α pathway is required to enhance glycolysis and confers resistance to lenvatinib in LC. The combination of LY294002 with lenvatinib offers a promising strategic approach for overcoming resistance and enhancing the clinical efficacy of lenvatinib in patients with LC.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 5","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12434331/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961803","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] Hepatitis B core antigen regulates dendritic cell proliferation and apoptosis through regulation of PKC/NF‑κB signaling pathway.","authors":"Lan Liu, Yanxin Huang, Kaili Zhang, Shupeng Song, Shuangxing Li, Yongguo Li, Yinghua Lan","doi":"10.3892/mmr.2025.13651","DOIUrl":"10.3892/mmr.2025.13651","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 four plots shown for the flow cytometric (FCM) data in Fig. 2 on p. 5728 contained overlapping areas, where differently performed experiments were intended to have been represented. Moreover, there were also indications that certain of the data were potentially overlapping with Figs. 4 and 5 (the other pair of figures containing FCM data in this paper). Owing to the fact that the abovementioned data bore notable similarities comparing across different quadrants among these three figures, the Editor of <i>Molecular Medicine Reports</i> has decided that this paper should be retracted from the Journal on the grounds 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 for any inconvenience caused. [Molecular Medicine Reports 18: 5726‑5732, 2018; DOI: 10.3892/mmr.2018.9604].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 5","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12369451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144847590","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] Renal denervation attenuates cardiac hypertrophy in spontaneously hypertensive rats via regulation of autophagy.","authors":"Jionghua Huang, He Huang, Wei Pan, Dejin Ou, Wenjun Dai, Yuhui Lin, Jinlei Wu, Wenjie Xie, Ximing Chen","doi":"10.3892/mmr.2025.13663","DOIUrl":"10.3892/mmr.2025.13663","url":null,"abstract":"<p><p>Following the publication of the above paper, a concerned reader drew to the Editor's attention that data featured in Figs. 1B, 3 and 4 had previously appeared in different contexts in three papers published in other journals (two papers in <i>PLoS One</i>, and one article in <i>Cardiovascular Journal of Africa</i>) that had been written by the same research group, or which contained members thereof. Moreover, the two articles featured in <i>PLoS One</i> have subsequently been retracted on account of the misassembly of various of the figures. An independent investigation of the data in this paper performed by the Editorial Office confirmed these concerns; therefore, the Editor of <i>Molcular Medicine Reports</i> has determined that this paper should be retracted from the Journal on account of a lack of confidence in the presented data. The Editor regrets any inconvenience that has been caused to the readership of the Journal. [Molcular Medicine Reports 16: 2023-2029, 2017; DOI: 10.3892/mmr.2017.6790].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 5","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12404012/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961640","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] Protective effects of atorvastatin on cerebral vessel autoregulation in an experimental rabbit model of subarachnoid hemorrhage.","authors":"Jun-Hui Chen, Ting Wu, Li-Kun Yang, Lei Chen, Jie Zhu, Pei-Pei Li, Xu Hu, Yu-Hai Wang","doi":"10.3892/mmr.2025.13673","DOIUrl":"10.3892/mmr.2025.13673","url":null,"abstract":"<p><p>Following the publication of the above paper, an interested reader drew the authors' attention to the fact that images showing TUNEL staining of hippocampus following SAH induction in Fig. 2A, and the western blot data in Fig. 7, apparently had already been previously published in an article written by the same research group in the journal <i>International Journal of Molecular Medicine</i>. After asking the authors to provide an explanation for the inclusion of the same data in the above paper, the authors responded to say that these two studies were finished at around the same time in their laboratory, both of which explored the neuroprotective effects of atorvastatin following subarachnoid hemorrhage. The study published in <i>International Journal of Molecular Medicine</i> focused on the effect of atorvastatin on AQP4 expression and early brain injury following subarachnoid hemorrhage, whereas the above study explored the protective effects of atorvastatin on cerebral vessel autoregulation and early brain injury after subarachnoid hemorrhage. As the results of the apoptosis experiments were applicable to both studies, the authors deemed it appropriate to include the same data and figures (which were the TUNEL staining data in Fig. 4 and the caspase‑3 western data in Fig. 7 in the above paper) in the two studies. In response to the identification of the matching data in these two papers that were published by this research group, the authors have submitted revised versions of Figs. 4 and 7, now featuring data from the repeated experiments in either case. The Editor of <i>Molecular Medicine Reports</i> has considered that it would be prudent to publish a corrigendum for the above paper featuring these alternative data, and the revised versions of Figs. 4 and 7 are presented on the next page. The authors are grateful to the Editor for allowing them the opportunity to publish this corrigendum for the purposes of the scientific record. [Molecular Medicine Reports 17: 1651‑1659, 2018; DOI: 10.3892/mmr.2017.8074].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 5","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12427605/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000901","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":"Glycolysis to lactylation: Unraveling the metabolic and epigenetic landscape in tissue fibrosis (Review).","authors":"Luna Zhang, Qianqian Li, Yuxin Deng, Yuanxia Zou, Li Wang, Jianchun Li","doi":"10.3892/mmr.2025.13655","DOIUrl":"https://doi.org/10.3892/mmr.2025.13655","url":null,"abstract":"<p><p>Tissue fibrosis represents a pathological condition characterized by excessive accumulation of extracellular matrix (ECM) components. Although historically considered a byproduct of glycolysis, lactate has emerged as a key signaling molecule influencing diverse physiological and pathological processes, including fibrosis. Roles have emerged for lactate metabolism and lactylation, a novel post‑translational modification, in regulating fibroblast activation, ECM deposition and fibrotic progression. The present review provides a comprehensive analysis of the current understanding of glycolysis, lactate and lactylation in tissue fibrosis, with emphasis on cardiac, liver, renal and pulmonary fibrosis. The present review examines how enhanced glycolysis supports the energetic and biosynthetic requirements of activated fibroblasts, how lactate functions as a signaling molecule promoting fibrogenesis and how lactylation connects metabolic changes to epigenetic regulation of gene expression. Furthermore, the present review explores potential therapeutic approaches targeting metabolic pathways and lactylation to mitigate fibrosis, while highlighting future directions in this rapidly evolving field.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 5","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12382434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961721","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":"Reg3β promotes chondrocyte proliferation and ECM metabolism during acetabular roof remodeling in a rat model of DDH‑induced residual dysplasia.","authors":"Peng Wang, Mengxia Li, Wenxuan Wang, Weiguo Sun, Wen Zhen, Qian Sun, Bo Ning, Guanghao Su, Xiaodong Wang","doi":"10.3892/mmr.2025.13653","DOIUrl":"https://doi.org/10.3892/mmr.2025.13653","url":null,"abstract":"<p><p>Residual acetabular dysplasia (RAD) is a common complication after the successful management of developmental dysplasia of the hip (DDH). RAD remodeling is important for predicting the outcome of the affected hip, and optimal treatment can be chosen accordingly. Regenerating islet‑derived protein 3‑β (Reg3β), a multifaceted cytokine, is a prognostic marker for inflammation and cardiac disease. Nevertheless, the roles of Reg3β in RAD remain unclear. Consequently, the aim of the present study was to assess the role of Reg3β in RAD and explore its related functions in chondrocytes <i>in vitro</i>. First, remodeling of the affected hip after fixation removal was observed in a neonatal rat DDH model, which simulated the process of RAD. Reg3β expression in RAD was upregulated at weeks 1, 2 and 4, as determined by western blot analysis. The serum concentration of Reg3β was greater than that of normal rats at 2 weeks and returned to normal levels at 4 weeks. Subsequently, it was found that Reg3β promoted cell proliferation and extracellular matrix (ECM) metabolism via the Jak2/Stat3/Socs3 signaling pathway through gene knockdown and addition of recombinant Reg3β protein. These findings suggest that Reg3β is a novel potent prognostic biomarker for the remodeling of RAD via regulation of chondrocyte proliferation and metabolism of the ECM.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 5","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12382431/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961734","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 monocytes in the pathogenesis of antiphospholipid syndrome and potential therapeutic targets (Review).","authors":"Rongxiu Huo, Chengcheng Wei, Yanting Yang, Yang Yang, Xiaocong Huo, Bangqin Wang, Danli Meng, Yijia Huang, Rongjun Huang, Jinying Lin, Xinxiang Huang","doi":"10.3892/mmr.2025.13670","DOIUrl":"10.3892/mmr.2025.13670","url":null,"abstract":"<p><p>Antiphospholipid syndrome (APS) is an autoimmune disorder characterized primarily by arterial and/or venous thrombosis, obstetric complications and persistent positivity for antiphospholipid antibodies (aPLs). It has been proposed that the pathogenesis of APS is closely associated with vascular endothelial cell activation, complement activation and platelet activation. Notably, APS may be key to understanding the relationship between innate immune cells, and thrombosis and obstetric complications. Monocytes are activated by aPLs, adopting a pro‑inflammatory and pro‑coagulant phenotype, and producing inflammatory cytokines; however, the exact mechanisms of action of monocytes in APS remain unclear. Monocytes may act as an intermediary, triggering immune dysregulation, closely linking them to thrombosis and obstetric complications. Therefore, a better understanding of the potential pathogenic role of monocytes in APS is required, which could assist clinicians in gaining deeper insights into the pathogenesis of APS and identifying new therapeutic targets. This may provide new options for the management of APS. Therefore, the present study aimed to review monocytes and their role in APS.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 5","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12426590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000895","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}