Molecular medicine reports最新文献

{"title":"Research progress in the regulatory mechanism of silent information regulator 1 in sepsis (Review).","authors":"Qilong Zhou, Weijie Gao, Weijin Zhang, Shu Tang, Hongxue Fu, Pengfei Pan","doi":"10.3892/mmr.2025.13573","DOIUrl":"https://doi.org/10.3892/mmr.2025.13573","url":null,"abstract":"<p><p>Sepsis is characterized by a dysregulated systemic inflammatory response to infection. Despite substantial advances in its treatment, sepsis remains a significant global health burden. An understanding of the underlying mechanisms driving sepsis is crucial for the development of targeted therapeutic strategies. Silent information regulator 1 (SIRT1), a member of the class III histone deacetylases, plays a pivotal role in regulating gene expression by catalyzing the deacetylation of lysine residues on non‑histone and histone proteins. SIRT1 has been shown to exert significant anti‑inflammatory, anti‑oxidative, anti‑apoptotic and metabolic regulatory effects, making it a potential therapeutic target for sepsis. The present study reviewed the latest research progress on the signaling pathways modulated by SIRT1 in sepsis and its associated regulatory mechanisms to further elucidate the pathogenesis of sepsis and guide its clinical treatment.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143046","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":"Exosomal miRNAs in pancreatitis: Mechanisms and potential applications (Review).","authors":"Liwei Wang, Jiaying Zhang, Ziwei He, Xiangding Kong, Chengxiang Liu, Yingzhi Xia, Ming Yang, Kuanyu Wang","doi":"10.3892/mmr.2025.13575","DOIUrl":"https://doi.org/10.3892/mmr.2025.13575","url":null,"abstract":"<p><p>Pancreatitis, an inflammatory disorder of the pancreas, remains a significant clinical challenge owing to its complex pathogenesis and the lack of reliable biomarkers for early diagnosis and effective treatment. Exosomes, small extracellular vesicles containing a variety of biomolecules including microRNAs (miRNAs), have been identified as key mediators of intercellular communication. Emerging evidence highlight the pivotal role of exosomal miRNAs in the regulation of pancreatic inflammation, fibrosis and cellular responses during pancreatitis. The present review comprehensively examined the mechanisms by which exosomal miRNAs contribute to the pathophysiology of pancreatitis. It discussed the effect of exosomal miRNAs on various cell types, such as pancreatic acinar cells, immune cells and pancreatic stellate cells, highlighting their roles in modulating inflammation, fibrosis and tissue remodeling. Furthermore, it explored the potential of exosomal miRNAs as non‑invasive biomarkers for diagnosing pancreatitis and predicting disease progression. The present review provided an overview of current research and discusses future directions for exosomal miRNA‑based therapies, offering new insights into potential strategies for managing pancreatitis.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142962","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":"METTL3‑mediated m6A methylation and its impact on OTUD1 expression in chronic obstructive pulmonary disease.","authors":"Jiameng Gao, Zheyi Shen, Weibin Tian, Junyi Xia, Weixin Cao, Zhuoru Chen, Zhihua Wang, Yao Shen","doi":"10.3892/mmr.2025.13571","DOIUrl":"https://doi.org/10.3892/mmr.2025.13571","url":null,"abstract":"<p><p>Chronic obstructive pulmonary disease (COPD) is characterized by persistent airflow limitation and chronic inflammation, often exacerbated by cigarette smoke exposure. Ovarian tumor protease domain‑containing protein 1 (OTUD1), a deubiquitinase, has previously been identified as a negative regulator of inflammation through its suppression of NF‑κB signaling. The present study explored the role of OTUD1 in COPD and the regulatory effects of N6‑methyladenosine (m6A) methylation on OTUD1 expression. The expression of OTUD1 in COPD was analyzed using public datasets (GSE38974 and GSE69818). In addition, BEAS‑2B cells were exposed to cigarette smoke extract (CSE) to investigate OTUD1 expression changes. OTUD1 overexpression and knockdown models were also constructed, and the levels of inflammation‑related genes and proteins, inflammatory cytokines and cell pyroptosis were measured using reverse transcription‑quantitative PCR, western blotting, ELISA and flow cytometry. The role of methyltransferase‑like 3 (METTL3)‑mediated m6A methylation in regulating OTUD1 was also examined. Notably, OTUD1 expression was significantly reduced in advanced COPD compared with that in the earlier stage. Furthermore, CSE exposure suppressed OTUD1 expression, which was associated with increased cell pyroptosis and elevated levels of the inflammatory cytokines IL‑1β and IL‑18. OTUD1 overexpression mitigated these effects, indicating its protective role against CSE‑induced cellular damage. Furthermore, METTL3‑mediated m6A methylation inhibited OTUD1 expression, with YTH m6A RNA binding protein 2 (YTHDF2) acting as the reader of this modification. Knockdown of METTL3 or YTHDF2 reduced m6A methylation and restored OTUD1 expression, highlighting a potential mechanism by which cigarette smoke suppresses OTUD1 through enhanced m6A methylation. In conclusion, OTUD1 may serve a protective role in COPD by inhibiting inflammation and reducing cell damage caused by cigarette smoke exposure. The suppression of OTUD1 through METTL3‑mediated m6A methylation and YTHDF2 interaction represents a novel mechanism contributing to COPD pathogenesis, suggesting potential therapeutic targets for mitigating disease progression.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143039","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] Slit2 suppresses endothelial cell proliferation and migration by inhibiting the VEGF‑Notch signaling pathway.","authors":"Guo-Jian Li, Yong Yang, Guo-Kai Yang, Jia Wan, Dao-Lei Cui, Zhen-Huan Ma, Ling-Juan Du, Gui-Min Zhang","doi":"10.3892/mmr.2025.13572","DOIUrl":"https://doi.org/10.3892/mmr.2025.13572","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 the Transwell migration assay data shown in Fig. 2 on p. 1984 had already appeared in an article written by different authors at different research institutes that was published previously in the journal <i>Drug Design, Development and Therapy</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. 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. [Molecular Medicine Reports 15: 1981‑1988, 2017; DOI: 10.3892/mmr.2017.6240].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142955","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":"Mechanistic exploration of hexokinase 2 and metabolism in diabetic cardiomyopathy.","authors":"Bo Li, Xu Zhao, Liming Ma, Xiaoying Wang, Yan Ding, Yi Zhang","doi":"10.3892/mmr.2025.13576","DOIUrl":"https://doi.org/10.3892/mmr.2025.13576","url":null,"abstract":"<p><p>The pathogenesis of diabetic cardiomyopathy (DCM) remains incompletely understood. The present study employed weighted gene co‑expression network analysis to analyze the DCM transcriptome dataset from the Gene Expression Omnibus (GEO) database to identify genes associated with this disease. Subsequently, both internal and external validation of the expression of the characterized genes was performed using additional GEO datasets. Key DCM genes were validated at both the <i>in vitro</i> and <i>in vivo</i> levels by Western blot and immunohistochemistry, IHC). Furthermore, the mechanisms of gene and metabolite co‑expression in DCM were investigated through transcriptome sequencing of cells overexpressing disease‑associated genes, combined with quantitative measurements of metabolites. Notably, hexokinase 2 (HK2) was downregulated in both DCM cell and db/db mouse models. Low expression of HK2 was implicated in the disruption of organic acids and their derivatives, as well as the receptor for advanced glycation end‑products pathway.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143034","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":"Chimeric antigen receptor T cell immunotherapy‑associated hemophagocytic lymphohistiocytosis: Pathogenesis, clinical manifestation, diagnosis and management compared with cytokine release syndrome (Review).","authors":"Jinglin Hu, Cuicui Feng, Lingbo He, Yini Wang","doi":"10.3892/mmr.2025.13578","DOIUrl":"https://doi.org/10.3892/mmr.2025.13578","url":null,"abstract":"<p><p>Chimeric antigen receptor (CAR) T cell therapy is used to treat hematological malignancy. However, it carries the risk of life‑threatening inflammatory toxicity, including cytokine release syndrome (CRS) and CAR T cell‑associated hemophagocytic lymphohistiocytosis (CARHLH). CRS is a common side effect of CAR T cell therapy, with fever and multiorgan functional impairment as the primary clinical manifestation. CARHLH and CRS have similar clinical manifestations. However, CARHLH is associated with a high mortality rate. CARHLH was previously considered a specific type of CRS, however, it must be promptly differentiated from CRS for treatment initiation, with management differing from that of CRS. The pathogenesis of CARHLH differs from that of CRS. The present review aimed to summarize the pathogenesis, diagnosis and treatment of CARHLH to assist in its early identification and management.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142958","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":"Insulin‑like growth factor in cancer: New perspectives (Review).","authors":"Duoming Wu, Shi Dong, Wence Zhou","doi":"10.3892/mmr.2025.13574","DOIUrl":"https://doi.org/10.3892/mmr.2025.13574","url":null,"abstract":"<p><p>The complex nature and heterogeneity of cancer present challenges for cancer treatment. As a class of single‑chain peptides, insulin‑like growth factors (IGFs) play key roles in cell growth, proliferation, differentiation and metabolic regulation. IGFs promote the proliferation, migration and invasive ability of tumor cells and are closely associated with poor prognosis. Furthermore, IGFs can influence the interactions between immune cells in the tumor microenvironment leading to immune escape. Moreover, the activation of signals associated with IGFs mediates the resistance of tumor cells to chemotherapeutic drugs. With the increasing incidence of tumor events, the desire for new therapies is becoming more urgent. This article comprehensively summarizes the molecular biological mechanisms of IGFs in tumorigenesis and the development of therapies related to targeting IGFs, with the hope of providing new insights into cancer treatment.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143031","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":"Role of amino acid metabolism in osteoporosis: Effects on the bone microenvironment and treatment strategies (Review).","authors":"Chang Zhou, Jiaheng Zhang, Qizhi Liu, Yanghongxu Guo, Mengyuan Li, Jing Tao, Sujuan Peng, Ronghui Li, Xianguang Deng, Guomin Zhang, Huiping Liu","doi":"10.3892/mmr.2025.13577","DOIUrl":"https://doi.org/10.3892/mmr.2025.13577","url":null,"abstract":"<p><p>Osteoporosis is a metabolic disease characterized by an imbalance in bone remodeling. Its pathogenesis involves a functional imbalance of osteoblasts, osteoclasts and bone marrow mesenchymal stem cells. Amino acid metabolism is a key biochemical process for maintaining biological activities, including protein synthesis, energy supply and signal transduction. Amino acid metabolism affects bone homeostasis by regulating osteocyte function and the bone microenvironment. Branched‑chain amino acid and aromatic amino acid metabolism are involved in the regulation of bone mineral density. The present review demonstrates the mechanism of amino acid metabolism in osteoporosis and its potential therapeutic value. In addition, the present review aimed to summarize the application of Mendelian randomization and metabolomic methods to provide a reference for future research and clinical interventions.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142984","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] Effect of selective inhibition or activation of PGE2 EP1 receptor on glomerulosclerosis.","authors":"Xu Chen, Jun Yin, Yuyin Xu, Zhi Qiu, Jing Liu, Xiaolan Chen","doi":"10.3892/mmr.2025.13538","DOIUrl":"https://doi.org/10.3892/mmr.2025.13538","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 immunohistochemical images shown in Fig. 2C and 3A, at least four pairs of data panels showed evidence of overlapping data, both within the same figure parts and comparing between them. Owing to the large number of data duplication events that have been identified in this paper, the Editor of <i>Molecular Medicine Reports</i> has decided that it 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 satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 22: 2887‑2895, 2020; DOI: 10.3892/mmr.2020.11353].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12046370/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144024577","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":"Anticancer effects of salvianolic acid A through multiple signaling pathways (Review).","authors":"Cheng-Xia Li, Qi Xu, Shi-Ting Jiang, Dan Liu, Chao Tang, Wen-Li Yang","doi":"10.3892/mmr.2025.13541","DOIUrl":"https://doi.org/10.3892/mmr.2025.13541","url":null,"abstract":"<p><p><i>Salvia miltiorrhiza</i> Bunge (<i>Salvia miltiorrhiza</i>), commonly referred to as Danshen, is a well‑known herb in traditional Chinese medicine, the active ingredients of which are mostly categorized as water soluble and lipid soluble. Salvianolic acids are the major water‑soluble phenolic acid constituents of Danshen; salvianolic acid B is the most prevalent, with salvianolic acid A (SAA) being the next most predominant form. SAA offers a wide array of pharmacological benefits, including cardiovascular protection, and anti‑inflammatory, antioxidant, antiviral and anticancer activities. SAA is currently undergoing phase III clinical trials for diabetic peripheral neuropathy and has shown protective benefits against cardiovascular illnesses; furthermore, its safety and effectiveness are encouraging. By targeting several signaling pathways, preventing cell cycle progression, tumor cell migration, invasion and metastasis, normalizing the tumor vasculature and encouraging cell apoptosis, SAA can also prevent the growth of malignancies. In addition, it enhances sensitivity to chemotherapeutic drugs, and alleviates their toxicity and side effects. However, the broad therapeutic use of SAA has been somewhat limited by its low content in <i>Salvia miltiorrhiza</i> Bunge and the difficulty of its extraction techniques. Therefore, the present review focuses on the potential mechanisms of SAA in tumor prevention and treatment. With the anticipation that SAA will serve a notable role in clinical applications in the future, these discoveries may offer a scientific basis for the combination of SAA with conventional chemotherapeutic drugs in the treatment of cancer, and could establish a foundation for the development of SAA as an anticancer drug.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12056544/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144018437","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}