Molecular medicine reports最新文献

{"title":"Recent advances in the antileukemic mechanisms of fucoidan based on epigenetic regulation (Review).","authors":"Guangyan Yu, Qiuling Xu, Ran An","doi":"10.3892/mmr.2025.13671","DOIUrl":"https://doi.org/10.3892/mmr.2025.13671","url":null,"abstract":"<p><p>Leukemia is a malignant clonal disease originating from hematopoietic stem cells, whose complex pathogenesis is associated with multiple factors. Epigenetic regulation has been found to play an important role in the occurrence and development of leukemia, and has become a major focus of research. Fucoidan (FPS), a natural sulfated polysaccharide primarily extracted from marine brown algae, is rich in L‑fucose and sulfate groups. It has a variety of biological activities, including antioxidant, antiviral, immunomodulatory and antitumor activities. Notably, FPS exhibits antileukemic potential by epigenetically inhibiting the protein expression of DNA methyltransferases, regulating methylation levels at the promoter regions of specific genes such as peroxiredoxin 2, influencing the activity of histone‑modifying enzymes, and controlling the expression of non‑coding RNAs (ncRNAs), including microRNAs and long ncRNAs. These effects collectively suppress the proliferative and differentiation of leukemic cells. The present review examines the epigenetic regulatory mechanisms by which FPS may inhibit leukemia, including DNA methylation, histone modification and ncRNA‑associated mechanisms. In addition, it also discusses the potential advantages and challenges of FPS in the treatment of leukemia, as well as future research directions for FPS in leukemia therapy, aiming to provide a stronger theoretical basis for its clinical application.</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":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000923","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":"Circular RNAs: Fundamental mechanisms in tumor metastasis and detection strategies (Review).","authors":"Xiangjun Dong, Yinwei Che, Yuzhuo Jiao, Hao Dong, Qingchao Ren, Huashan Sun, Tao Zhao","doi":"10.3892/mmr.2025.13667","DOIUrl":"10.3892/mmr.2025.13667","url":null,"abstract":"<p><p> As a class of endogenous non‑coding RNAs, circular RNAs (circRNAs) are produced by an event known as back‑splicing. Although circRNAs were initially considered to be the product of abnormal splicing events, increasing evidence has shown their vital role in the development of various diseases, especially malignant tumors. Tumor metastasis is the leading cause of tumor deterioration and cancer‑associated mortality, and involves biological changes to malignant cells. A number of circRNAs can mediate tumor progression, especially tumor metastasis. Furthermore, due to their unique structural features, circRNAs are highly stable in body fluids, and have temporal and tissue specificity, making them potentially ideal non‑invasive biomarkers for sensitive monitoring of tumor changes. The present review focuses on circRNAs associated with tumor metastasis and discusses their functional mechanisms. Furthermore, the current review summarizes advances regarding circRNAs as biomarkers and detection strategies.</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/PMC12439457/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961773","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] Sevoflurane attenuates brain damage through inhibiting autophagy and apoptosis in cerebral ischemia‑reperfusion rats.","authors":"Cun-Xian Shi, Jin Jin, Xue-Qin Wang, Teng Song, Guang-Hong Li, Ke-Zhong Li, Jia-Hai Ma","doi":"10.3892/mmr.2025.13656","DOIUrl":"https://doi.org/10.3892/mmr.2025.13656","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 immunohistochemistry experiments shown in Fig. 4A, the 'Tak‑242' and the 'Se+Tak‑242' panels appeared to show an overlapping section of data, and for the western blot data shown in Figs. 6 and 7, the β‑actin data in Fig. 6A were strikingly similar to the NF‑κB data in Fig. 7A, such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original sources. Following an independent analysis of the data in the Editorial Office, a small overlapping section of data was also identified comparing the 'Tak‑242' and 'Se' panels for the cellular morphological images in Fig. 5A, and the western blots featured in Fig. 6A were found to have subsequently reappeared in a paper written by different authors at different research institutes in the journal <i>Drug Design, Development and Therapy</i>. In view of the various instances of data duplication identified in this paper, and the reappearance of certain of the data in a subsequent article, the Editor of <i>Molecular Medicine Reports</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 satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 21: 123‑130, 2020; DOI: 10.3892/mmr.2019.10832].</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/PMC12395214/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961725","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":"How transcription factors regulate apoptosis in endometriosis (Review).","authors":"Zhuqing Ouyang, Juexiao Deng, Lanyue Zhang, Fujin Shen","doi":"10.3892/mmr.2025.13654","DOIUrl":"https://doi.org/10.3892/mmr.2025.13654","url":null,"abstract":"<p><p>Endometriosis (EM) is a common chronic gynaecological disease that affects 10% of women of reproductive age globally. EM is defined as the presence of endometrial glands and stroma in extrauterine locations, and it can result in pelvic pain and infertility. Inflammation, oxidative stress and apoptosis dysregulation serve a key role in endometriotic lesions. The pathogenesis of EM remains unclear, posing major clinical challenges in its diagnosis and treatment. Apoptosis contributes to the maintenance of cellular homeostasis during the menstrual cycle by eliminating ageing cells from the functional layer of the uterine endometrium. Inhibition of apoptosis facilitates ectopic endometrial cell invasion, implantation and survival, and it promotes the occurrence and development of EM. Transcription factors are pivotal regulators of cellular processes and serve key roles in regulating apoptosis to promote EM. Therefore, identifying the mechanisms by which transcription factors regulate apoptosis in EM may help identify novel targets for the treatment of this disease. The present review summarizes the regulation of apoptosis by different transcription factors in the pathogenesis of EM, contributing to the development of promising biomarkers and therapeutic strategies.</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/PMC12382432/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961801","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":"Hyperbaric oxygen therapy for sudden sensorineural hearing loss (Review).","authors":"Yuting Sun, Shangyuan Wang, Huimin Fu, Xiaoli Ge, Shuming Pan","doi":"10.3892/mmr.2025.13672","DOIUrl":"10.3892/mmr.2025.13672","url":null,"abstract":"<p><p>Sudden sensorineural hearing loss (SSNHL) is an acute hearing disorder that develops rapidly and is an otolaryngology emergency. Hyperbaric oxygen therapy (HBOT), a non‑pharmacological treatment, has gained increasing attention for SSNHL management. HBOT exerts therapeutic effects by increasing inner ear oxygen partial pressure, improving the microcirculation and reducing inflammation, as its main mechanisms. When combined with glucocorticoids, HBOT can significantly improve treatment outcomes, particularly when initiated as an early intervention. However, its optimal clinical application has not yet been determined, mainly due to the lack of standardized treatment parameters, such as pressure settings, the duration of treatment and the therapeutic time window. In addition, clinical studies have yielded inconsistent results. The purpose of the present review is to explore the biological mechanisms, clinical efficacy and existing controversies of HBOT in the treatment of SSNHL, review and summarize the latest research progress, and discuss potential directions for future development.</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/PMC12427607/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000968","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":"The role of Na,K‑ATPase in lung diseases (Review).","authors":"Zhenyu Liu, Tingyan Dong, Fei Li, Chunmei He, Weizhen Zhang, Biyun Li","doi":"10.3892/mmr.2025.13665","DOIUrl":"10.3892/mmr.2025.13665","url":null,"abstract":"<p><p>Na,K‑ATPase, commonly referred to as the sodium pump, is known for its essential function as an ion pump, which is key for transporting Na⁺ and K⁺ across plasma cell membranes. Additionally, Na,K‑ATPase has multiple biological functions, independent of ion pumping, which are involved in regulating cell proliferation, apoptosis, differentiation and other processes associated with the development and progression of various diseases; particularly cancer, cardiovascular diseases, nervous system diseases, kidney diseases and lung diseases. As a potential therapeutic target, Na,K‑ATPase may represent a novel strategy for treating these diseases in the future. The present review aims to summarize the role of Na,K‑ATPase in lung diseases.</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/PMC12409250/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961754","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":"Asprosin activates multiple placental pathways <i>in vitro</i>: Evidence for potential involvement in angiogenesis, fatty acid metabolism and the mTOR, NOTCH and WNT signalling pathways.","authors":"Sophie Orton, Seley Gharanei, Jovile Kazileviciute, Sayeh Saravi, Vanlata Patel, Jayanta Chatterjee, Ioannis Kyrou, Emmanouil Karteris, Harpal S Randeva","doi":"10.3892/mmr.2025.13674","DOIUrl":"10.3892/mmr.2025.13674","url":null,"abstract":"<p><p>Asprosin is glucogenic adipokine that exerts a wide repertoire of actions, including the regulation of appetite, insulin resistance and cell proliferation. At present, little is known about the actions of asprosin in the human placenta. The present study investigated the effects of asprosin on the transcriptome of the BeWo and JEG‑3 placental cell lines, and assessed the expression of FBN1/Furin and asprosin's candidate receptors in healthy placentas when compared against placentas from pregnancies where the carrier had gestational diabetes mellitus (GDM). A number of methods, including tissue culture, clinical sample collection, RNA extraction, RNA sequencing, reverse transcription‑quantitative PCR and gene enrichment analyses were used in the present study. RNA sequencing revealed that asprosin induced cell specific differential expression for 51 genes in BeWo cells, and 204 in JEG‑3 cells, with nine common differentially expressed genes in both <i>in vitro</i> models including <i>SLCA1</i> and <i>HK2</i>. Specific pathways involved in angiogenesis, fatty acid metabolism and mTOR/NOTCH/WNT/p53 signalling were also enriched. Only <i>TLR4</i> was significantly downregulated in GDM placentas when compared with controls. The present study provides novel insight into the actions of asprosin in two well‑established <i>in vitro</i> placental (trophoblast) models, identifying key genes and signalling pathways. A common theme identified from these findings is that of glucose homeostasis, in accordance with the role of this adipokine.</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/PMC12446899/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000954","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":"Mitophagy as a pivotal axis in non‑alcoholic fatty liver disease: From pathogenic mechanisms to therapeutic strategies (Review).","authors":"Yushu Huang, Xueqing Xia, Jingyang Xu, Zihan Wang, Yanting You, Qingfeng Du","doi":"10.3892/mmr.2025.13664","DOIUrl":"10.3892/mmr.2025.13664","url":null,"abstract":"<p><p>Non‑alcoholic fatty liver disease (NAFLD), characterized by excessive lipid accumulation in hepatocytes, has emerged as the leading cause of chronic liver disorders globally. As the central metabolic organ, the liver critically depends on mitochondrial integrity. Mitophagy, a selective form of autophagy, plays a pivotal role in sustaining mitochondrial homeostasis by eliminating dysfunctional mitochondria. Dysregulated mitophagy contributes to the progression of NAFLD, while its restoration mitigates disease severity. The present review outlines the tripartite axis of mitophagy, namely, the PTEN‑induced putative kinase 1/Parkin, PI3K/AKT/mTOR and AMP‑activated protein kinase pathways, in NAFLD pathogenesis across the various stages of disease development, including steatosis, nonalcoholic steatohepatitis and fibrosis, and explores their therapeutic potential. Additionally, emerging regulators, including FUN14 domain‑containing protein 1, prohibitin 2, ceramide signaling and non‑coding RNAs, which fine‑tune mitophagy in NAFLD are highlighted. By integrating evidence from pharmacological and natural agents, including traditional Chinese medicines, mitophagy‑centric strategies to promote hepatic lipid metabolism, mitigate disease progression and inform novel NAFLD therapeutics are discussed. This exploration of the mechanisms that govern mitochondrial‑autophagic crosstalk not only advances mechanistic insights but also opens new avenues for precision medicine in the treatment of metabolic liver diseases.</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/PMC12409231/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961787","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":"MitoQ alleviates malathion‑induced hepatorenal toxicity via oxidative stress and inflammation modulation.","authors":"Saed A Althobaiti","doi":"10.3892/mmr.2025.13661","DOIUrl":"10.3892/mmr.2025.13661","url":null,"abstract":"<p><p>Malathion, a commonly used organophosphate pesticide, induces severe hepatorenal toxicity, mitochondrial dysfunction and inflammatory responses primarily through oxidative stress and apoptosis. The present study investigated the protective effects of mitoquinol (MitoQ), a mitochondria‑targeted antioxidant, against malathion‑induced toxicity in male Wistar albino rats. A total of 50 rats were divided into the following five groups: i) Control; ii) malathion‑only; iii) malathion + MitoQ; iv) MitoQ‑only; and v) vehicle. Malathion exposure significantly elevated the levels of aspartate aminotransferase, alkaline phosphatase, creatinine, urea and uric acid and decreased total protein, albumin and globulin levels. At the mitochondrial level, malathion reduced antioxidant enzyme activity (superoxide dismutase, glutathione peroxidase and glutathione) and ATP production while increasing reactive oxygen species, leading to oxidative damage. Furthermore, malathion induced upregulation of pro‑apoptotic markers such as Bax, and downregulation of the anti‑apoptotic marker, Bcl‑2. In addition, malathion increased TNF‑α, NF‑κB, Toll‑like receptor (TLR) 2 and TLR4 expression, and malathion toxicity induced severe hepatorenal damage, including vascular congestion, inflammatory infiltration and tubular degeneration. MitoQ co‑administration revealed a trend towards mitigating altered hepatorenal markers, inflammatory markers and regulated apoptotic/antiapoptotic gene markers, with partial restoration in mitochondrial function and histopathological changes. In parallel, MitoQ normalized cellular changes induced by malathion in the liver and kidneys. In conclusion, malathion toxicity in the liver and kidneys is mediated by mitochondrial oxidative stress, apoptosis and inflammation. MitoQ exerts protective effects by restoring mitochondrial homeostasis, reducing inflammatory signaling and mitigating tissue damage. Future research should explore longer treatment durations and potential synergistic effects with other antioxidants to optimize protection against pesticide‑induced toxicity.</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/PMC12404019/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961710","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 the tumor microenvironment in promoting treatment resistance in urothelial carcinoma (Review).","authors":"Li Yan, Pengxiao Su, Xiaoke Sun","doi":"10.3892/mmr.2025.13658","DOIUrl":"https://doi.org/10.3892/mmr.2025.13658","url":null,"abstract":"<p><p>Urothelial carcinoma (UC) presents considerable treatment challenges, primarily due to the high rates of therapeutic resistance observed in affected patients. Currently, therapeutic strategies often fail to yield satisfactory outcomes; therefore, there is a need for innovative treatment approaches. The tumor microenvironment (TME) serves a key role in driving treatment resistance in UC, revealing that components such as cancer‑associated fibroblasts, tumor‑associated macrophages and the extracellular matrix contribute to tumor survival and evasion of therapy. Understanding the mechanisms through which the TME influences treatment resistance is key for developing effective countermeasures. Targeting the TME may be an effective therapeutic strategy, as this approach may increase the efficacy of existing treatments and overcome barriers to response. The present review aims to summarize current knowledge regarding the role of the TME in UC treatment resistance, discuss potential strategies for targeting the TME and highlight future research directions. The translation of insights from studies on the TME into therapeutic strategies may improve clinical outcomes for patients suffering from this challenging malignancy.</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/PMC12395220/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961756","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}