Molecular medicine reports最新文献

{"title":"Advances in research on the intestinal microbiota in the mechanism and prevention of colorectal cancer (Review).","authors":"Weitong Sun, Shize Ma, Dongdong Meng, Chaoxing Wang, Jinbo Zhang","doi":"10.3892/mmr.2025.13498","DOIUrl":"10.3892/mmr.2025.13498","url":null,"abstract":"<p><p>The intestinal microbiota represents a diverse population that serves a key role in colorectal cancer (CRC) and its treatment outcomes. Advancements in sequencing have revealed notable shifts in microbial composition and diversity among individuals with CRC. Concurrently, animal models have elucidated the involvement of specific microbes such as <i>Lactobacillus fragilis</i>, <i>Escherichia coli</i> and <i>Fusobacterium nucleatum</i> in the progression of CRC. The present review aimed to highlight contributions of intestinal microbiota to the pathogenesis of CRC, the effects of traditional treatments on intestinal microbiota and the potential for microbiota modulation as a therapeutic strategy for CRC.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11948985/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670510","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] The role of Zeb1 in the pathogenesis of morbidly adherent placenta.","authors":"Na Li, Tian Yang, Wenqian Yu, Hao Liu, Chong Qiao, Caixia Liu","doi":"10.3892/mmr.2025.13493","DOIUrl":"10.3892/mmr.2025.13493","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the flow cytometric assay data shown in Fig. 2C and 3C on p. 2817 and p. 2818 respectively were strikingly similar to data that had already been submitted for publication in a paper written by different authors at a different research institute. Owing to the fact that the contentious data in the above article were already under consideration for publication 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 20: 2812‑2822, 2019; DOI: 10.3892/mmr.2019.10490].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11938022/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670509","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] lncRNA MNX1‑AS1 promotes prostate cancer progression through regulating miR‑2113/MDM2 axis.","authors":"Dong Liang, Chuanjie Tian, Xiaowen Zhang","doi":"10.3892/mmr.2025.13480","DOIUrl":"10.3892/mmr.2025.13480","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the cell migration assay data shown in Fig. 2D on p. 5 were strikingly similar to data that had already been published in different form in the journal <i>OncoTargets and Therapy</i> in an article written by different authors at different research institutes (which has subsequently been retracted). In addition, there were instances of overlapping data panels identified comparing the data in Fig. 2E and F with those in Fig. 5E and F, such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original sources. 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 26: 231, 2022; DOI: 10.3892/mmr.2022.12747].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905196/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573507","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":"Heme oxygenase 1‑overexpressing bone marrow mesenchymal stem cell‑derived exosomes suppress interleukin‑1 beta‑induced apoptosis and aging of nucleus pulposus cells.","authors":"Hao Zhang, Di Zhang, Hui Wang, Yilei Liu, Wenyuan Ding, Guangpu Fan, Xianzhong Meng","doi":"10.3892/mmr.2025.13481","DOIUrl":"10.3892/mmr.2025.13481","url":null,"abstract":"<p><p>Exosomes derived from bone marrow mesenchymal stem cells (BMSCs) and heme oxygenase 1 (HO‑1) attenuate intervertebral disc degeneration (IVDD). However, whether BMSC‑derived exosomes attenuate IVDD by delivering HO‑1 to nucleus pulposus (NP) cells remains to be elucidated. Mouse BMSCs were characterized by multilineage differentiation and surface marker molecule detection. Exosomes Exo and Exo‑HO‑1 were isolated from BMSCs and HO‑1‑overexpressing BMSCs by ultracentrifugation and characterized by observing their morphology, detecting the exosome marker proteins, tumor susceptibility gene 101 (TSG101) and CD63 and analyzing their particle size. Interleukin‑1 β (IL‑1β)‑stimulated NP cells were used as the IVDD cell model. The influence of Exo or Exo‑HO‑1 on IL‑1β‑urged apoptosis and senescence in NP cells was determined by flow cytometry, western blotting and senescence‑associated β‑galactosidase (SA‑β‑gal) staining. Exo and Exo‑HO‑1 did not vary in size or morphology. Exo‑HO‑1 markedly repressed IL‑1β‑prompted apoptosis in NP cells, accompanied with a prominent increase in Cleaved caspase 3 and Bax protein levels and a marked decrease in Bcl‑2 protein levels. Exo and Exo‑HO‑1 both decreased the number of SA‑β‑gal‑positive NP cells and arrested NP cells in the G₁ phase. Exo‑HO‑1 had stronger effects than Exo, suggesting that Exo‑HO‑1 can weaken IL‑1β‑induced NP cell senescence. In addition, Exo and Exo‑HO‑1 repressed IL‑1β mediating the phosphorylation of p65 and nuclear translocation of p65. In conclusion, HO‑1‑overexpressing BMSC‑derived exosomes blocked the nuclear factor‑kappa B signaling in IL‑1β‑stimulated NP cells, thus impairing cell apoptosis and senescence.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905203/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573442","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":"Efficacy of exosomes in acute kidney injury treatment and the associated mechanism (Review).","authors":"Zehao Zhang, Lecheng She, Ming Bai","doi":"10.3892/mmr.2025.13503","DOIUrl":"10.3892/mmr.2025.13503","url":null,"abstract":"<p><p>Acute kidney injury (AKI) is a syndrome characterized by rapid loss of renal function with a high morbidity and mortality. However, due to the complex pathophysiologic mechanisms of AKI, no specific treatment for this disease is currently available. Animal models have demonstrated the protective effects of exosomes on AKI; however, the underlying mechanisms require further investigation. The present review focuses on the efficacy of exosomes derived from different cell sources, including mesenchymal stem cells, endothelial progenitor cells and tubular epithelial cells, in the treatment of AKI and the associated mechanism. Furthermore, the effects of exosomal contents, including microRNAs, circular RNAs, long non‑coding RNAs, messenger RNAs and proteins, on the repair of renal tubules, protection against renal tubular epithelial cell injury, protection against fibrosis, inhibition of early endoplasmic reticulum stress and mediation of inflammation during AKI are also summarized in the present review.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720657","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 2 in spermatogenesis dysfunction (Review).","authors":"Pingping Tang, Jiale Wang, Xiaohan Tang, Yichun Li, Suyun Li","doi":"10.3892/mmr.2025.13494","DOIUrl":"10.3892/mmr.2025.13494","url":null,"abstract":"<p><p>Spermatogenesis dysfunction is characterized by abnormal morphology, destruction, atrophy of seminiferous tubules, blocked differentiation of spermatogenic cells, decreased sperm count and increased sperm abnormalities. Inflammation, oxidative stress, endoplasmic reticulum stress and obesity are important factors leading to spermatogenesis dysfunction. It has been demonstrated that insulin‑like growth factor 2 (IGF2) is closely related to the aforementioned factors. In the present review, the relationship between IGF2 and inflammation, oxidative stress, ER stress and obesity was investigated, providing theoretical and experimental evidence on the role of IGF2 in the prevention and treatment of spermatogenesis dysfunction of male infertility.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11938415/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670511","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":"Obacunone inhibits ferroptosis through regulation of Nrf2 homeostasis to treat diabetic nephropathy.","authors":"Yi Ou, Wenjuan Zhang","doi":"10.3892/mmr.2025.13500","DOIUrl":"10.3892/mmr.2025.13500","url":null,"abstract":"<p><p>Diabetic nephropathy (DN), a prevalent and severe microvascular complication of diabetes, often leads to end‑stage renal disease and poses a threat to patient survival. However, to the best of our knowledge, there are currently no effective strategies available for the treatment of DN. Obacunone (OB), a small‑molecule natural compound derived from Citrus plants, exhibits various pharmacological effects; however, the impact of OB on DN remains to be fully elucidated. Therefore, the present study aimed to explore the effects and potential mechanisms of OB in DN. In the current study, DN models were created <i>in vitro</i> by treating HK‑2 cells with high‑glucose (HG) levels, and in vivo by administering a HG and high‑fat diet along with intraperitoneal injections of streptozotocin to Sprague‑Dawley rats. Subsequently, cell viability was evaluated using the Cell Counting Kit‑8 assay, while ferroptosis‑related marker levels were determined using biochemical kits, immunofluorescence and western blotting. Activation and homeostasis of the nuclear factor erythroid 2‑related factor 2 (Nrf2) signaling pathway were analyzed using western blotting, co‑immunoprecipitation and reverse transcription‑quantitative PCR. In addition, alterations in renal function parameters and the severity of renal pathological injury in rats were examined. The <i>in vitro</i> experiments demonstrated that OB significantly promoted cell viability and inhibited ferroptosis, as evidenced by increased glutathione peroxidase 4 and SLC7A11 expression, and decreased levels of malondialdehyde, ferrous ion and reactive oxygen species (P<0.05). Additionally, OB activated the Nrf2 signaling pathway, blocked the interaction between Nrf2 and Kelch‑like ECH‑associated protein 1, and suppressed Nrf2 ubiquitination and degradation (P<0.05). In vivo, OB administration improved renal function parameters, including serum creatinine and blood urea nitrogen levels (P<0.05), and reduced renal pathological injury, in comparison with the DN group. The results of the present study indicated that OB, a natural small molecule, exhibited significant anti‑DN effects, possibly through the regulation of Nrf2 homeostasis to inhibit ferroptosis. Overall, this study provides new evidence for OB as a potential clinical treatment for DN.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11948956/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670478","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] miR‑593 inhibits proliferation and invasion and promotes apoptosis in non‑small cell lung cancer cells by targeting SLUG‑associated signaling pathways.","authors":"Fang Wei, Mofei Wang, Zhen Li, Yong Wang, Yong Zhou","doi":"10.3892/mmr.2025.13490","DOIUrl":"10.3892/mmr.2025.13490","url":null,"abstract":"<p><p>Following the publication of this paper, and subsequently to the publication of a corrigendum (DOI: 10.3892/mmr.2021.12555) that was intended to address the issue of a pair of duplicated data panels in Fig. 5D, it was drawn to the Editor's attention by a concerned reader that certain of the flow cytometric plots shown in Fig. 4A and B and cell migration assay data shown in the originally published version of Fig. 5A were strikingly similar to data that had appeared previously in other papers written by different authors at different research institutes. In view of the fact that the abovementioned data had already apparently been published prior to its submission to <i>Molecular Medicine Reports</i>, the Editor has decided that this paper should now 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 20: 5172‑5182, 2019; DOI: 10.3892/mmr.2019.10776].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11920771/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625308","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":"New developments in the role of ferroptosis in sepsis‑induced cardiomyopathy (Review).","authors":"Dingdeng Wang, Xinguang Qu, Zhaohui Zhang, Gaosheng Zhou","doi":"10.3892/mmr.2025.13483","DOIUrl":"10.3892/mmr.2025.13483","url":null,"abstract":"<p><p>Sepsis is a life‑threatening organ dysfunction disorder caused by dysfunctional host response to infection. Sepsis‑induced cardiomyopathy (SIC) is a common and serious complication of sepsis, and it is associated with increased mortality rates; however, its specific pathogenesis is still unclear. Ferroptosis, which is an iron‑dependent form of programmed cell death, is involved in the pathophysiology of SIC. Further study on the mechanism and therapeutic targets of ferroptosis in SIC may provide new strategies for clinical diagnosis and treatment of this condition. The present article reviews the mechanisms between SIC and ferroptosis, summarizes the progress in research of the involvement of ferroptosis in SIC and provides new potential strategies for further research and treatment in the future.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11904766/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573445","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":"Semaglutide enhances PINK1/Parkin‑dependent mitophagy in hypoxia/reoxygenation‑induced cardiomyocyte injury.","authors":"Liqin Li, Lili Jin, Yaping Tian, Jun Wang","doi":"10.3892/mmr.2025.13476","DOIUrl":"10.3892/mmr.2025.13476","url":null,"abstract":"<p><p>The present study aimed to explore how semaglutide can help protect the heart from injury caused by hypoxia/reoxygenation (H/R) and to reveal the underlying mechanism. Briefly, AC16 cardiomyocytes were subjected to 8 h of hypoxia followed by 12 h of reoxygenation to simulate H/R. The cells were divided into the following five groups: Normoxia, H/R, H/R + semaglutide, H/R + semaglutide + rapamycin (autophagy inducer), and H/R + semaglutide + 3‑methyladenine (3‑MA; autophagy inhibitor) groups. Cell viability was examined using a Cell Counting Kit‑8 assay, ATP levels were examined using a bioluminescent detection kit, reactive oxygen species (ROS) production was detected using a ROS Assay Kit, and monomeric red fluorescent protein (mRFP)‑green fluorescent protein (GFP)‑LC3 was assessed using tandem mRFP‑GFP fluorescence microscopy, while autophagosomes were observed using transmission electron microscopy. Furthermore, the protein expression levels of autophagy markers (LC3, p62 and Beclin1) and regulators of mitochondrial autophagy [PTEN‑induced putative kinase protein‑1 (PINK1) and Parkin] were examined using western blot analysis. In AC16 cells, exposure to hypoxia followed by reoxygenation led to an increase in oxidative stress. This condition also induced an increase in autophagy activity, as evidenced by an increase in the number of autophagosomes, elevated LC3‑II/LC3‑I ratio, and upregulation of p62, Beclin1, PINK1 and Parkin expression compared with those in cells cultured under normoxia. Notably, treatment with semaglutide or rapamycin effectively reversed the H/R‑induced oxidative stress, enhanced the changes in autophagy activity, autophagosome levels and elevated LC3BII/LC3BI ratio, and increased the expression levels of Beclin1, PINK1, Parkin and p62 expression. Notably, the use of 3‑MA exhibited distinct effects under the same conditions; it exacerbated oxidative stress, decreased autophagy activity and reduced the LC3BII/LC3BI ratio. In conclusion, semaglutide was found to reduce oxidative stress caused by H/R and to increase autophagy via the ROS/PINK1/Parkin/p62 pathway. The present study offers a novel understanding of how semaglutide may protect the heart, and suggests its potential use in the treatment of myocardial ischemia/reperfusion injury.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11884227/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143523968","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}