International journal of molecular medicine最新文献

{"title":"Function and application of brain‑derived neurotrophic factor precursors (Review).","authors":"Risheng Chen, Weixin Chen, Ping Li, Yingchang Zhao, Qianqian Zeng, Wenqing Chen, Dequan Cao","doi":"10.3892/ijmm.2025.5546","DOIUrl":"10.3892/ijmm.2025.5546","url":null,"abstract":"<p><p>Brain‑derived neurotrophic factor precursor (proBDNF) plays a critical role in the pathogenesis and progression of various human diseases. Through its interaction with p75NTR and sortilin receptors, proBDNF promotes apoptosis, impairs synaptic plasticity, and contributes to the regulation of immune system function, inflammatory responses and cellular metabolic processes. proBDNF is widely distributed throughout the body, and as such, extensive research has demonstrated that proBDNF is significantly associated with the pathophysiological mechanisms underlying several diseases. In the present review, the mechanisms by which proBDNF contributes to different diseases are summarized to highlight its potential therapeutic and diagnostic implications. Specifically, the role of proBDNF in cognitive disorders, focusing on its effects on synaptic function and neural network dynamics, while analyzing the cascade reactions involving proBDNF and downstream effector molecules in inflammatory diseases, to elucidate its bidirectional regulatory effects in tumor initiation and progression. Furthermore, the function of proBDNF in neurogenesis, the mechanism by which it regulates the memory of fear, and enhances individual behavioral flexibility is discussed. Finally, the potential of proBDNF as a biomarker for disease diagnosis and the therapeutic prospects of targeting it using monoclonal antibodies are highlighted while also proposing future research directions. The present review can serve as a reference for translational medical research on proBDNF and its receptors.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081033/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144009585","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":"Molecular mechanisms of programmed cell death and potential targeted pharmacotherapy in ischemic stroke (Review).","authors":"Wan-Li Duan, Li-Hui Gu, Ai Guo, Xue-Jie Wang, Yi-Yue Ding, Peng Zhang, Bao-Gang Zhang, Qin Li, Li-Xia Yang","doi":"10.3892/ijmm.2025.5544","DOIUrl":"10.3892/ijmm.2025.5544","url":null,"abstract":"<p><p>Stroke poses a threat to the elderly, being the second leading cause of death and the third leading cause of disability worldwide. Ischemic stroke (IS), resulting from arterial occlusion, accounts for ~85% of all strokes. The pathophysiological processes involved in IS are intricate and complex. Currently, tissue plasminogen activator (tPA) is the only Food and Drug Administration‑approved drug for the treatment of IS. However, due to its limited administration window and the risk of symptomatic hemorrhage, tPA is applicable to only ~10% of patients with stroke. Additionally, the reperfusion process associated with thrombolytic therapy can further exacerbate damage to brain tissue. Therefore, a thorough understanding of the molecular mechanisms underlying IS‑induced injury and the identification of potential protective agents is critical for effective IS treatment. Over the past few decades, advances have been made in exploring potential protective drugs for IS. The present review summarizes the specific mechanisms of various forms of programmed cell death (PCD) induced by IS and highlights potential protective drugs targeting different PCD pathways investigated over the last decade. The present review provides a theoretical foundation for basic research and insights for the development of pharmacotherapy for IS.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081036/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144017539","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":"Multifaceted regulatory mechanisms of the EGR family in tumours and prospects for therapeutic applications (Review).","authors":"Rongqi Guo, Rui Wang, Weisong Zhang, Yangyang Li, Yihao Wang, Hao Wang, Xia Li, Jianxiang Song","doi":"10.3892/ijmm.2025.5554","DOIUrl":"10.3892/ijmm.2025.5554","url":null,"abstract":"<p><p>The early growth response (EGR) family comprises four zinc finger transcription factors: EGR1, EGR2, EGR3 and EGR4. These transcription factors belong to the Cys₂‑His₂‑type zinc finger protein family and are essential in cell differentiation, proliferation, apoptosis and stress response. Initially, EGR1 was recognised for its essential regulatory role in tumourigenesis. Recent studies have identified similarities between other members of the EGR family and EGR1 in tumour regulation and the multifaceted regulatory mechanism employed by the EGR family to affect tumours. Therefore, the present review describes the dual roles of the EGR family in tumours and their regulatory mechanisms in immunity, metabolism and differentiation. Additionally, the present review offers a new perspective on relevant tumour therapeutic studies based on current EGR targeting.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12121985/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144181808","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] MicroRNA‑7 functions as a tumor‑suppressor gene by regulating ILF2 in pancreatic carcinoma.","authors":"Yiliang Bi, Wei Shen, Min Min, Yan Liu","doi":"10.3892/ijmm.2025.5542","DOIUrl":"10.3892/ijmm.2025.5542","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 Transwell cell migration and invasion assay data shown in Fig. 3C on p. 304 were strikingly similar to data appearing in different form in an article written by different authors at different research institutes that had already been published in the journal <i>Oncotarget</i>. Upon performing an independent analysis of the data in this paper, the data shown in Fig. 2B were also strikingly similar to data that had appeared in another previously published article. In view of the fact that the abovementioned data had already apparently been published previously, the Editor of <i>International Journal of Molecular Medicine</i> 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 satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 39: 900‑906, 2017; DOI: 10.3892/ijmm.2017.2894].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081025/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143964620","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":"Gossypin induces apoptosis and autophagy via the MAPK/JNK pathway in HT‑29 human colorectal cancer cells.","authors":"Jun-Mo Moon, Sang-Woo Lee, Yun-Seo Jang, Su-A Lee, Soo-Hyun Jung, Sang-Ki Kim, Byung-Kwon Park, Young-Seok Park, Byeong-Soo Kim, Myeon-Sik Yang, Ji-Youn Jung","doi":"10.3892/ijmm.2025.5548","DOIUrl":"10.3892/ijmm.2025.5548","url":null,"abstract":"<p><p>Gossypin, a flavone found in <i>Hibiscus vitifolius</i>, exhibits antioxidant, antidiabetic, anti‑inflammatory and anticancer effects. The present study investigated the potential of gossypin to induce apoptosis and autophagy in HT‑29 human colorectal cancer (CRC) cells, and assessed its association with the MAPK/JNK pathway. Cell viability assays, DAPI staining, flow cytometry, acridine orange staining, western blotting, hematoxylin and eosin staining, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and immunohistochemistry were performed. The results revealed an increased number of apoptotic bodies, higher apoptosis rates and enhanced autophagy in gossypin‑treated HT‑29 cells. To investigate autophagy during cell death, the effects of the early autophagy inhibitor 3‑methyladenine (3‑MA) and the late autophagy inhibitor hydroxychloroquine on cell viability and the expression of apoptosis‑related proteins were assessed. Significant increases in cell viability were observed following 3‑methyladenine pretreatment, as well as a decrease in the expression levels of Bcl‑2 and an increase in Bax. The analysis of MAPK pathway proteins following treatment with gossypin revealed that the levels of phosphorylated (p‑)JNK and p‑p38 were significantly increased in a concentration‑dependent manner. The JNK inhibitor SP600125 was used to confirm the role of the JNK pathway in gossypin‑induced apoptosis and autophagy. Moreover, gossypin reduced the volume of HT‑29 tumors in mice, and western blotting indicated the induction of apoptosis and autophagy in these tumors <i>in vivo</i>. Finally, TUNEL and immunohistochemistry experiments confirmed the induction of apoptosis and p‑JNK upregulation in these tumors <i>in vivo</i>. In conclusion, the present study suggested that gossypin may induce MAPK/JNK‑mediated apoptosis and autophagy in HT‑29 CRC cells, highlighting the potential of gossypin as an anticancer agent.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101101/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077722","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 vitamins in the development and treatment of osteoporosis (Review).","authors":"Mingze Jiang, Genghan Li, Keda Yang, Lin Tao","doi":"10.3892/ijmm.2025.5550","DOIUrl":"10.3892/ijmm.2025.5550","url":null,"abstract":"<p><p>Osteoporosis has escalated into a pressing public health challenge amidst global demographic aging. Conventional diagnostic approaches and therapeutic interventions demonstrate growing limitations in both risk stratification and epidemiological control. In this context, serological monitoring and targeted nutrient supplementation emerge as promising preventive strategies. Vitamins, fundamental regulators of cellular homeostasis, demonstrate particular significance in bone remodeling processes. The present comprehensive review elucidates the pathophysiological mechanisms through which specific vitamins differentially modulate osteoblastic activity and osteoclastic regulation, summarizing contemporary evidence from the molecular to clinical research levels. While vitamin A exhibits dual effects, other vitamins predominantly show positive impacts on bone homeostasis. Oxidative stress and inflammation are key pathological changes associated with osteoporosis. Vitamins play a protective role by enhancing the expression of antioxidant enzymes, activating antioxidant pathways and inhibiting the secretion of inflammatory cytokines, thereby mitigating these conditions. Serum vitamin concentrations exhibit significant correlations with bone mineral density alterations and osteoporosis progression, providing predictive biomarkers for fracture risk assessment. However, serum vitamin profiles exhibit marked heterogeneity across osteoporosis risk strata, necessitating population‑specific therapeutic protocols. Precision‑adjusted supplementation strategies effectively attenuate pathological bone resorption while preserving physiological remodeling homeostasis. The present review systematically delineates the therapeutic potential of vitamins in osteoporotic management, underscoring the necessity for evidence‑based precision nutrient protocols tailored to at‑risk populations to prevent disease progression.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077730","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] Endothelial cell‑derived exosomes protect SH‑SY5Y nerve cells against ischemia/reperfusion injury.","authors":"Bing Xiao, Yi Chai, Shigang Lv, Minhua Ye, Miaojing Wu, Liyuan Xie, Yanghua Fan, Xingen Zhu, Ziyun Gao","doi":"10.3892/ijmm.2025.5549","DOIUrl":"10.3892/ijmm.2025.5549","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 flow cytometric data shown in Figs. 3A and 5E, and certain of the EdU assay data shown in Fig. 5C were strikingly similar to data that had either already appeared in previously published articles that were written by different authors at different research institutes, or were featured in articles that were submitted for publication to different journals at around the same time, or have otherwise subsequently appeared in print elsewhere. Owing to the fact that the contentious data in the above article had already been published prior to its submission to <i>International Journal of Molecular Medicine</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. [International Journal of Molecular Medicine 40: 1201‑1209, 2017; DOI: 10.3892/ijmm.2017.3106].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12121983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077060","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] Effect of apelin on the cardiac hemodynamics in hypertensive rats with heart failure.","authors":"Hui Pang, Bing Han, Tao Yu, Zhenkun Zong","doi":"10.3892/ijmm.2025.5536","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5536","url":null,"abstract":"<p><p>Following the publication of the above article, a concerned reader drew to the authors' attention that, regarding the western blot data shown in Fig. 7B on p. 762, a number of the bands shown to represent phosphorylated (p)‑ERK‑1/2 bands were strikingly similar to bands that were showing the results from the total (t)‑ERK‑1/2 experiments; moreover, certain of the bands in question were non‑contiguous in terms of how they were positioned in the gels. Upon examining these data independently in the Editorial Office, the Editor of <i>International Journal of Molecular Medicine</i> has determined that this article should be retracted from the Journal on the basis 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 of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 34: 756‑764, 2014; DOI: 10.3892/ijmm.2014.1829].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 6","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12045472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144007565","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] Paeonol induces the apoptosis of the SGC‑7901 gastric cancer cell line by downregulating ERBB2 and inhibiting the NF‑κB signaling pathway.","authors":"Jun Fu, Luhua Yu, Jie Luo, Rui Huo, Bing Zhu","doi":"10.3892/ijmm.2025.5532","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5532","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 flow cytometric plots shown in Fig. 7 on p. 1479, although the number of data points increased with an increasing concentration of paenol, the patterning of the dots were similar comparing across the panels, which would not have been anticipated as the result if these experiments had been performed discretely, suggesting a fundamental flaw in the way in which these experiments were performed. The Editor of <i>International Journal of Molecular Medicine</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 reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 42: 1473‑1483, 2018; DOI: 10.3892/ijmm.2018.3704].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 6","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12021388/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978978","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] Hypoxia‑induced expression of CXCR4 favors trophoblast cell migration and invasion via the activation of HIF‑1α.","authors":"Zhan Zhang, Pengyun Li, Yan Wang, Huan Yan","doi":"10.3892/ijmm.2025.5528","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5528","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 Transwell migration and invasion assay experiments shown in Figs. 3A, 4C, 5C and G, a number of the individual panels contained overlapping sections of data, both within and across the figure parts, such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original sources. In view of the fact that these figures were assembled erroneously, the Editor of <i>International Journal of Molecular Medicine</i> has decided that this paper should be retracted from the Journal on account of a lack of confidence in the presented data. 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. [International Journal of Molecular Medicine 42: 1508‑1516, 2018; DOI: 10.3892/ijmm.2018.3701].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 6","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12005362/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144006342","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}