Molecular medicine reports最新文献

{"title":"[Retracted] AKR1C1 alleviates LPS‑induced ALI in mice by activating the JAK2/STAT3 signaling pathway.","authors":"Xianjun Wang, Baocheng Yang, Yuyu Li, Jiye Luo, Yanli Wang","doi":"10.3892/mmr.2025.13449","DOIUrl":"https://doi.org/10.3892/mmr.2025.13449","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 immunohistochemical data shown in Fig. 1C on p. 5 were strikingly similar to data appearing in different form in another article written by different authors at different research institutes that had already been published in the journal Archives of Biochemistry and Biophysics prior to the submission of this paper to <i>Molecular Medicine Reports</i>. In view of the fact that the abovementioned data had already apparently been published previously, the Editor of <i>Molecular Medicine Reports</i> 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 24: 833, 2021; DOI: 10.3892/mmr.2021.12473].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066790","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":"Adaptation mechanisms in cancer: Lipid metabolism under hypoxia and nutrient deprivation as a target for novel therapeutic strategies (Review).","authors":"Shiro Koizume, Yohei Miyagi","doi":"10.3892/mmr.2025.13448","DOIUrl":"https://doi.org/10.3892/mmr.2025.13448","url":null,"abstract":"<p><p>Tumor tissues generally exist in a relatively hypovascular state, and cancer cells must adapt to severe tissue conditions with a limited molecular oxygen and nutrient supply for their survival. Lipid metabolism serves a role in this adaptation. Lipids are supplied not only through the bloodstream but also through autonomous synthesis by cancer cells, and they function as sources of adenosine triphosphate and cell components. Although cancer‑associated lipid metabolism has been widely reviewed, how this metabolism responds to the tumor environment with poor molecular oxygen and nutrient supply remains to be fully discussed. The main aim of the present review was to summarize the findings on this issue and to provide insights into how cancer cells adapt to better cope with metabolic stresses within tumors. It may be suggested that diverse types of lipid metabolism have a role in enabling cancer cells to adapt to both hypoxia and nutrient‑poor conditions. Gaining a deeper understanding of these molecular mechanisms may reveal novel possibilities of exploration for cancer treatment.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066707","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":"Protective effect of soluble protein hydrolysate against H₂O₂‑induced intestinal injury: An interventional study.","authors":"Jingjing Wei, Guozhong Tao, Junlin Liu, Bomi Framroze, Karl G Sylvester","doi":"10.3892/mmr.2025.13450","DOIUrl":"https://doi.org/10.3892/mmr.2025.13450","url":null,"abstract":"<p><p>The present study aimed to investigate whether soluble protein hydrolysate (SPH) protects against intestinal oxidative stress injury. An <i>in vitro</i> lactate dehydrogenase assay was used to assess the cytotoxicity and protective effect of SPH. For <i>in vivo</i> assessment, friend virus B NIH Jackson mouse pups aged 21 days were administered with 5% w/v soluble protein hydrolysate (SPH) through drinking water for 14 days and then luminally injected with 0.3% or 0.6% H₂O₂. Thereafter, the fecal samples of mice were collected, and the mice were sacrificed. Intestinal epithelial injury was assessed, and the expressions of 84 oxidative stress‑related genes in intestinal tissues was determined. SPH prophylactically protected against H₂O₂‑induced oxidative stress injury in human intestinal epithelial cells. An animal model of oxidative stress‑induced intestinal injury was established using 0.3 and 0.6% H₂O₂. SPH treatment reduced oxidative stress (0.3% H₂O₂)‑induced gut injury in mice. As no accelerated body growth was observed in SPH‑treated mice, it was hypothesized that the underlying protective mechanism of SPH is not related to nutrient oversupply. Treatment with SPH upregulated five oxidative protective genes that were not consistent between the sexes. Some antioxidative genes, including ferritin heavy polypeptide‑1 (<i>Fth1</i>), heme oxygenase‑1 (<i>Hmox1</i>), NAD(P)H dehydrogenase quinone 1 (<i>Nqo1</i>) and superoxide dismutase 1 (<i>Sod1</i>), were commonly upregulated in both male and female mice. Overall, an antioxidative protective effect was observed following SPH treatment, which may be attributed to the upregulation of genes that protect against oxidative damage. The findings of the present study highlight the promising potential of SPH as a functional food for alleviating intestinal oxidative stress injury.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066815","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] Tan IIA inhibits H1299 cell viability through the MDM4‑IAP3 signaling pathway.","authors":"Yukun Zu, Jianning Wang, Wei Ping, Wei Sun","doi":"10.3892/mmr.2025.13435","DOIUrl":"10.3892/mmr.2025.13435","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editors' attention by a concerned reader that certain of the western blotting data shown in Fig. 1C and D on p. 2386 were strikingly similar to data appearing in different form in a pair of other articles written by different authors at a different research institute that had already been published elsewhere prior to the submission of this paper to <i>Molecular Medicine Reports</i>. Moreover, some of the data featured in Fig. 6A and C were strikingly similar, also suggesting that the data in this figure had been misassembled. In view of the fact that the abovementioned data had already apparently been published previously, the Editor of <i>Molecular Medicine Reports</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 reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 2384‑2392, 2018; DOI: 10.3892/mmr.2017.8152].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11751589/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143008521","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":"Preconditioning with acteoside ameliorates myocardial ischemia‑reperfusion injury by targeting HSP90AA1 and the PI3K/Akt signaling pathway.","authors":"Jing Li, Yuxin Guo, Yang Yang, Qing Xue, Hong Cao, Guangyuan Yang, Linlin Jia, Haibo Yu","doi":"10.3892/mmr.2025.13442","DOIUrl":"10.3892/mmr.2025.13442","url":null,"abstract":"<p><p>The present study aimed to investigate the cardioprotective effects of acteoside (AC) on myocardial ischemia‑reperfusion injury (MIRI). To meet this aim, a network pharmacological analysis was conducted to search for key genes and signaling pathways associated with AC and MIRI. The infarct size of the rat heart was evaluated using 2,3,5‑triphenyltetrazolium chloride staining, and the serum levels of creatine kinase MB isoenzyme, cardiac troponin I, malondialdehyde and superoxide dismutase were subsequently detected in an <i>in vivo</i> experiment. The inhibitory effect of AC on oxidative stress was further confirmed by assessing the intracellular accumulation of reactive oxygen species (ROS). Hematoxylin and eosin staining was subsequently carried out to observe cardiac histopathological damage. The anti‑apoptotic effects of AC were determined using terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labeling assay and Hoechst 33342 staining, and the expression levels of apoptosis‑associated proteins in the myocardial tissue were assessed using immunohistochemical analysis. In addition, cell viability was determined using a Cell Counting Kit‑8 assay, and the expression levels of key target proteins associated with AC and MIRI were detected by western blot analysis. The results suggested that pretreatment with AC could mitigate MIRI‑induced myocardial damage, oxidative stress and apoptosis. The anti‑apoptotic effects of AC were associated with elevated Bcl‑2 levels, and reduced caspase‑3 and Bax expression levels in myocardial tissue. <i>In vitro</i>, AC pretreatment both led to an increased rate of cell survival and alleviated oxidative stress, as demonstrated by a decreased level of intracellular ROS accumulation. Moreover, guided by the network pharmacological analysis, heat‑shock protein 90AA1 (HSP90AA1) and the phosphoinositide 3‑kinase (PI3K)/serine‑threonine protein kinase (Akt) signaling pathway emerged as key targets for the action of AC against MIRI. Furthermore, the western blot analysis results showed that pretreatment with AC led to a significant increase in the activity of the PI3K/Akt signaling pathway, in addition to increased expression levels of glycogen synthase kinase‑3β and HSP90AA1. Taken together, the findings of the present study revealed that AC may exert cardioprotective effects on MIRI through suppressing apoptosis and oxidative stress by regulating the expression and activity of key proteins.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066698","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":"NGR1 reduces neuronal apoptosis through regulation of ITGA11 following subarachnoid hemorrhage.","authors":"Yu Hou, Lihan Zhang, Wenzhe Ma, Yong Jiang","doi":"10.3892/mmr.2025.13432","DOIUrl":"10.3892/mmr.2025.13432","url":null,"abstract":"<p><p>Subarachnoid hemorrhage (SAH), a prevalent cerebrovascular condition associated with a high mortality rate, frequently results in neuronal apoptosis and an unfavorable prognosis. The adjunctive use of traditional Chinese medicine (TCM) with surgical interventions exerts a therapeutic impact on SAH, potentially by facilitating apoptosis. However, the mechanism by which TCM mediates apoptosis following SAH remains unclear. In the present study, C57BL/6J mice were subjected to the modified single‑clamp puncture method to produce an <i>in vivo</i> model of SAH. Treatment of these mice with notoginsenoside R1 (NGR1) prevented short‑term neurological deficits, reduced the expression levels of apoptosis‑associated proteins and mitigated brain edema. In addition, an <i>in vitro</i> model of SAH was established by treating HT22 mouse neuronal cells with oxyhemoglobin (OxyHb). Treatment of these cells with NGR1 resulted in attenuation of the OxyHb‑induced apoptosis. Furthermore, RNA sequencing analysis was used to examine NGR1 + OxyHb and OxyHb groups. Statistically significant changes in the expression levels of apoptosis‑associated genes in OxyHb‑stimulated HT22 cells upon administration of NGR1 were observed. The present study investigated the potential mechanism by which NGR1 mitigates neuronal apoptosis, presenting a novel therapeutic approach for treating SAH through the use of a single TCM component.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736250/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142951905","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":"Prospects for potential therapy targeting immune‑associated factors in endometriosis (Review).","authors":"Wenwen Zhang, Kang Li, Aiwen Jian, Guanran Zhang, Xiaoli Zhang","doi":"10.3892/mmr.2024.13422","DOIUrl":"10.3892/mmr.2024.13422","url":null,"abstract":"<p><p>Endometriosis (EM) is a chronic inflammatory disease that is one of the most common causes of gynecological systemic lesions in women before menopause. The most representative histological feature of EM is that the endometrium appears outside of the uterine cavity, often in the ovary. Although it is generally accepted that the epithelial and stromal cells of the ectopic endometrium are not malignant, they still have numerous similarities to malignant tumors, including considerable changes to the immune microenvironment (immune monitoring disorder), the creation of a specific hormone environment, high levels of oxidative stress, chronic inflammation and abnormal immune cell regulation. The pathogenesis of EM is not fully understood, which makes it difficult to identify specific biomarkers and potential therapeutic targets for early disease diagnosis and effective treatment. However, considerable progress has been made in this field over the past few decades. The purpose of the present review is to summarize the confirmed and potential biomarkers for EM, and to identify potential therapeutic targets based on changes in immunological factors (including natural killer cells, macrophages, the complement system, miRNA and P‑selectin) in the ectopic endometrial tissue. It is hoped that this work can be used as the basis for identifying accurate diagnostic markers for EM and developing personalized immune‑targeted therapy.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11715623/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882564","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":"Quercetin attenuates the symptoms of osteoarthritis <i>in vitro</i> and <i>in vivo</i> by suppressing ferroptosis via activation of AMPK/Nrf2/Gpx4 signaling.","authors":"Shiyu Dong, Xiaoliang Li, Genrong Xu, Liming Chen, Jiyang Zhao","doi":"10.3892/mmr.2024.13425","DOIUrl":"10.3892/mmr.2024.13425","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a common joint disorder involving the cartilage and other joint tissues. Quercetin (QCT) serves a protective role in the development of OA. However, to the best of our knowledge, the regulatory mechanisms of QCT in the progression of OA have not yet been fully elucidated. In order to mimic a model of OA <i>in vitro</i>, IL‑1β was used to stimulate chondrocytes. Furthermore, an <i>in vivo</i> animal model of OA was induced by anterior cruciate ligament transection (ACLT). 5‑Ethynyl‑2'‑deoxyuridine assays, TUNEL assays, ELISAs, western blotting and immunohistochemical assays were conducted to assess the chondroprotective properties of QCT in the development of OA. The results revealed that 100 µM QCT significantly promoted the proliferation, reduced the apoptosis and inflammation, and inhibited the extracellular matrix (ECM) degradation in IL‑1β‑stimulated chondrocytes. Additionally, QCT attenuated the IL‑1β‑induced ferroptosis of chondrocytes, as demonstrated by the reduced lipid reactive oxygen species and Fe²⁺ levels. Conversely, the inhibitory effects of QCT on the apoptosis and inflammatory responses were reversed by the activation of ferroptosis by erastin in IL‑1β‑stimulated chondrocytes. Furthermore, QCT significantly elevated the level of phosphorylated (p‑)5' AMP‑activated protein kinase (AMPK) and the levels of two negative regulators of ferroptosis [nuclear factor erythroid 2‑related factor 2 (Nrf2) and glutathione peroxidase 4 (Gpx4)] in IL‑1β‑stimulated chondrocytes. The AMPK inhibitor compound C notably reversed the promoting effects of QCT on phosphorylated‑AMPK, Nrf2 and Gpx4 expression in IL‑1β‑stimulated chondrocytes. Additionally, QCT markedly ameliorated the destruction and degradation of articular cartilage, and elevated the p‑AMPK, Nrf2 and Gpx4 levels in the mouse model of ACLT‑induced OA. Overall, the present study demonstrated that QCT inhibited the development of OA by suppressing ferroptosis via the activation of the AMPK/Nrf2/Gpx4 signaling pathway. These findings provide novel insights into the regulatory mechanisms of QCT for the treatment of patients with OA.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11711930/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882570","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":"Adiponectin targets the AMPK/mTOR signaling pathway to alleviate cognitive impairment in epilepsy.","authors":"Yaoyuan Zhang, Zhenzhen Qu, Zhuofeng Mao, Hu Liu, Weiping Wang, Lijing Jia","doi":"10.3892/mmr.2025.13429","DOIUrl":"10.3892/mmr.2025.13429","url":null,"abstract":"<p><p>Among patients with chronic epilepsy, 70‑80% have cognitive impairment. To investigate the relationship between adiponectin (ADPN) and the cognitive level in epilepsy and its mechanism, 20 epileptic patients and 20 healthy controls were included for the assessment of the cognitive level. An ELISA was used to evaluate the serum ADPN level. An epileptic rat model was established and treated with AdipoRon, an ADPN receptor (AdipoR) agonist, which binds to AdipoR1 and AdipoR2. The Morris water maze test was used to assess the cognitive function of rats, and the expression levels of the synapsis‑associated proteins postsynaptic density protein 95 (PSD95), synaptosomal associated protein 25 (SNAP25) and synaptophysin (SYP), as well as AMP‑activated protein kinase (AMPK), mTOR, phosphorylated (p‑)AMPK and p‑mTOR were determined by immunoblotting. Serum ADPN levels were positively correlated with the Montreal cognitive assessment score. AdipoRon improved the cognitive function of epileptic rats, maintained the structural integrity of hippocampal neurons and reduced neuronal damage. It also promoted the mRNA expression of AdipoR1 and AdipoR2 in the hippocampus. Furthermore, AdipoRon increased the expression of the synapsis‑associated proteins PSD95, SNAP25 and SYP by activating the AMPK/mTOR signaling pathway. ADPN improved cognitive impairment in epilepsy by targeting the AMPK/mTOR signaling pathway, providing novel insights for the treatment of epilepsy.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11726285/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142921669","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":"Annexin A1: The dawn of ischemic stroke (Review).","authors":"Chen Tang, Rui Lan, Dong-Rui Ma, Min Zhao, Yong Zhang, Hong-Yu Li, Shuang Liu, Bo-Yang Li, Jie-Li Yang, Hui-Jie Yang, Zhen-Qiang Zhang","doi":"10.3892/mmr.2024.13427","DOIUrl":"10.3892/mmr.2024.13427","url":null,"abstract":"<p><p>Ischemic stroke is a prevalent clinical condition that poses a significant global challenge. Developing innovative strategies to address this issue is crucial. Annexin A1 (ANXA1), a key member of the annexin superfamily, performs various functions, such as inhibiting inflammatory factor release, promoting phagocytosis, and blocking leukocyte migration. Evidence indicates that ANXA1 plays a pivotal role in the pathogenesis of ischemic stroke. The present article reviews involvement of ANXA1 in anti‑atherosclerosis, inflammatory processes, blood‑brain barrier protection, platelet aggregation and anti‑apoptotic mechanisms. The potential applications of ANXA1 in treating ischemic stroke are also explored.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11726294/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142921711","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}