Molecular medicine reports最新文献

{"title":"Role of CALCR expression in liver cancer: Implications for the immunotherapy response.","authors":"Sijia Wang, Wei Wang, Jia Zeng","doi":"10.3892/mmr.2024.13406","DOIUrl":"10.3892/mmr.2024.13406","url":null,"abstract":"<p><p>Liver hepatocellular carcinoma (LIHC) is a prevalent and lethal malignancy with a complex molecular landscape. Fibrosis and ferroptosis are implicated in LIHC progression, yet their roles remain to be elucidated. The present study investigated the expression and prognostic significance of calcitonin receptor (CALCR), a gene that intersects the pathways of fibrosis and ferroptosis, across LIHC and other types of cancer. Data were obtained from The Cancer Genome Atlas and the Molecular Signatures Database. LIHC patients were classified into two clusters based on fibrosis‑related gene expression using ConsensusClusterPlus. Single‑sample gene set enrichment analysis was employed to quantify fibrosis and ferroptosis levels. Correlation, survival and nomogram analyses were performed to assess the prognostic value of CALCR. Additionally, single‑cell RNA sequencing data from the Tumor Immune Single Cell Hub 2 (TISCH2) and pan‑cancer analyses of genomic heterogeneity features were incorporated. The present study also identified a putative regulatory role for CALCR in LIHC cell migration, proliferation and apoptosis. CALCR was identified as a significant prognostic marker for LIHC. Patients with high CALCR expression exhibited shortened overall survival (OS) and disease‑specific survival (DSS). Specifically, the hazard ratios (HRs) for OS and DSS were 1.76 [95% confidence interval (CI): 1.23=2.49) and 1.77 (95% CI: 1.13=2.78], respectively, with corresponding P‑values of 0.002 for OS and 0.013 for DSS. Analyses of immune cell infiltration revealed a more complex immune environment in patients with low CALCR expression, suggesting differential responses to immunotherapy. Furthermore, in HepG‑2 and HuH‑7 cells, small interfering (si)‑CALCR increased apoptosis while reducing proliferation and migration compared with si‑negative control. CALCR serves as a significant prognostic biomarker for LIHC, influencing both molecular pathways and the immune landscape. Its expression is associated with improved survival outcomes and distinct genomic features, positioning it as a potential therapeutic target and predictor of immunotherapy efficacy.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11622006/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142751022","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] A disintegrin and metalloprotease 17 promotes microglial cell survival via epidermal growth factor receptor signalling following spinal cord injury.","authors":"Zijian Wei, Deshui Yu, Yunlong Bi, Yang Cao","doi":"10.3892/mmr.2024.13414","DOIUrl":"https://doi.org/10.3892/mmr.2024.13414","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 apoptotic data shown in Fig. 3A, the flow cytometric (FCM) data in Fig. 3B on p. 67, and the western blot data shown in Fig. 5 on p. 68 were strikingly similar to data that had either already been submitted for publication elsewhere, or which subsequently appeared in different form in other articles/publications. Moreover, patterns of data featured within certain quadrants of the FCM plots featured in Fig. 5 appeared to be strikingly similiar to other patterns of data when comparing between the quadrants of the FCM plots within this same figure, such that the similarities were difficult to attribute to coincidence. Owing to the fact that the abovementioned data have apparently subsequently appeared in other unrelated articles, and owing to the potentially anomalous presentation of data in the FCM plots in Fig. 5, the Editor of <i>Molecular Medicine Reports</i> has decided that this paper should be retracted from the Journal on the grounds 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 for any inconvenience caused. [Molecular Medicine Reports 12: 63‑70, 2015; DOI: 10.3892/mmr.2015.3395].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818509","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":"Comprehensive bioinformatics analysis of metabolism‑related microRNAs in high myopia in young and old adults with age‑related cataracts.","authors":"Fanfan Huang, Yanyi Chen, Jiaxue Wu, Shijie Zheng, Rongxi Huang, Wenjuan Wan, Ke Hu","doi":"10.3892/mmr.2024.13411","DOIUrl":"10.3892/mmr.2024.13411","url":null,"abstract":"<p><p>High myopia and age‑related cataracts are prevalent ocular disorders that compromise visual acuity. The molecular mechanisms underlying these conditions remain largely unclear. Here, microRNA (miRNA or miR) sequencing was performed on aqueous humor samples obtained from individuals with age‑related cataracts and high myopia (AH, n=9), young patients with high myopia (YH, n=9) and a control group of elderly patients with age‑related cataracts, matched in terms of sex and age (AN, n=9). miRNA sequencing and differential expression were performed. Intersecting miRNAs were identified, as well as metabolism‑related genes from MsigDB were intersected with miRNA target genes. Functional enrichment was performed and disease targets predicted using DisGeNET. A protein‑protein interaction network was built with STRING, and hub genes were identified via Cytoscape. GeneMANIA analyzed hub genes, while drug predictions were made using Comparative Toxicogenomics Database. Long non‑coding RNAs and transcription factors were predicted via mirNet and ChEA3. Results were validated by RT‑qPCR. A total of 18 miRNAs were significantly differential expressed between AH and AN group, of which eight were up‑ and 10 were downregulated. A total of 23 miRNAs were significantly differential expressed between the YH and AN group, of which six were up‑ and 17 were downregulated. hsa‑miR‑490‑3p, hsa‑miR‑4423‑3p and hsa‑miR‑4485‑3p may serve as characteristic miRNAs. A total of 289 target genes were predicted. Functional enrichment analysis yielded 169 terms, with 'herpes simplex virus 1 infection' the most significantly enriched. There were 19 metabolism‑associated target genes linked with these miRNAs, suggesting a potential role of metabolic processes in pathogenesis of these conditions. The biosynthetic process of carbohydrate derivatives may serve a key role during the development of high myopia. There were 10 hub genes and Propionyl‑CoA Carboxylase Subunit β could potentially serve as a biomarker. Drugs that could modulate their function were predicted; cyclosporine, tretinoin and acetaminophen may exert a broad influence on these hub genes. Hub gene networks based on the miRNAs were constructed to predict 44 associated long non‑coding RNAs and 98 transcription factors. The present findings offer novel insights into the molecular mechanisms of age‑related cataracts and high myopia and propose potential therapeutic targets.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11638740/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142786227","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":"Advances in research on malignant tumors and targeted agents for TOP2A (Review).","authors":"Tao Zhou, Yiting Niu, Yanjun Li","doi":"10.3892/mmr.2024.13415","DOIUrl":"10.3892/mmr.2024.13415","url":null,"abstract":"<p><p>The DNA topoisomerase isoform topoisomerase IIα (TOP2A) is essential for the condensation and segregation of cellular mitotic chromosomes and the structural maintenance. It has been demonstrated that TOP2A is highly expressed in various malignancies, including lung adenocarcinoma (LUAD), hepatocellular carcinoma (HCC) and breast cancer (BC), associating with poor prognosis and aggressive tumor behavior. Additionally, TOP2A has emerged as a promising target for cancer therapy, with widespread clinical application of associated chemotherapeutic agents. The present study explored the impact of TOP2A on malignant tumor growth and the advancements in research on its targeted drugs. The fundamental mechanisms of TOP2A have been detailed, its specific roles in tumor cells are analyzed, and its potential as a biomarker for tumor prognosis and therapeutic targeting is highlighted. Additionally, the present review compiles findings from the latest clinical trials of relevant targeted agents, information on newly developed inhibitors, and discusses future research directions and clinical application strategies in cancer therapy, aiming to propose novel ideas and methods.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818569","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":"Influence of lactate in resistance to anti‑PD‑1/PD‑L1 therapy: Mechanisms and clinical applications (Review).","authors":"Yi Zeng, Yu Huang, Qiaoyun Tan, Ling Peng, Jian Wang, Fan Tong, Xiaorong Dong","doi":"10.3892/mmr.2024.13413","DOIUrl":"10.3892/mmr.2024.13413","url":null,"abstract":"<p><p>Metabolic reprogramming is a prominent characteristic of tumor cells, evidenced by heightened secretion of lactate, which is linked to tumor progression. Furthermore, the accumulation of lactate in the tumor microenvironment (TME) influences immune cell activity, including the activity of macrophages, dendritic cells and T cells, fostering an immunosuppressive milieu. Anti‑programmed cell death protein 1 (PD‑1)/programmed death‑ligand 1 (PD‑L1) therapy is associated with a prolonged survival time of patients with non‑small cell lung cancer. However, some patients still develop resistance to anti‑PD‑1/PD‑L1 therapy. Lactate is associated with resistance to anti‑PD‑1/PD‑L1 therapy. The present review summarizes what is known about lactate metabolism in tumor cells and how it affects immune cell function. In addition, the present review emphasizes the relationship between lactate secretion and immunotherapy resistance. The present review also explores the potential for targeting lactate within the TME to enhance the efficacy of immunotherapy.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818665","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":"Diagnostic and predictive values of m5C‑associated genes in idiopathic pulmonary fibrosis.","authors":"Lan Tian, Wanting Song, Jiabao Wu, Yi Lan, Limin Chen","doi":"10.3892/mmr.2024.13418","DOIUrl":"https://doi.org/10.3892/mmr.2024.13418","url":null,"abstract":"<p><p>In patients with idiopathic pulmonary fibrosis (IPF), the role of 5‑methylcytosine (m5C)‑associated genes in the pathogenesis and development of the disease remains unclear. The present study aimed to identify reliable diagnostic markers based on the expression of m5C‑associated genes for the early detection of IPF. Count data were obtained by screening the IPF genome‑wide assay in the Gene Expression Omnibus database, followed by a comparison of m5C gene expression in patients with IPF and controls. The GSE150910 and GSE173355 datasets yielded a total of 23 differentially expressed m5C‑associated genes, which were then investigated for their functions. A diagnostic model was built using eight m5C genes and validated with training sets and the GSE124685 dataset. IPF subtypes were identified based on expression of m5C‑related genes as well as clinical and immunological characteristics. Furthermore, a pulmonary fibrosis model was established in mice by administering bleomycin into the trachea. Lungs were harvested and analyzed using quantitative PCR to determine the expression of m5C‑related genes. The Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed that these genes were significantly enriched in 'base excision repair'. Immunoassay results revealed that 13 immune cell markers (naive, memory and B cell plasma, T cell CD4 naive, T cell CD4 memory resting, T cell follicular helper, T cell regulatory Tregs, NK cell resting, Monocyte, Macrophage M0, Mast cell activated, Eosinophil, and Neutrophil) were significantly associated with IPF. Patients with IPF had lower levels of resting memory CD4+ T cells, which were positively associated with Tet methylcytosine dioxygenase2 (TET2) and Thymine‑DNA glycosylase (TDG) but negatively correlated with NOP2/Sun RNA methyltransferase5 (NSUN5) expression. All samples were classified into based on the levels of the eight diagnostic m5C genes. Samples with high m5C scores are subtype 1, and those with low m5C scores are subtype 2. In subtype 2, male patients had lower levels of CD27 and CD70 but higher levels of CD274, CD86, Cytotoxic T‑lymphocyte‑associated protein4 and Hepatitis A virus cellular receptor2 (HAVCR2). When compared with normal mouse lung tissue samples, expression levels of NOP2/Sun RNA methyltransferase6 (NSUN6), Ubiquitin‑like with PHD and RING Finger Domains1, TDG and TET2 in lung fibrosis tissue samples were significantly higher, while expression levels of NSUN5, NTH‑like DNA glycosylase1, DNA (cytosine‑5‑)‑methyltransferase3 β and Methyl‑CpG binding domain protein 3) were lower. It is possible that m5C‑associated genes play an important role in the diagnosis and typing of IPF. These genes may facilitate investigation of the pathophysiology of IPF and identification of potential treatment targets.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864890","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":"Risk factors and treatment strategies for adjacent segment disease following spinal fusion (Review).","authors":"Xing Huang, Yong Cai, Kai Chen, Qiang Ren, Bo Huang, Gang Wan, Yuchen Wang, Jincheng Lin, Jun Zhao","doi":"10.3892/mmr.2024.13398","DOIUrl":"10.3892/mmr.2024.13398","url":null,"abstract":"<p><p>Adjacent segment disease (ASD) is a significant clinical complication following cervical and lumbar spinal fusion surgery, characterized by the degeneration of spinal segments adjacent to the fused area. The present literature review aimed to elucidate the risk factors contributing to ASD and to evaluate current and emerging treatment strategies. Epidemiological data indicate that patient‑related factors such as age, pre‑existing spinal degeneration and comorbidities, along with surgical factors including the type of fusion, instrumentation and alignment correction, play pivotal roles in ASD development. Biomechanical alterations post‑fusion further exacerbate the risk. The underlying mechanisms of ASD involve changes in spinal kinematics and disc degeneration, driven by inflammatory and degenerative processes. Diagnostic modalities, such as magnetic resonance imaging and computed tomography scans, are essential for early detection and accurate diagnosis. Preventive strategies emphasize meticulous preoperative planning, advanced surgical techniques and postoperative rehabilitation. Treatment approaches range from conservative methods such as physical therapy and pharmacological interventions to surgical solutions, including revision surgeries and the use of motion‑preserving technologies. Emerging therapies, particularly in regenerative medicine, show promise in mitigating ASD. The present review underscored the necessity of a multidisciplinary approach to optimize patient outcomes and highlighted the need for ongoing research to address gaps in the current understanding of ASD in both cervical and lumbar regions.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11605282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142687691","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":"Stattic suppresses p‑STAT3 and induces cell death in T‑cell acute lymphoblastic leukemia.","authors":"Chia-Ling Li, Han-Yu Chen, Jiin-Cherng Yen, Sheng-Jie Yu, Ting-Yu Chou, Sih-Wen Yeh, Huai-Yu Chuang, Fang-Liang Huang","doi":"10.3892/mmr.2024.13416","DOIUrl":"https://doi.org/10.3892/mmr.2024.13416","url":null,"abstract":"<p><p>The present study investigated the therapeutic potential of Stattic, a selective inhibitor of STAT3, in treating T‑cell acute lymphoblastic leukemia (T‑ALL). The effects of Stattic on cell viability, STAT3 phosphorylation, apoptosis and autophagy in T‑ALL cell lines, and on tumor growth in a xenograft mouse model of T‑ALL, were assessed. Methods, including the Cell Counting Kit‑8 assay for cell viability, propidium iodide/Annexin V staining for apoptosis detection, western blotting for protein expression analysis, and a xenograft mouse model for evaluating <i>in vivo</i> tumor growth, were employed. The results showed that Stattic effectively reduced cell viability in a dose‑dependent manner, with significant reductions observed at concentrations of 1.25 <i>µ</i>M and above in CCRF‑CEM cells (IC₅₀=3.188 <i>µ</i>M) and at 2.5 <i>µ</i>M and above in Jurkat cells (IC₅₀=4.89 <i>µ</i>M) after 24 h of treatment. Concurrently, Stattic significantly suppressed the expression of phosphorylated STAT3, indicating its mechanism of action as a STAT3 pathway inhibitor. Furthermore, Stattic treatment induced both apoptosis and autophagy in CCRF‑CEM and Jurkat cells, as evidenced by the respective upregulation of cleaved caspase‑3 and LC3B. In a xenograft mouse model of T‑ALL, Stattic markedly inhibited tumor growth, with the greatest effect occurring at the highest dose of 30 mg/kg. These results suggested that Stattic holds promise as a therapeutic agent in T‑ALL by modulating key pathways involved in cell survival and proliferation. In conclusion, Stattic exhibited a significant therapeutic potential for T‑ALL via a dose‑dependent reduction of cell viability, inhibiting STAT3 phosphorylation, and promoting both apoptotic and autophagic cell death; however, further studies are required before clinical application.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818669","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":"Ciliary neurotrophic factor activation of astrocytes mediates neuronal damage via the IL‑6/IL‑6R pathway.","authors":"Hong-Tao Wang, Si-Tong Lu, Zhi-Hui Xia, Tao Xu, Wei-Yan Zou, Mei-Qun Sun","doi":"10.3892/mmr.2024.13396","DOIUrl":"10.3892/mmr.2024.13396","url":null,"abstract":"<p><p>The occurrence of epilepsy is a spontaneous and recurring process due to abnormal neuronal firing in the brain. Epilepsy is understood to be caused by an imbalance between excitatory and inhibitory neurotransmitters in the neural network. The close association between astrocytes and synapses can regulate the excitability of neurons through the clearance of neurotransmitters. Therefore, the abnormal function of astrocytes can lead to the onset and development of epilepsy. The onset of epilepsy can produce a large number of inflammatory mediators, which can aggravate epileptic seizures, leading to a vicious cycle. Neurons and glial cells interact to promote the onset and maintenance of epilepsy, but the specific underlying molecular mechanisms need to be further studied. Ciliary neurotrophic factor (CNTF) belongs to the IL‑6 cytokine family and is mainly secreted by astrocytes and Schwann cells. In the normal physiological state, CNTF levels are low, but in an epileptic state, CNTF levels in the serum and tears of patients are elevated. Astrocyte activation plays an important role in epileptic seizures. CNTF activates astrocytes to produce a variety of secreted proteins, which are secreted into the astrocyte culture medium (ACM), thus forming a distinct culture medium (CNTF‑ACM) that can be used to study the effect of astrocytes on neurons <i>in vitro</i>. CNTF‑activated astrocytes increase the secretion of the pro‑inflammatory factor IL‑6. In the present study, CNTF‑ACM was applied to primary cerebral cortical neurons to observe the specific effects of IL‑6 in CNTF‑ACM on neuronal activity and excitability. The results suggested that CNTF‑ACM can reduce neuronal activity via the IL‑6/IL‑6R pathway, promote neuronal apoptosis, increase Ca²⁺ inflow, activate the large conductance calcium‑activated potassium channel and enhance neuronal excitability. The results of the present study further revealed the functional changes of astrocytes after CNTF activated astrocytes and the effects on neuronal activity and excitability, thereby providing new experimental evidence for the role of communication between astrocytes and neurons in the mechanism of epileptic seizures.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11600100/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142687689","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] Protection of rat intestinal epithelial cells from ischemia/reperfusion injury by (D‑Ala2, D‑Leu5)‑enkephalin through inhibition of the MKK7‑JNK signaling pathway.","authors":"Zhenran Wang, Bo Tang, Fang Tang, Yang Li, Guangyu Zhang, Li Zhong, Chencheng Dong, Songqing He","doi":"10.3892/mmr.2024.13403","DOIUrl":"10.3892/mmr.2024.13403","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the cell apoptotic assay data shown in Fig. 2A on p. 4082 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 <i>Life Sciences</i> 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. 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 12: 4079‑4088, 2015; DOI: 10.3892/mmr.2015.3991].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11613647/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142751068","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}