Molecular medicine reports最新文献

{"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":"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":"Insulin receptor tyrosine kinase substrate in health and disease (Review).","authors":"Xueyan Zhang, Zhewen Zhang","doi":"10.3892/mmr.2025.13437","DOIUrl":"10.3892/mmr.2025.13437","url":null,"abstract":"<p><p>Insulin receptor (IR) tyrosine kinase substrate (IRTKS) was first identified >20 years ago as a tyrosine‑phosphorylated IR substrate and subsequently characterized as a protein containing an inverse‑Bin‑amphiphysin‑Rvs domain. Subsequent research has shown that IRTKS functions as a scaffold protein with multiple domains, which results in diverse functions in a variety of cell activities. For example, IRTKS plays roles in regulating the formation of membrane protrusions; triggering pathogen‑driven actin assembly; modulating insulin signaling, antiviral immunity and embryonic development; and promoting tumor occurrence and progression. It is also a candidate forensic biomarker of hypothermia. Nevertheless, a systematic summary of the biological functions of IRTKS and its underlying molecular mechanism is lacking. Therefore, the present review provides a comprehensive summary of the latest advancements in IRTKS research, thereby establishing a framework for understanding the contribution of IRTKS to diverse cell processes.</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/PMC11795247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143391296","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}

{"title":"Triptolide reverses cis‑diamminedichloroplatinum resistance in esophageal squamous cell carcinoma by suppressing glycolysis and causing mitochondrial malfunction.","authors":"Kuiyuan Liu, Jia Liu, Tiebao Meng, Nan Wu, Juntao Liu, Mingxu Qiao, Liangyi Dong, Jingeng Liu","doi":"10.3892/mmr.2025.13439","DOIUrl":"10.3892/mmr.2025.13439","url":null,"abstract":"<p><p>The present study investigated the sensitization mechanism of triptolide (TPL) in esophageal squamous cell carcinoma (ESCC) resistant to cis‑diamminedichloroplatinum (CDDP). CDDP‑resistant TE‑1/CDDP and KYSE30/CDDP cells were created using an incremental drug concentration approach. TPL and CDDP treatment conditions were screened based on the Cell Counting Kit‑8 cell viability assay and cell proliferation was detected using 5‑ethynyl‑2'‑deoxyuridine and clone formation assays. Flow cytometry combined with Hoechst 33258 staining was used to assess cell cycle progression and apoptosis. Scratch healing assay, Transwell assay and western blotting were used to investigate the malignant behaviors of the cells. Changes in cellular glycolysis were investigated by measuring glucose uptake, lactate production and the levels of related regulatory factors. Changes in mitochondrial function were examined by detecting ATP and reactive oxygen species levels, as well as mitochondrial membrane potential and cytochrome c release. Furthermore, a nude mouse subcutaneous graft tumor model assay was used to assess the in vivo effect of TPL. <i>In vitro</i> dosages of TPL and CDDP were tested at 2 nM and 4 <i>µ</i>M, respectively. Notably, TPL decreased the proliferation, migration, invasion and epithelial‑mesenchymal transition of CDDP‑resistant ESCC cells, increased their apoptosis and significantly suppressed tumor growth in a nude mouse model of ESCC. TPL was shown to have a strong CDDP‑sensitizing effect <i>in vitro</i> and <i>in vivo</i> and its mechanism may involve inhibiting anaerobic glycolysis and causing mitochondrial energy metabolism impairment to induce apoptosis. In conclusion, TPL may be considered a potential CDDP sensitizer with substantial clinical implications for ESCC 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/PMC11795233/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066784","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":"Establishment and verification of a prognostic signature associated with fatty acid metabolism in endometrial cancer.","authors":"Lu Peng, Rui Sun, Tingting Hao, Yulong Mu, Qing Zhang, Jie Jiang, Helgi B Schiöth, Ruifen Dong","doi":"10.3892/mmr.2025.13444","DOIUrl":"10.3892/mmr.2025.13444","url":null,"abstract":"<p><p>Endometrial carcinoma (EC) is one of the leading causes of mortality in women. Metabolic disorders, such as abnormal fatty acid metabolism (FAM), are considered to be indicators of tumorigenesis. However, to the best of our knowledge, the relationship between EC and FAM remains unclear. The process of FAM is associated with the function of immune cells, thus samples from The Cancer Genome Atlas were grouped according to immune infiltration levels. Subsequently, prognostic gene signatures were constructed based on selected FAM‑associated genes. The signature effect was validated, and enrichment analyses were conducted based on sample classification. Nomograms were used to predict survival, merging clinical data and the gene signature. Samples were divided into high‑ and low‑risk groups based on the gene signature. The survival status, clinical characteristics, enrichment analysis and immune infiltration were significantly different between high‑ and low‑risk groups. According to the nomogram, low microsatellite instability‑high as well as a high tumor mutation burden can be observed in the low‑nomo‑score group. Immune checkpoint inhibitor‑associated genes were differentially expressed between groups and 35 sensitive compounds were identified. Comprehensive bioinformatics analysis in EC revealed potential roles of FAM in tumorigenesis, the tumor microenvironment and prognosis, suggesting that FAM‑associated signatures are promising biomarkers for EC. These findings may improve the understanding of FAM in EC and pave the way for a more accurate assessment of prognosis and immunotherapy outcomes.</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/PMC11795235/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066659","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":"Viruses and psychiatric disorders: We have not crossed the borderline from hypothesis to proof yet (Review).","authors":"Nikolaos Siafakas, Cleo Anastassopoulou, Spyridon Pournaras, Athanasios Tsakris, Evangelos Alevizakis, Stylianos Kympouropoulos, Demetrios A Spandidos, Emmanouil Rizos","doi":"10.3892/mmr.2024.13426","DOIUrl":"10.3892/mmr.2024.13426","url":null,"abstract":"<p><p>Most psychiatric disorders are heterogeneous and are attributed to the synergistic action of a multitude of factors. It is generally accepted that psychiatric disorders are the outcome of interactions between genetic predisposition and environmental perturbations, which involve psychosocial stress, or alterations in the physiological state of the organism. A number of hypotheses have been presented on such environmental influences that may include direct insults such as injury, malnutrition and hostile living conditions, or indirect sequelae following infection from viruses such as influenza, arboviruses, enteroviruses and several herpesviruses, or the differential expression of human endogenous retroviruses. It is known that the concept of viruses is far more extensive than their perception as mere agents of acute infections, or chronic debilitating diseases, such as AIDS or some forms of cancer. Notably, an apparent causal connection between viruses and the pathophysiology of diseases has been suggested; however, it remains unclear as to how to establish this causal connection. There are inherent difficulties in answering this question with certainty, which may be due to the multitude of genetic and environmental influences that can lead to psychopathology; the latent state of chronic infection exhibited by a number of neurotropic viruses; the late onset of psychiatric disorders with respect to the acute phase of viral infection at which detection tests would be successful; the complexity of the virome; and the existence of thousands of viral species. The present review aims to provide an outline of the conclusions that have thus far been reached regarding a possible association between viral infection and psychiatric disease, and the obstacles confronted during the quest for the truth behind the role of viruses.</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/PMC11711936/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142921733","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] Tanshinone IIA improves hypoxic ischemic encephalopathy through TLR‑4‑mediated NF‑κB signal pathway.","authors":"Chengzhi Fang, Lili Xie, Chunmei Liu, Chunhua Fu, Wei Ye, Hong Liu, Binghong Zhang","doi":"10.3892/mmr.2025.13428","DOIUrl":"10.3892/mmr.2025.13428","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 IL‑1 protein data shown in the western blotting data in Fig. 5A on p. 1905, the hippocampal images shown in Fig. 6A and certain of the immunohistochemical data shown in Fig. 6B on p. 1906 were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had either already been published elsewhere prior to the submission of this paper to <i>Molecular Medicine Reports</i>, or were under consideration for publication at around the same time. In view of the fact that certain of 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 satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 18: 1899‑1908, 2018; DOI: 10.3892/mmr.2018.9227].</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/PMC11726297/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142921623","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":"Application of integrated omics in aseptic loosening of prostheses after hip replacement.","authors":"Yun-Ke Liu, Yong-Hui Dong, Xia-Ming Liang, Shuo Qiang, Meng-En Li, Zhuang Sun, Xin Zhao, Zhi-Hua Yan, Jia Zheng","doi":"10.3892/mmr.2025.13430","DOIUrl":"10.3892/mmr.2025.13430","url":null,"abstract":"<p><p>Aseptic loosening (AL) of artificial hip joints is the most common complication following hip replacement surgery. A total of eight patients diagnosed with AL following total hip arthroplasty (THA) undergoing total hip replacement and eight control patients diagnosed with avascular necrosis of femoral head (ANFH) or femoral neck fracture undergoing THA were enrolled. The samples of the AL group were from synovial tissue surrounding the lining/head/neck of the prosthesis, and the samples of the control group were from the synovium in the joint cavity. The present study utilized second‑generation high‑throughput sequencing and mass spectrometry to detect differentially expressed genes, proteins and metabolites in the samples, as well as Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis. Key genes cytokine receptor‑like factor‑1 (CRLF1) and glutathione‑S transferase <i>µ</i>1 (GSTM1) expression levels were verified by reverse transcription‑quantitative PCR and western blotting. The integrated transcriptomics, proteomics and untargeted metabolomics analyses revealed characteristic metabolite changes (biosynthesis of guanine, L‑glycine and adenosine) and decreased CRLF1 and GSTM1 in AL, which were primarily associated with amino acid metabolism and lipid metabolism. In summary, the present study may uncover the underlying mechanisms of AL pathology and provide stable and accurate biomarkers for early warning and diagnosis.</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/PMC11726296/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142921728","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":"Expression of the IGF‑1Ea isoform in human placentas from third trimester normal and idiopathic intrauterine growth restriction singleton pregnancies: Correlations with clinical and histopathological parameters.","authors":"Apostolos Fasoulopoulos, Michail Varras, Fani-Niki Varra, Anastasios Philippou, Despina Myoteri, Viktoria-Konstantina Varra, Evgenia Kouroglou, Alexandros Gryparis, Argyro Papadopetraki, Iakovos Vlachos, Konstantinos Papadopoulos, Michael Koutsilieris, Anastasia Evangelia Konstantinidou","doi":"10.3892/mmr.2025.13434","DOIUrl":"10.3892/mmr.2025.13434","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Intrauterine growth restriction (IUGR) is the second most common obstetric complication after preterm labor. Appropriate trophoblast differentiation and placental structure, growth and function are key for the maintenance of pregnancy and normal fetal growth, development and survival. Extravillous trophoblast cell proliferation, migration and invasion are regulated by molecules produced by the fetomaternal interface, including autocrine factors produced by the trophoblast, such as insulin‑like growth factor (IGF)‑1. The aim of the present study was to investigate expression patterns of IGF‑1Ea isoform in IUGR placenta compared with appropriate for gestational age (AGA) pregnancies. Placental frozen tissues were collected from 13 AGA and 15 IUGR third trimester pregnancies for detection of IGF‑1Ea mRNA expression using reverse transcription‑quantitative PCR. Formalin‑fixed paraffin‑embedded samples from 15 AGA and 47 IUGR pregnancies were analyzed immunohistochemically for the identification and localization of the IGF‑1Ea peptide and comparison of clinical and histopathological parameters. To the best of our knowledge, the present study is the first to show IGF‑1Ea expression in third trimester human placenta. The results indicated that similar IGF‑1Ea mRNA expression levels were present in placental specimens from both groups. Cytoplasmic IGF‑1Ea expression was localized in the perivillous syncytiotrophoblast, extravillous trophoblast and endothelium of the villous and decidual vessels in both groups. No significant difference in the scores and intensity of IGF‑1Ea expression in perivillous syncytiotrophoblasts were noted in the IUGR vs. AGA pregnancies. Most IUGR cases showed negative IGF‑1Ea expression in the extravillous trophoblast, whereas AGA pregnancies showed predominantly positive immunostaining. A sex‑specific expression pattern was noted in the extravillous trophoblast, with negative IGF‑1Ea expression in the placentas of female IUGR cases. Additionally, positive immunostaining for IGF‑1Ea peptide in fetal villous and maternal decidual vessels, was more frequently observed in the IUGR group compared with AGA. In conclusion, no difference in total IGF‑1Ea mRNA placental expression was observed between IUGR and AGA pregnancies, likely due to heterogeneity of histological structures expressing this isoform. Negative IGF‑1Ea immunohistological expression in the extravillous trophoblast from IUGR placentas, associated with histological changes of maternal malperfusion, may reflect the involvement of this isoform in defective placentation. The presence of IGF‑1Ea peptide in the endothelium of the villous vessels in IUGR placentas may indicate a reactive autocrine regulation to compensate for malperfused villi in IUGR pregnancy by regulating angiogenesis and vasodilation. The observed sex differences in IGF‑1Ea expression between IUGR and AGA placentas may indicate interactions between sex hormones and selective IGF‑1 binding proteins ","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/PMC11751665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142951891","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}