Molecular medicine reports最新文献

{"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":"","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":"","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":"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":"","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":"","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}

{"title":"Mitochondrial DNA copy number alterations: Key players in the complexity of glioblastoma (Review).","authors":"Abdul Aziz Mohamed Yusoff, Siti Zulaikha Nashwa Mohd Khair, Siti Muslihah Abd Radzak","doi":"10.3892/mmr.2025.13443","DOIUrl":"https://doi.org/10.3892/mmr.2025.13443","url":null,"abstract":"<p><p>Renowned as a highly invasive and lethal tumor derived from neural stem cells in the central nervous system, glioblastoma (GBM) exhibits substantial histopathological variation and genomic complexity, which drive its rapid progression and therapeutic resistance. Alterations in mitochondrial DNA (mtDNA) copy number (CN) serve a crucial role in GBM development and progression, affecting various aspects of tumor biology, including energy production, oxidative stress regulation and cellular adaptability. Fluctuations in mtDNA levels, whether elevated or diminished, can impair mitochondrial function, potentially disrupting oxidative phosphorylation and amplifying reactive oxygen species generation, thereby fueling tumor growth and influencing treatment responses. Understanding the mechanisms of mtDNA‑CN variations, and their interplay with genetic and environmental elements in the tumor microenvironment, is essential for advancing diagnostic and therapeutic strategies. Targeting mtDNA alterations could strengthen treatment efficacy, mitigate resistance and ultimately enhance the prognosis of patients with this aggressive brain tumor. The present review summarizes the existing literature on mtDNA alterations, specifically emphasizing variations in mtDNA‑CN and their association with GBM by surveying articles published between 1996 and 2024, sourced from databases such as Scopus, PubMed and Google Scholar. In addition, the review provides a brief overview of mitochondrial genome architecture, knowledge regarding the regulation of mtDNA integrity and CN, and how mitochondria significantly impact GBM tumorigenesis. This review further presents information on therapeutic approaches for restoring mtDNA‑CN that contribute to optimized mitochondrial function and improved health 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":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066771","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] NG25, an inhibitor of transforming growth factor‑β‑activated kinase 1, ameliorates neuronal apoptosis in neonatal hypoxic‑ischemic rats.","authors":"Hua Wang, Zhong Chen, Yu Li, Qiaoyun Ji","doi":"10.3892/mmr.2024.13423","DOIUrl":"10.3892/mmr.2024.13423","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 TUNEL assay data shown in Fig. 4B were strikingly similar to data appearing in different form in another article written by different authors at different research institutes that had already been submitted for publication to the journal <i>Experimental and Therapeutic Medicine</i> (which has subsequently been retracted). Owing to the fact that these contentious data had already apparently been submitted for publication prior to the receipt of this paper to <i>Molecular Medicine Reports</i>, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 1710-1716, 2018; DOI: 10.3892/mmr.2017.8024].</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/PMC11715618/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New insights into the role of complement system in colorectal cancer (Review).","authors":"Yuwen Xu, Jiaqi Zhou, Yuanyuan Wu, Jie Shen, Xiaoyan Fu, Meifang Liu, Shujuan Liang","doi":"10.3892/mmr.2025.13433","DOIUrl":"10.3892/mmr.2025.13433","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is one of the most common cancers worldwide. With the growing understanding of immune regulation in tumors, the complement system has been recognized as a key regulator of tumor immunity. Traditionally, the complement cascade, considered an evolutionarily conserved defense mechanism against invading pathogens, has been viewed as a crucial inhibitor of tumor progression. Complement components or activation products produced via cascade‑dependent or ‑independent processes are associated with the regulation of tumor‑associated inflammation. Various forms of complement activation products present in body fluids or inside cells, along with complement regulatory proteins and complement receptors, are involved in tumor cell growth and modulating the tumor microenvironment. In the present review, the role of the complement system in the tumor immunity of CRC is discussed. In addition, the contribution of the unconventional cascade‑independent pathway of complement activation in CRC progression is highlighted. A deeper understanding of the mechanism underlying the complement system in colitis‑associated colorectal cancer (CAC) may provide novel insights to assist the development of methods to prevent tumor progression and identify potential targets for the treatment of CAC.</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/PMC11751662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142951896","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":"Insights into renal damage in hyperuricemia: Focus on renal protection (Review).","authors":"Hang Yang, Jie Ying, Tong Zu, Xiao-Ming Meng, Juan Jin","doi":"10.3892/mmr.2024.13424","DOIUrl":"10.3892/mmr.2024.13424","url":null,"abstract":"<p><p>The incidence of hyperuricemia has increased recently, posing a serious threat to public health. Hyperuricemia is associated with an increased risk of gout, chronic kidney disease (CKD), obesity, metabolic syndrome, type 2 diabetes mellitus, hypertension, hypertriglyceridaemia, metabolic dysfunction‑associated steatotic liver disease, acute kidney injury, coronary heart disease and cardiovascular disease (CVD). These diseases are commonly accompanied by varying degrees of kidney damage. A number of randomized controlled clinical trials have investigated the effectiveness of UA‑lowering therapies in preventing kidney disease progression. The present review provided fundamental insights into the pathogenesis, principles and therapeutic approaches for managing hyperuricemia in patients with aforementioned diseases and assesses the effect of uric acid‑lowering therapy on diabetic nephropathy, systemic lupus erythematosus, CKD, CVD and obesity progression.</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/PMC11711934/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882559","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}