Current molecular medicine最新文献

{"title":"Dynamic Changes of Extracellular Matrix in Sepsis: A Review.","authors":"Mingjie Fu, Wenwei Xu, Jie Zhao, Shi Fu, Shuiqiao Fu, Liang Ma","doi":"10.2174/0115665240407854251202120058","DOIUrl":"https://doi.org/10.2174/0115665240407854251202120058","url":null,"abstract":"<p><p>During the pathogenesis of sepsis, extracellular matrix (ECM) impairment represents a critical pathological hallmark. The ECM not only plays pivotal roles in maintaining tissue architecture and physiological functions, but also actively participates in cellular signaling transduction and tissue repair mechanisms. Sepsisinduced systemic inflammatory responses and oxidative stress provoke ECM component degradation and structural remodeling, which, in turn, activate multiple intracellular and intercellular signaling cascades. Bioactive fragments derived from ECM degradation can function as signaling ligands that bind to specific cell surface receptors, triggering downstream pathways that regulate critical cellular processes, including survival, proliferation, migration, and inflammatory activation. The sustained activation of these signaling networks exerts profound pathophysiological consequences, potentially leading to vascular endothelial dysfunction, dysregulated immune cell hyperactivation, and coagulation system abnormalities. Furthermore, these signaling pathways mediate essential regulatory functions during the tissue remodeling phase in late-stage sepsis. While this dynamic ECM remodeling may facilitate tissue repair and regeneration, persistent dysregulation could result in maladaptive fibrosis and permanent organ dysfunction. Collectively, the ECM demonstrates multifaceted involvement in sepsis pathophysiology through its regulatory effects on cellular signaling, functional modulation, and tissue remodeling processes. This article systematically synthesizes current knowledge regarding ECM dynamics in sepsis pathogenesis.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147303480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional Roles of Non-Coding RNAs in Graves' Disease.","authors":"Omid Anbiyaee, Abdolah Mousavi Salehi, Bahar Jaberian Asl, Fatemeh Jamshidi, Farhoodeh Ghaedrahmati, Maryam Farzaneh","doi":"10.2174/0115665240380518251113092158","DOIUrl":"https://doi.org/10.2174/0115665240380518251113092158","url":null,"abstract":"<p><p>Graves' disease (GD) is a disorder marked by an enlarged and overactive thyroid gland (Graves' hyperthyroidism), ocular abnormalities (Graves' orbitopathy; GO), and localized dermopathy (pretibial myxoedema; PTM). It is recognized as the most common cause of hyperthyroidism worldwide. Patients with GD most frequently exhibit elevated thyroid hormone secretion from thyroid cells as a result of autoantibodies acting as thyroid-stimulating hormone receptor (TSHR) agonists. Numerous investigations have examined the elements that contribute to the pathogenesis of GD, focusing on different components, such as molecular factors like non-coding RNAs (ncRNAs). NcRNAs represent a type of RNA transcript that, while not encoding proteins, are essential in the regulation of numerous aspects of cellular biology. NcRNAs include major groups, such as circular RNAs (circRNAs), long noncoding RNAs (lncRNAs), and small non-coding RNAs (sncRNAs), all of which are garnering increasing interest in the scientific community. This review will provide a comprehensive analysis of the function of ncRNAs in the development, diagnosis, and treatment of GD, and investigate the latest research in this area.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146225727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alterations in the Expression of Toll-Like Receptors (TLRs) 3, 4, and 7 in Patients with COVID-19: The Role of Disease Severity and Gender.","authors":"Zohreh-Al-Sadat Ghoreshi, Mohsen Sharif-Zak, Gholamreza Asadikaram, Mojtaba Abbasi-Jorjandi, Alireza Afsharipur, Fatemeh Seyedi, Hamidreza Reshidinejad, Mohammad Kazemiarababadi, Fardin Khajepour, Nasir Arefinia, Moslem Abolhassani","doi":"10.2174/0115665240394369251208174759","DOIUrl":"https://doi.org/10.2174/0115665240394369251208174759","url":null,"abstract":"<p><p><P> Introduction: The expression dynamics of Toll-like receptors (TLRs) in response to SARS-CoV-2, particularly regarding disease severity, remain poorly understood. This study aimed to investigate the gene expression of TLR3, TLR4, and TLR7 in COVID-19 patients and correlate them with disease severity and gender. </P> <P> Methods: This case-control study enrolled 470 COVID-19 patients (categorized as moderate, severe, and critical) and 100 healthy controls. The mRNA expression levels of these genes in peripheral blood leukocytes were quantified using RT-qPCR. </P> <P> Results: Expression of all three TLRs was significantly higher in patients than in the control group. Overall, male patients exhibited higher expression than females. Notably, a significant decrease in TLR3, TLR4, and TLR7 expression was observed in the critical group compared with the moderate and severe groups. </P> <P> Discussion: This paradoxical downregulation of TLRs in critical patients, reported for the first time in such a large cohort (N=470), aligns with reports of 'immunoparalysis' or 'immune exhaustion' observed in other severe inflammatory conditions. This phenomenon might represent a negative feedback mechanism to prevent overwhelming systemic inflammation, although it may concurrently compromise pathogen clearance. </P> <P> Conclusion: The findings suggest that while TLR expression is upregulated in COVID-19, its downregulation in critical stages may be associated with an unfavorable disease outcome. Therefore, TLR expression levels could be considered potential biomarkers for identifying patients at risk of progressing to the critical phase of the disease.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA HULC/miR-556-5p Axis Attenuates Ang II-Induced Cardiac Microvascular Endothelial Cell Dysfunction by Suppressing the AMPK/FOXO3 Pathway.","authors":"Yafeng Hao, Mingming Fu, Zhiqian Wang","doi":"10.2174/0115665240395360251112160900","DOIUrl":"https://doi.org/10.2174/0115665240395360251112160900","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to investigate the regulatory mechanism of the LncRNA HULC/miR-556-5p axis in endothelial cell injury associated with heart failure and its impact on endothelial cell function. Specifically, we explored how HULC interacts with miR-556-5p to modulate cell survival, apoptosis, inflammation, and autophagy in response to Ang II-induced injury.</p><p><strong>Methods: </strong>Human cardiac microvascular endothelial cells (HCMECs) were utilized as the study model. Ang II-induced HCMEC injury was simulated by treating cells with 100 nM Ang II for 24 hours. The expression levels of HULC, miR-556-5p, and related proteins were assessed using techniques, such as real-time quantitative PCR and Western blot. Cell apoptosis was detected using flow cytometry, and inflammatory cytokine release (TNF-α, IL-1β, and IL-6) was analyzed via ELISA. Cell viability was assessed using MTT assays. Immunoblotting was employed to evaluate the phosphorylation status of key signaling molecules, including AMPK and FOXO3.</p><p><strong>Results: </strong>We observed a crucial role of the LncRNA HULC/miR-556-5p axis in Ang IIinduced HCMEC injury. Overexpression of HULC significantly suppressed miR-556-5p activity, thereby reducing cell apoptosis and the release of inflammatory cytokines while promoting cell survival. Further experimental results indicated that miR-556-5p regulated cell function by reducing the expression level of FOXO3 and modulating the AMPK signaling pathway. Additionally, miR-556-5p markedly decreased cellular autophagy levels, further supporting its regulatory role in endothelial cell injury associated with heart failure.</p><p><strong>Conclusion: </strong>This study elucidates the important role of the LncRNA HULC/miR-556- 5p axis in endothelial cell injury associated with heart failure. Our findings provide new insights into the pathophysiological mechanisms of heart failure and highlight the potential therapeutic value of targeting this axis to improve endothelial cell function.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146060766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phosphatidylethanolamine: Structural Component and Beyond.","authors":"Swaroop Kumar Pandey, Ayush Kulshreshtha, Anuja Mishra","doi":"10.2174/0115665240415642251205104453","DOIUrl":"https://doi.org/10.2174/0115665240415642251205104453","url":null,"abstract":"<p><p>Phosphatidylethanolamine (PE) is a major phospholipid in biological membranes and plays essential roles in autophagy, cell signaling, protein function, and membrane integrity. Its dynamic, conical structure supports membrane fluidity and curvature, which are crucial for processes such as signaling, autophagosome formation, membrane fusion, vesicle trafficking, and proper protein folding. Although PE is abundant, its significance for human health and disease has only recently come to light. Altered PE levels or disruptions in its metabolism have been associated with various conditions, including metabolic disorders such as non-alcoholic fatty liver disease (NAFLD), neurodegenerative diseases like Alzheimer's and Parkinson's, and several cancers. PE is synthesized primarily via two pathways: the CDP-ethanolamine (Kennedy) pathway and the mitochondrial phosphatidylserine decarboxylase (PSD) pathway, both of which are critical for maintaining lipid homeostasis. Advances in lipidomics now allow comprehensive profiling of PE species, facilitating the identification of disease-specific lipid biomarkers. This review expands current knowledge on the physiological roles of PE and elucidates mechanisms underlying PErelated lipid dysregulation in human disease.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146028577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell Sequencing Reveals Key Biological Insights into Intervertebral Disc Development and Degeneration.","authors":"Chaorong Yu, Wei Yang, Yanyan Wang, Yujie Zhang","doi":"10.2174/0115665240418547251215053012","DOIUrl":"https://doi.org/10.2174/0115665240418547251215053012","url":null,"abstract":"<p><p>Intervertebral disc degeneration (IDD) is a common spinal disease that imposes a significant economic burden on healthcare systems. Understanding the biological processes involved in IDD development and degeneration is critical for developing potential therapeutic approaches. Single-cell RNA sequencing (scRNAseq) technology has revolutionized our understanding of cellular heterogeneity at the single-cell level and provided profound insights into the transcriptional landscape of IDD. This review provides an overview of research progress on the cellular biological characteristics of IDD occurrence and degeneration using scRNA-seq. It systematically summarizes the applications and key findings of scRNA-seq in subtyping cell populations, detecting transcriptomic changes, regulating signaling pathways, and elucidating cell-cell interactions in IDD. Additionally, it emphasizes the potential role of scRNA-seq in maintaining and repairing intervertebral disc tissues, from both preventive and therapeutic perspectives. In summary, this study underscores the extensive application of scRNA-seq in degenerative disc research and provides a foundation for future investigations and potential treatment strategies.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146028564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neonatal Anaesthesia and Neuronal Injury: Molecular Mechanisms and Insights.","authors":"Ryo-En Tan, Anna Xin Yi Ko, Khai Ee Tan, Zi Ni Ngai, Soi Moi Chye, Anna Pick Kiong Ling, Shamala Salvamani, Rhun Yian Koh","doi":"10.2174/0115665240416611251208191736","DOIUrl":"https://doi.org/10.2174/0115665240416611251208191736","url":null,"abstract":"<p><p>Despite widespread use of general anaesthesia (GA) in neonatal procedures, its effects on the developing brain are still not fully understood, raising ongoing questions in both research and clinical practice. Experimental studies have demonstrated that GA can cause neuronal cell injury, and neonates may be vulnerable due to their physiological immaturity, necessitating exact dosing and constant monitoring. To optimise anaesthesia protocols and minimise risks in this vulnerable population, it is imperative to thoroughly evaluate the mechanisms underlying anaesthesia-induced neuronal cell damage in neonates. This review article will explore the following mechanisms: apoptosis, pyroptosis, gamma-aminobutyric acid (GABA) and N-methyl-D-aspartate (NMDA), oxidative stress and mitochondrial damage, calcium imbalance, neural circuit impairment, and neuroinflammation, with particular focus on studies utilising animal models. It will also highlight recent studies on therapeutic strategies against reducing neuronal cell damage. However, as most of these findings remain preclinical, their translational potential requires cautious interpretation. In conclusion, although current evidence highlights plausible mechanisms and emerging neuroprotective approaches, more clinical trials are needed to ensure the reliability and efficacy of the treatment strategies to confirm their effects on neonatal anaesthesia-induced cell damage.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146028513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nanolayered Topsheet Integration for Enhanced Antimicrobial Properties in Sanitary Napkins.","authors":"Harini A, Seethalakshmi K, Balasubramanian Deepika, Anbazhagan Thirumalai, Sharon Sofini P S, Ilaiyaraja Perumal, Agnishwar Girigoswami, Koyeli Girigoswami","doi":"10.2174/0115665240420228251206201238","DOIUrl":"https://doi.org/10.2174/0115665240420228251206201238","url":null,"abstract":"<p><strong>Introduction: </strong>Menstrual hygiene practices are a critical health concern, and if neglected, they may lead to reproductive tract infections (RTIs), toxic shock syndrome, and other vaginal diseases. To prevent these conditions, antiseptic and antibacterial properties must be incorporated into sanitary napkins.</p><p><strong>Methods: </strong>In this study, nanolayered topsheets were synthesized by embedding silver nanoparticles (AgNPs) into PVA in Aloe vera extract, which was then coated onto a non-woven fabric. The polymer-entrapped AgNPs in Aloe vera (AgNPs + PVA + Aloe vera) were characterized using UV-visible spectrometry, dynamic light scattering (DLS), zeta potential, FTIR, and SEM analyses.</p><p><strong>Results: </strong>The release kinetics of AgNPs from the coated fabric were studied in simulated vaginal fluid (SVF), showing an initial burst release followed by sustained release. The toxicity of the released nanosilver was evaluated both in vitro using A375 cells and in vivo using zebrafish embryos, establishing a safe dose of 3 μM. The antimicrobial effect of the coated fabric was tested against S. aureus and E. coli, showing clear zones of inhibition.</p><p><strong>Discussion: </strong>The AgNPs and the coated fabric demonstrated comparable antimicrobial activity.</p><p><strong>Conclusion: </strong>This product has potential for use in coating sanitary napkins to provide skin-soothing and antimicrobial effects.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146028723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Toll/Interleukin-1 Receptor Domain Protein C on Mesenchymal Stem Cells Mitochondrial Protein Expression: A Proteomic Study.","authors":"Yameng Wang, Jiaqi Fang, Dongyang Guo, Liang Xia","doi":"10.2174/0115665240411988251128121911","DOIUrl":"https://doi.org/10.2174/0115665240411988251128121911","url":null,"abstract":"<p><strong>Introduction: </strong>Stem cells play a pivotal role in immunomodulation and tissue repair, and their functions can be influenced by TLR signaling. The Toll/interleukin-1 receptor domain-containing protein C (TcpC), secreted by Uropathogenic Escherichia coli, can inhibit host immunity by interfering with TLR pathways. As mitochondria are crucial for stem cell function, there may be links between TcpC and mitochondrial homeostasis.</p><p><strong>Methods: </strong>We isolated MSC mitochondria using magnetic beads coated with a monoclonal antibody against the outer mitochondrial membrane protein OMP25 and conducted a proteomic study to examine the MSC mitochondrial proteome with or without TcpC. Bioinformatics analyses, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, and proteinprotein interaction (PPI) network analysis, were employed.</p><p><strong>Results: </strong>A total of 33 proteins with significant changes in abundance were identified: 4 increased in abundance, including glycolytic enzymes (Pkm [FC=1.6599, p=0.0217]) and stress response proteins (Ywhaq [FC=1.4666, p=0.04502]); and 29 decreased, mainly related to mitochondrial oxidative phosphorylation (e.g., Atp5f1e [FC=0.001, p=0.00120], Ndufa11 [FC=0.001, p=0.00674]) and protein quality control (e.g., Grpel1 [FC=0.46663, p=0.02083], Hspa9 [FC=0.48089, p=0.0435], Pitrm1 [FC=0.12764, p=0.01388]).</p><p><strong>Discussion: </strong>The possible effects of TcpC on the MSC mitochondrial proteome are reported here for the first time. This information provides a clearer understanding of MSCs in the context of infectious disease and offers a scientific basis for future stem cell therapy research.</p><p><strong>Conclusion: </strong>TCP-C intervention leads to a series of differentially expressed proteins in MSC mitochondria, which are involved in several functional clusters, including oxidative phosphorylation, respiratory electron transport, the tricarboxylic acid cycle, glyoxylate and dicarboxylate metabolism, branched-chain amino acid catabolism, and cristae formation.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146028749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SLC39A8 Inhibits Ferroptosis by Regulating the Β-Catenin/TCF4/ GPX4 Signaling in Osteosarcoma.","authors":"Siliang Tang, Guojun Tang, Liangyuan Chen, Mingjiang Luo, Jingshan Huang, Zihan Zhang, Shuo Wen, Zhihong Xiao","doi":"10.2174/0115665240400149251029112234","DOIUrl":"10.2174/0115665240400149251029112234","url":null,"abstract":"<p><strong>Introduction: </strong>SLC39A8 has been implicated in various cancers; however, its specific role in osteosarcoma (OS) remains poorly understood. This study aims to elucidate the functional significance of SLC39A8 in OS progression.</p><p><strong>Methods: </strong>Using qRT-PCR and Western blot analysis, we analyzed SLC39A8 expression in osteosarcoma cells. Functional assays, including CCK-8, colony formation, and transwell assays, were employed to assess the impact of SLC39A8 on cell proliferation, migration, and invasion. Ferroptosis was evaluated by measuring lipid peroxidation, labile iron pool (LIP), Fe²⁷, malondialdehyde (MDA), reactive oxygen species (ROS), glutathione (GSH), and GPX4 expression.</p><p><strong>Results: </strong>Our results revealed that SLC39A8 is upregulated in osteosarcoma cells. The knockdown of SLC39A8 significantly suppressed cell proliferation, migration, and invasion while inducing ferroptosis, as evidenced by increased levels of LIP, Fe²⁷, MDA, and ROS, and decreased GSH and GPX4 expression. These effects were reversed by the ferroptosis inhibitor ferrostatin-1 (Fer-1). Furthermore, SLC39A8 overexpression activated the Wnt/β-catenin signaling pathway and upregulated GPX4 expression, effects that were abrogated by silencing β-catenin or TCF4. In vivo experiments confirmed that SLC39A8 knockdown inhibited tumor growth.</p><p><strong>Discussion: </strong>SLC39A8 is a key zinc and iron transporter. Studies have reported that SLC39A8 was significantly dysregulated in some cancers and was associated with their prognosis. SLC39A8 has been identified as an iron metabolism- and ferroptosisrelated gene related to the prognosis of esophageal squamous cell carcinoma. Our study showed that SLC39A8 promotes osteosarcoma cell proliferation, migration, and invasion while suppressing ferroptosis by regulating β-catenin signaling. Our study further indicated that LF3 reversed SLC39A8-mediated ferroptosis in osteosarcoma cells by reducing GPX4 expression. Although our study shows that SLC39A8 regulates the β-catenin signaling pathway, the upstream regulatory mechanism remains to be investigated.</p><p><strong>Conclusion: </strong>Our findings demonstrate that SLC39A8 plays a pivotal role in osteosarcoma progression by modulating ferroptosis via the β-catenin/TCF4/GPX4 signaling pathways.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146017381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}