Molecular medicine reports最新文献

{"title":"Biological mechanisms of atropine in myopia control (Review).","authors":"Qin Zhu, Guanglong Zhou, Lingguo Wang, Xuejiao Li, Zhijuan Hua, Jie Yin, Jieying Zhang, Yuan Zhou, Xiaofan Zhang, Allison Wilde, Yingting Zhu, Liping Xue","doi":"10.3892/mmr.2026.13993","DOIUrl":"10.3892/mmr.2026.13993","url":null,"abstract":"<p><p>Myopia is now recognized as a progressive, potentially sight‑threatening disease rather than just a refractive error, with its prevalence rising rapidly worldwide due to its high occurrence, major vision losses and huge public health cost. The World Health Organization estimates that 2.6 billion individuals in the world were myopic in 2020 this figure is projected to increase to 3.364 billion by 2030. Although myopia may be better controlled in its early stages, it may not be completely reversed at this time. Of all of the methods for controlling myopia, atropine, a muscarinic receptor antagonist, remains an effective pharmacological option for slowing myopia progression in children. However, the mechanisms of action of atropine remain to be fully elucidated. This review provided a systematic review for myopia epidemiology, pathogenesis, the effects and side effects, as well as up‑to‑date possible mechanisms, in the hope of facilitating that researchers in this field elucidate its underlying mechanisms so that clinical ophthalmologists may be able to better control this disease.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13504464/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795558","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":"Deubiquitinating enzymes in kidney diseases: Molecular mechanisms, pathological roles and therapeutic opportunities (Review).","authors":"Qianqian Li, Yufang Ni, Zhaoyang Li, Jianchun Li, Li Wang","doi":"10.3892/mmr.2026.13994","DOIUrl":"10.3892/mmr.2026.13994","url":null,"abstract":"<p><p>The ubiquitin‑proteasome system maintains cellular protein turnover and quality control through the coordinated action of ubiquitin ligases and deubiquitinating enzymes (DUBs). While the functions of E3 ubiquitin ligases have been extensively investigated in renal disease, the ~100 human DUBs distributed across seven structurally distinct families have recently emerged as important regulators of renal physiology and pathology. The present review organizes current knowledge of DUB‑mediated regulation in kidney disease around functional themes rather than individual disease categories. The present review discusses how DUBs regulate inflammatory signaling, TGF‑β‑mediated fibrotic responses, epithelial‑to‑mesenchymal transition (EMT), mitochondrial homeostasis, multiple forms of programmed cell death, podocyte homeostasis, and oncogenic pathways in renal cell carcinoma. Several DUBs, including A20 (TNFAIP3), CYLD, USP25 and OTUD5, restrain inflammation and fibrosis, whereas USP11, OTUD1, and USP22 promote disease progression through substrate stabilization. The translational landscape of DUB inhibitors, PROTAC degraders, and the DUBTAC platform for targeted protein stabilization, along with the selectivity and delivery challenges that remain, were discussed. Key unanswered questions, including cell‑type‑specific DUB functions, ubiquitin chain linkage context, and the therapeutic window for DUB modulation in the kidney, are outlined as priorities for future investigation.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13504441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795589","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":"Ginsenosides alleviate the progression of hepatic fibrosis by targeting the liver circadian clock gene <i>CLOCK</i>.","authors":"Jiawen Yu, Chunmei Qian, Renye Que, Yi Zhou","doi":"10.3892/mmr.2026.13973","DOIUrl":"10.3892/mmr.2026.13973","url":null,"abstract":"<p><p>Hepatic fibrosis (HF) serves as a critical pathological process underlying the progression of cirrhosis and hepatocellular carcinoma. Despite its clinical relevance, effective anti‑fibrotic therapies remain scarce. Although total ginsenosides (GSS) can ameliorate hepatic oxidative damage and attenuate the development of HF, the molecular mechanism mediating their anti‑fibrotic effects remains incompletely elucidated. Notably, circadian clock gene dysregulation is associated with hepatic metabolic dyshomeostasis and the fibrotic process. As a core circadian gene in the liver, clock circadian regulator (CLOCK) serves a role in the progression of fibrosis. The present study hypothesized that GSS may exert anti‑fibrotic effects by restoring hepatic circadian rhythmicity through circadian clock‑dependent pathways. Using a well‑established carbon tetrachloride‑induced murine model of HF in C57BL/6 mice, GSS was administered intraperitoneally at graded doses of 50, 100 and 200 mg/kg. Subsequently, serum and liver tissues were collected from mice for histopathological examination. Furthermore, the expression levels of fibrotic markers (α‑smooth muscle actin and collagen type 1) and circadian rhythm genes [CLOCK, basic helix‑loop‑helix ARNT‑like 1, cryptochrome (CRY)1, CRY2, period circadian protein homolog (PER)1 and PER2 were assessed. At the cellular level, LX‑2 hepatic stellate cells (HSCs) were activated with TGF‑β1 and treated with GSS, after which, RNA sequencing was performed on GSS‑treated cells. In addition, the CLOCK inhibitor (CLK8) was used for <i>in vitro</i> experiments. The results of the present study revealed that GSS intervention effectively reversed the dysregulation of circadian gene expression and alleviated the progression of fibrosis. Molecular docking analysis further supported the interaction between GSS active components and the CLOCK protein. Thus, the current study focused on GSS and explored its role in ameliorating HF through regulation of the core circadian gene CLOCK. Collectively, the findings demonstrated that GSS may alleviate HF by rescuing circadian clock‑driven circadian homeostasis in hepatocytes and HSCs, thereby providing mechanistic insight into traditional Chinese medicine‑based interventions and identifying CLOCK as a druggable node for fibrosis therapy.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13454752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148630810","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":"Uric acid enhances tumor stemness in breast cancer cells by upregulating GMPS.","authors":"Zhiying Wang, Mingzhang Huang, Yuanqi Zhang, Siqi Huang, Wei Lei, Xiaorong Shui","doi":"10.3892/mmr.2026.13990","DOIUrl":"10.3892/mmr.2026.13990","url":null,"abstract":"<p><p>Metabolic reprogramming is closely associated with the development and progression of cancer and is considered an emerging hallmark of cancer. To meet the bioenergetic and biosynthetic demands, tumor cells tend to initiate the metabolic reprogramming process, creating a tumor microenvironment that is adaptable for cancer cell growth and further promote oncogenic signaling, cell proliferation and metastasis. As a final byproduct of purine metabolism, the uric acid (UA) concentration rises in the quickly growing tumor microenvironment. However, whether elevated UA affects the development and prognosis of patients with tumors has not been demonstrated. In the present study, Cell Counting Kit‑8 and scratch healing test were used to investigate the effects of UA on the proliferation and migration of breast cancer cells. The effects of UA on nucleotide <i>de novo </i>synthesis genes in breast cells were validated using quantitative PCR (qPCR) and western blotting (WB). The activation of stemness in breast cancer cells by UA was validated using colony formation assays, ELISA, qPCR and WB. Finally, clinical data and The Cancer Genome Atlas database were analyzed to examine the expression of <i>de novo</i> nucleotide synthesis genes in cancerous and adjacent tissues, as well as in different types of breast cancer tissues. The present study investigated the potential effect of UA on the function of breast cancer; it also determined how UA affected the genes involved in nucleotide <i>de novo</i> synthesis, as well as how it contributes to tumor stemness. It was discovered that UA could enhance tumor stemness in breast cancer cells through the upregulation of guanosine 5'‑monophosphate synthase (GMPS). It was notable that GMPS expression in patients with breast cancer may be strongly associated with the course of the disease and the prognosis of patients. In conclusion, the present study demonstrated that elevated UA upregulates GMPS and stimulates the migration and proliferation of breast cancer cells through the cyclic guanosine monophosphate/protein kinase G/mitogen‑activated protein kinase pathway axis.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13501391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148765283","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":"[Corrigendum] CLEC4M overexpression inhibits progression and is associated with a favorable prognosis in hepatocellular carcinoma.","authors":"Qianle Yu, Kai Gao","doi":"10.3892/mmr.2026.14003","DOIUrl":"10.3892/mmr.2026.14003","url":null,"abstract":"<p><p>Following the publication of the above article, the authors have contacted the Editorial Office to explain that certain of the western blots featured in Figs. 3A and B, and 6A and B, on p. 2248 and 2250 respectively were chosen incorrectly. Specifically, the data chosen for the CLEC4M blots in Fig. 3A and B, and the p‑JAK1 blots in Fig. 6A and the STAT3 blots in Fig. 6B, were presented incorrectly in these figures. However, the authors retained their original data, and have submitted corrected versions of Figs. 3 and 6, now showing the correct data for the CLEC4M blots in Fig. 3A and B, and the p‑JAK1 blots in Fig. 6A and the STAT3 blots in Fig. 6B. These figures are featured on the next page. Note that the errors made in compiling these figures did not affect the results or the main conclusions reported in the study. All the authors approve of the publication of this corrigendum, and are grateful to the Editor of <i>Molecular Medicine Reports</i> for allowing them the opportunity to publish this. The authors regret their oversight in allowing these errors to be included in the paper, and apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 22: 2245‑2252, 2020; DOI: 10.3892/mmr.2020.11336].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13573278/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891770","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":"Licoisoflavone A ameliorates adipose tissue dysfunction in diet‑induced obesity by promoting METTL3 expression.","authors":"Shuangxi Tu, Xiaodan Wang, Zhenbo Wang, Haojun Tang, Kai Yin, Xiao Zhu","doi":"10.3892/mmr.2026.14007","DOIUrl":"10.3892/mmr.2026.14007","url":null,"abstract":"<p><p>With the development of obese adipose tissue (AT), adipocytes undergo pathological changes from inert energy storage to excessive and active endocrine organs associated with disease hazards. Methyltransferase 3 (METTL3) is an RNA methyltransferase with key roles in AT development, functional maintenance and metabolic homeostasis. Licoisoflavone A (LIC‑A) is a prenylated flavonoid compound derived from licorice, which has anti‑inflammatory, antihypertrophic and antiproliferative activities; however, whether it directly modulates METTL3 expression and affects AT function in obesity remains unknown. In the present study, molecular docking of compounds from the traditional Chinese medicine formula Fangji‑Huangqi Decoction against METTL3, identified 16 top‑ranked candidate molecules. Among these candidates, LIC‑A was identified as a potential upstream regulator of METTL3 and markedly increased METTL3 expression. The effects of TNF‑α and lipopolysaccharide treatments on the inhibition of adipogenesis were successfully recovered by LIC‑A treatment of the adipogenic 3T3‑L1 cells, via the regulation of adipogenic cytokines, as well as the expression of inflammatory factors. These protective effects were similarly abolished by METTL3 knockdown, suggesting that the role of LIC‑A relies on METTL3. Moreover, <i>in vivo</i> data demonstrated that the administration of LIC‑A could notably recover body weight lipid metabolism, insulin resistance and gluconeogenesis in mice with reduced adipose deposition, as well as abate systemic inflammation. The novelty of the present study lies in three aspects: i) LIC‑A was identified as a previously unrecognized upstream positive regulator of METTL3 expression; ii) LIC‑A was demonstrated to alleviate adipokine dysregulation and AT inflammation through a METTL3‑dependent mechanism; and iii) the first <i>in vivo</i> experimental evidence that LIC‑A can improve obesity‑related metabolic disorders by promoting METTL3‑mediated m6A methylation in AT was provided. To the best of our knowledge, this is the first study to link a natural isoflavone compound from licorice to METTL3‑mediated post‑transcriptional regulation in the context of AT dysfunction.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13573282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891759","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] Aberrant expression of miR‑130a‑3p in ankylosing spondylitis and its role in regulating T‑cell survival.","authors":"Fengju Li, Dingran Si, Xuejun Guo, Ningru Guo, Dandan Li, Liujing Zhang, Xianan Jian, Jiasheng Ma","doi":"10.3892/mmr.2026.13991","DOIUrl":"10.3892/mmr.2026.13991","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the expression of BAX protein in Jurkat T cells, as shown in the western blots in Fig. 6A on p. 3392, was unexpected, since Jurkat cells have been reported to be BAX‑null [see the paper \"A genome‑wide survey of mutations in the Jurkat cell line\" by Gioia <i>et al</i>, Vol. 19, article no. 334 (2018)]. Furthermore, upon performing an independent analysis of the data in this paper, it came to light that the control β‑actin western blots featured in Fig. 4A and flow cytometric data included in Fig. 5B were strikingly similar to data that had already been submitted for publication to other journals in other articles written by different authors at different research institutes, one of which has since been retracted. Owing to the fact that the contentious data in the above article had already been submitted for publication prior to its submission 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 20: 3388‑3394, 2019; DOI: 10.3892/mmr.2019.10573].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13501390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795542","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 study of Sirt1 regulation and the effect of resveratrol on synoviocyte invasion and associated joint destruction in rheumatoid arthritis.","authors":"Liang Hao, Yuying Wan, Uhua Xiao, Qiang Tang, Huan Deng, Lu Chen","doi":"10.3892/mmr.2026.13986","DOIUrl":"10.3892/mmr.2026.13986","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that western blot data featured in Fig. 5 on p. 5103 were remarkably similar to data that had already been submitted to the same journal, <i>Molecular Medicine Reports</i>, in a paper that was written by different authors at different research insititutes, but which has subsequently been retracted. Similarly, western blot data featured in Fig. 2 on p. 5102 were strikingly similar to data that were featured in another paper written by different authors at different research institutes which was submitted to the journal <i>Biomed Research International</i> a few months afterwards. Owing to the fact that the contentious data in the above article had already been submitted for publication prior to its submission 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 16: 5099‑5106, 2017; DOI: 10.3892/mmr.2017.7299].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13488517/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148758407","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":"[Corrigendum] Identification of key differentially expressed genes associated with non‑small cell lung cancer by bioinformatics analyses.","authors":"Yubo Xiao, Min Feng, Haiying Ran, Xiao Han, Xuegang Li","doi":"10.3892/mmr.2026.13976","DOIUrl":"10.3892/mmr.2026.13976","url":null,"abstract":"<p><p>Subsequently to the publication of the above paper, an interested reader drew to the Editor's attention that the authors may have misstated the datasets used in their study at the start of the Results section. Specifically, at the beginning of the Materials and methods section (in the \"<i>Affymetrix microarray data</i>\" subsection), it is stated that \"Series matrix files of the <b>microarray data</b>: GSE21933, GSE33532, GSE44077 and GSE74706 were downloaded from the public GEO database\", whereas in the first sentence of the Results section, in the \"<i>Identification of DEGs</i>\" subsection, it is stated \"In order to identify the DEGs, we downloaded 4 public <b>RNA‑seq datasets</b> of NSCLC from the GEO database for our analysis: GSE21933, GSE33532, GSE44077 and GSE74706.\" After having considered this comment by the external reader, the Editor of <i>Molecular Medicine Reports</i> has judged that the four datasets in question should have also been described as microarray datasets in the Results section of this paper. Although we have been unable to reach the authors in this regard, we are continuing to ask them to confirm that the text in the Results section was indeed written incorrectly. We apologize to the readership of the Journal for any confusion in this matter. [Molecular Medicine Reports 17: 6379‑6386, 2018; DOI: 10.3892/mmr.2018.8726].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13454908/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148630809","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":"STC1 promotes osteogenic differentiation and represses inflammation via inhibition of NF‑κB signaling in mesenchymal stromal cells.","authors":"Chen Yang, Xin Li, Peng Wang, Yitong Chen, Erli Wu, Qian Chen, Jing Hu, Fu Zheng, Lamu Gongsang, Jiayu Li, Mengyuan Zhang, Jing Zhou, Bing Han, Amr A Badreldin, Yuka Miyamoto, Jin Koo Kim, Insoon Chang, Jia Chang, Paul H Krebsbach, Liyuan Huang, Xiaoping Xu, Xiaoyan Chen, Peng Deng, Qianming Chen, Lijie Fan","doi":"10.3892/mmr.2026.13983","DOIUrl":"10.3892/mmr.2026.13983","url":null,"abstract":"<p><p>The aging of mesenchymal stromal cells (MSCs) is characterized by impaired osteogenic differentiation and enhanced adipogenic differentiation. Studies have identified stanniocalcin‑1 (STC1) as a core component of the senescence‑associated secretory phenotype and a regulator of osteoblast maturation; however, its role in MSC biology remains poorly understood. In the present study, bone marrow‑derived MSCs were used and <i>in vitro</i> functional assays together with molecular and omics‑based analyses were performed to investigate the role of STC1. It was observed that STC1 expression was upregulated in aged MSCs and during both osteogenic and adipogenic differentiation. Small interfering RNA‑mediated depletion of STC1 reduced cellular senescence and notably impaired osteogenic differentiation, whereas adipogenic and chondrogenic differentiation were not significantly affected. RNA sequencing revealed that <i>STC1</i> knockdown led to the downregulation of osteogenesis‑related genes and the concomitant upregulation of inflammatory factors. Genes associated with closing differentially accessible regions (DARs) were enriched in osteogenic pathways, whereas those associated with opening DARs were predominantly involved in inflammatory responses. Mechanistically, <i>STC1</i> knockdown led to the activation of NF‑κB signaling. Pharmacological inhibition assays using NF‑κB inhibitors were performed to validate pathway involvement. Pharmacological inhibition of NF‑κB signaling significantly mitigated the impairment in osteogenic differentiation and attenuated the inflammatory response induced by STC1 depletion. Collectively, these findings suggest that STC1 is involved in the regulation of osteogenic differentiation and inflammatory signaling through the modulation of NF‑κB activity in MSCs. Furthermore, targeting STC1 while inhibiting NF‑κB signaling may represent a promising therapeutic strategy for alleviating MSC dysfunction and age‑related bone loss.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13469798/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685155","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}