Journal of Cellular and Molecular Medicine最新文献

Molecular Dynamics Reveals a Glycan Conformation Underlying IDUA Dysfunction in Attenuated MPS I. 分子动力学揭示减弱型MPS I中IDUA功能障碍的糖聚糖构象。

IF 4.2 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2026-10-01 DOI: 10.1111/jcmm.71396

Maria Giovanna Eva Papadopoulos, Giuseppe Bonapace, Lorenzo Taglietti, Barbara La Ferla, Rosanna Rizzi, Michele Pitaro, Daniela Concolino, Domenico Alberga, Giuseppe Felice Mangiatordi

{"title":"Molecular Dynamics Reveals a Glycan Conformation Underlying IDUA Dysfunction in Attenuated MPS I.","authors":"Maria Giovanna Eva Papadopoulos, Giuseppe Bonapace, Lorenzo Taglietti, Barbara La Ferla, Rosanna Rizzi, Michele Pitaro, Daniela Concolino, Domenico Alberga, Giuseppe Felice Mangiatordi","doi":"10.1111/jcmm.71396","DOIUrl":"10.1111/jcmm.71396","url":null,"abstract":"Mucopolysaccharidosis Type I (MPS I) is a rare autosomal recessive lysosomal storage disorder caused by mutations in α-ʟ-iduronidase (IDUA) enzyme, a glycosylated hydrolase responsible for glycosaminoglycan (GAG) degradation. Pathogenic variants are associated with a broad clinical spectrum, from severe Hurler syndrome to attenuated Scheie phenotype. The missense mutations L490P and P533R cause attenuated-intermediate MPS I, retaining residual enzyme activity. To investigate the structural mechanisms underlying these phenotypes, we performed all-atom molecular dynamics simulations -18 trajectories of 1.6 μs each- comparing wild type IDUA with L490P and P533R mutants at pH 7.5 and 4.5, mimicking the endoplasmic reticulum (ER) and lysosomal microenvironments, respectively. Backbone root-mean-square deviation and fluctuation analyses indicated that the overall protein fold was maintained across conditions; however, we identified a pH-dependent restricted conformational flexibility of the N372-linked glycan in both mutants. Cluster analysis performed on the obtained trajectories showed that both mutations affect the conformation of this glycan. Hydrogen bond analysis further revealed that P533R induces aberrant, persistent glycan-protein interactions, providing a possible structural explanation for reduced IDUA activity and, therefore, GAG processing. Our findings, supported by in vitro data, propose glycan conformational restriction as a possible new molecular mechanism that underpins enzymatic dysfunction in attenuated MPS I, opening new avenues for structure-informed therapeutic strategies.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 19","pages":"e71396"},"PeriodicalIF":4.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13654827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149170893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

GPX4-Mediated Inhibition of Ferroptosis by Sodium Selenite Ameliorates Bone Metabolic Disorders in Ovariectomized Mice. 亚硒酸钠对gpx4介导的铁下沉抑制改善去卵巢小鼠骨代谢紊乱

IF 4.2 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2026-10-01 DOI: 10.1111/jcmm.71414

Wei Luo, Haibo Xu, Xin Liu, Yongsheng Zhang, Hao Zhou, Xiangqiang Pan, Dechun Geng, Hanliang He

{"title":"GPX4-Mediated Inhibition of Ferroptosis by Sodium Selenite Ameliorates Bone Metabolic Disorders in Ovariectomized Mice.","authors":"Wei Luo, Haibo Xu, Xin Liu, Yongsheng Zhang, Hao Zhou, Xiangqiang Pan, Dechun Geng, Hanliang He","doi":"10.1111/jcmm.71414","DOIUrl":"10.1111/jcmm.71414","url":null,"abstract":"Postmenopausal osteoporosis (PMOP) and its associated fracture complications have emerged as pressing public health challenges due to rapidly accelerating global population ageing. The functional decline of bone marrow mesenchymal stem cells (BMSCs) under elevated oxidative stress is a recognised pathogenic cornerstone of PMOP, positioning redox imbalance as a critical therapeutic node. Here, we establish that sodium selenite (Na2SeO3) robustly counters oxidative insults in BMSCs, thereby restoring and enhancing their osteogenic lineage commitment. Furthermore, RNA sequencing analysis indicated that ferroptosis may be mechanistically associated with the underlying cellular responses. Ferroptosis is critically mediated by glutathione peroxidase 4 (GPX4), a selenoenzyme that functions as its principal enzymatic suppressor. Silencing GPX4 in BMSCs markedly reduced their osteogenic capacity and simultaneously upregulated ferroptotic protein expression. Notably, this impairment was not reversed by Na2SeO3 administration under conditions of GPX4 suppression. These findings suggest that Na2SeO3 enhances osteogenic differentiation primarily by upregulating GPX4 expression, thereby inhibiting ferroptosis. Thus, we have established Na2SeO3 as a potential therapeutic strategy for PMOP by identifying a previously unrecognised molecular axis through which selenium regulates bone metabolic homeostasis.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 20","pages":"e71414"},"PeriodicalIF":4.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13678664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149220158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Arachidonic Acid Disrupts PKM2-Linked Glycolysis-Related Metabolism and Exacerbates PAN-Induced Podocyte Injury. 花生四烯酸破坏pkm2相关糖酵解相关代谢并加剧pan诱导的足细胞损伤

IF 4.2 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2026-10-01 DOI: 10.1111/jcmm.71404

Kun Nie, Xiaowei Gao, Minggang Liu, Danyu You, Mengjie Weng, Tingting Zheng, Jiaqun Lin, Siyi Rao, Yongjie Zhuo, Jianxin Wan, Liyan Yang

{"title":"Arachidonic Acid Disrupts PKM2-Linked Glycolysis-Related Metabolism and Exacerbates PAN-Induced Podocyte Injury.","authors":"Kun Nie, Xiaowei Gao, Minggang Liu, Danyu You, Mengjie Weng, Tingting Zheng, Jiaqun Lin, Siyi Rao, Yongjie Zhuo, Jianxin Wan, Liyan Yang","doi":"10.1111/jcmm.71404","DOIUrl":"10.1111/jcmm.71404","url":null,"abstract":"Minimal change disease (MCD) frequently relapses, and infection is one of the most common clinical triggers. Arachidonic acid (AA), an inflammatory lipid mediator released during tissue injury and infection, has been implicated in podocyte injury, but its contribution to metabolic dysfunction in MCD remains unclear. Here, we investigated whether AA aggravates PAN-induced podocyte injury and examined the involvement of pyruvate kinase M2 (PKM2)-associated metabolic dysfunction. In a puromycin aminonucleoside (PAN)-induced rat model, AA exposure increased serum AA levels, aggravated proteinuria, reduced nephrin expression, promoted foot-process effacement and exacerbated mitochondrial dysfunction. AA was also associated with reduced PKM1 and PKM2 abundance, increased PKM2 (Tyr105) phosphorylation, decreased pyruvate kinase activity and lower pyruvate, lactate and ATP levels. In cultured human podocytes, AA intensified PAN-induced cytoskeletal disruption, mitochondrial dysfunction, oxidative stress and apoptosis. Pharmacological activation of PKM2 with TEPP-46 partially restored PK-associated metabolic activity, improved mitochondrial readouts and attenuated podocyte injury in vitro. These findings suggest that AA exacerbates PAN-induced podocyte injury in association with PKM2-associated metabolic dysfunction and mitochondrial stress.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 19","pages":"e71404"},"PeriodicalIF":4.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149171384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transcriptomics Implicates the G3BP1-SG Axis in Cochlear Hair-Cell Pyroptosis During Age-Related Hearing Loss. 转录组学暗示G3BP1-SG轴在年龄相关性听力损失耳蜗毛细胞焦亡中的作用。

IF 4.2 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2026-10-01 DOI: 10.1111/jcmm.71403

Chen Li, Yuan Cao, Jun Zhou, Yurun Chen, Qi Tang, Shuyi Wang, Zhiyuan Wu, Shu Wang, Zixin Zhang, Mengyao Xie, Hong Huo, Hua Yang

{"title":"Transcriptomics Implicates the G3BP1-SG Axis in Cochlear Hair-Cell Pyroptosis During Age-Related Hearing Loss.","authors":"Chen Li, Yuan Cao, Jun Zhou, Yurun Chen, Qi Tang, Shuyi Wang, Zhiyuan Wu, Shu Wang, Zixin Zhang, Mengyao Xie, Hong Huo, Hua Yang","doi":"10.1111/jcmm.71403","DOIUrl":"10.1111/jcmm.71403","url":null,"abstract":"Age-related hearing loss (ARHL) is a degenerative change in the auditory system, but its underlying mechanism remains unclear. In this study, using RNA sequencing technology, we analysed the expression profiles of mRNAs in the cochlear tissues of ARHL-susceptible C57BL/6J (C57) mice and relatively resistant CBA/CaJ (CBA) mice. We found that the mRNA related to stress granules (SGs) was significantly increased in the cochlear tissues of ARHL mice. Combined with current research on the pyroptosis of cochlear hair cells, we constructed an aging model of House Ear Institute-Organ of Corti 1 (HEI-OC1) in vitro and found that the expression of SG was upregulated and the expression of pyroptosis-related proteins showed a synergistic upregulation. Furthermore, functional studies involving both G3BP1 knockdown and overexpression suggested that stress granules exert a protective effect by negatively regulating pyroptosis in HEI-OC1 cells. In summary, the results of this study indicate that with aging, the formation of SG increases and the activation of pyroptosis-related markers is enhanced. The dysfunction of G3BP1 further exacerbates these pyroptosis markers, supporting the protective role of SG homeostasis in inhibiting pyroptosis activation under stress conditions. Preliminary verification suggests that the SG-pyroptosis axis may be a potential target for regulating the pyroptosis of cochlear hair cells.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 19","pages":"e71403"},"PeriodicalIF":4.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13654818/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

OIP5-AS1 Sponges miR-223-3p to Upregulate FoxO3 and Ameliorate Temporomandibular Joint Osteoarthritis by Inhibiting Chondrocyte Apoptosis. OIP5-AS1海绵miR-223-3p上调FoxO3，通过抑制软骨细胞凋亡改善颞下颌关节骨性关节炎。

IF 4.2 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2026-09-01 DOI: 10.1111/jcmm.71359

Xuesong Xu, Shichong Qiao

{"title":"OIP5-AS1 Sponges miR-223-3p to Upregulate FoxO3 and Ameliorate Temporomandibular Joint Osteoarthritis by Inhibiting Chondrocyte Apoptosis.","authors":"Xuesong Xu, Shichong Qiao","doi":"10.1111/jcmm.71359","DOIUrl":"10.1111/jcmm.71359","url":null,"abstract":"Apoptosis and functional loss of articular chondrocytes serve as initiating events in temporomandibular joint osteoarthritis (TMJOA), and FoxO3 represents a critical molecule for sustaining chondrocyte homeostasis. This study investigates the regulatory mechanism of the lncRNA-OIP5-AS1/hsa-miRNA-223-3p/FoxO3 axis in TMJOA, aiming to identify potential therapeutic targets for this disease. Single-cell database analysis first revealed markedly reduced FoxO3 expression in TMJOA-derived chondrocytes. A rat TMJOA model was then constructed and assigned to control, model, and FoxO3 overexpression groups; micro-CT and histological staining, including HE and Safranin O-fast green staining, were applied to assess articular cartilage injury, while immunohistochemistry was used to detect cartilage-associated proteins Col2a1, MMP-13, Aggrecan, and ADAMTS-5. Further in vitro experiments validated the chondroprotective function of FoxO3 as well as the binding interaction between FoxO3 and rno-miRNA-223-3p. Database screening confirmed significant down-regulation of FoxO3 in TMJOA cartilage. Animal experiments demonstrated that FoxO3 overexpression mitigated chondrocyte injury in rat TMJOA lesions, increased Col2a1 and Aggrecan levels, and suppressed MMP-13 and ADAMTS-5 expression. Cellular assays showed that FoxO3 overexpression enhanced chondrocyte proliferation and matrix synthesis and preserved chondrocyte function. Sequencing and cellular evidence indicated that rno-miRNA-223-3p directly targets FoxO3 mRNA to repress its transcription and negatively modulate FoxO3 abundance, consequently aggravating chondrocyte apoptosis. Collectively, rno-miRNA-223-3p suppresses FoxO3 activity to facilitate TMJOA pathogenesis, and the lncRNA-OIP5-AS1/rno-miRNA-223-3p/FoxO3 regulatory cascade may act as a promising molecular target for TMJOA clinical intervention.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 17","pages":"e71359"},"PeriodicalIF":4.2,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13564244/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

T1R3 Anchors ACE2 at the Pulmonary Endothelial Cell Surface to Attenuate Vascular Injury Following SARS-CoV-2 Spike 1 Protein Exposure In Vitro. T1R3在肺内皮细胞表面锚定ACE2以减轻体外暴露于SARS-CoV-2 Spike - 1蛋白后的血管损伤

IF 4.2 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2026-08-01 DOI: 10.1111/jcmm.71339

Zsuzsanna Kertesz, Lewis Spurrier-Best, Havovi Chichger

{"title":"T1R3 Anchors ACE2 at the Pulmonary Endothelial Cell Surface to Attenuate Vascular Injury Following SARS-CoV-2 Spike 1 Protein Exposure In Vitro.","authors":"Zsuzsanna Kertesz, Lewis Spurrier-Best, Havovi Chichger","doi":"10.1111/jcmm.71339","DOIUrl":"10.1111/jcmm.71339","url":null,"abstract":"The development of acute lung injury in COVID-19 patients is a major cause of lethality. Activation of the pulmonary vasculature, with inflammation, oxidative stress and barrier disruption, is initiated by the SARS-CoV-2 spike protein (Sp1) at the endothelial cell surface. We previously identified the presence of a novel G-Protein Coupled Receptor (GPCR) in the lung microvasculature, T1R3. The T1R3 agonist (T1R3-A) protects the endothelium from endotoxin-induced lung injury therefore we sought to investigate the effect of T1R3-A on Sp1-induced damage to the pulmonary endothelium. Sp1 induced significant disruption to the endothelium with elevated gap formation, monolayer leak and ROS accumulation. This damage was attenuated following exposure of the lung microvasculature to T1R3-A. We further demonstrated that this agonist promotes ACE2 expression at the endothelial cell surface. Using immunoprecipitation studies, we demonstrated that T1R3-A increases ACE2:T1R3 binding which may be a mechanism for protecting against Sp1-induced endothelial cell injury. Our findings highlight the protective effect of T1R3 activation in the pulmonary endothelium and that there is a close link between T1R3 and ACE2. We propose that T1R3 activation protects the endothelium by preventing Sp1-induced internalisation of ACE2, thereby blocking downstream ACE2 signalling leading to pulmonary vascular injury.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 16","pages":"e71339"},"PeriodicalIF":4.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13508132/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148818602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Machine Learning Stratification of Periodontal and Cerebrovascular Disease Status Using Salivary and Subgingival Lipopolysaccharide Activity. 利用唾液和龈下脂多糖活性对牙周和脑血管疾病状态进行机器学习分层。

IF 4.2 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2026-08-01 DOI: 10.1111/jcmm.71337

Anbo Dong, Zhenshan Xie, Muhammed Manzoor, Jaakko Leskelä, Jukka Putaala, Eija Könönen, Luigi Nibali, Pirkko Pussinen, Susanna Paju, Svetislav Zaric

{"title":"Machine Learning Stratification of Periodontal and Cerebrovascular Disease Status Using Salivary and Subgingival Lipopolysaccharide Activity.","authors":"Anbo Dong, Zhenshan Xie, Muhammed Manzoor, Jaakko Leskelä, Jukka Putaala, Eija Könönen, Luigi Nibali, Pirkko Pussinen, Susanna Paju, Svetislav Zaric","doi":"10.1111/jcmm.71337","DOIUrl":"10.1111/jcmm.71337","url":null,"abstract":"Oral dysbiosis may contribute to systemic inflammation, but taxonomic composition alone does not capture the host-relevant inflammatory activity of microbial products. This study investigated whether salivary and subgingival lipopolysaccharide (LPS) activities could reflect host-microbiome interactions across periodontal and cerebrovascular disease states. Participants from the SECRETO Oral study were stratified by periodontal status and cryptogenic ischaemic stroke. LPS activity was quantified using a recombinant Factor C assay. Log-transformed mean oral LPS activity and the subgingival-to-salivary LPS activity ratio were evaluated alongside demographic and behavioural variables in an exploratory machine-learning framework. Integrated oral LPS activity increased across disease groups and was highest in participants with both periodontitis and stroke, while the LPS activity ratio differed across disease states, indicating altered niche distribution. Models combining demographic, behavioural and LPS-derived features discriminated disease groups better than models using either feature set alone. LPS-derived features therefore provided complementary, but not independently sufficient, discriminatory information. Oral LPS activity may represent a functional marker of microbial inflammatory burden across periodontal and cerebrovascular disease states. These exploratory findings require validation in independent cohorts with paired microbiome and endotoxin data.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 16","pages":"e71337"},"PeriodicalIF":4.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13508137/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148818465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transcriptomic Profiling Associates Collagen-Rich Extracellular Matrix With Postoperative Angiogenesis in Moyamoya Disease. 转录组学分析将富含胶原的细胞外基质与烟雾病术后血管生成联系起来。

IF 4.2 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2026-08-01 DOI: 10.1111/jcmm.71267

Jing-Yi Chen, Shun-Fei Xu, Zi-Qing Wang, Wen-Xin Jin, Ri-Sheng Liang, Xian-Kun Tu

{"title":"Transcriptomic Profiling Associates Collagen-Rich Extracellular Matrix With Postoperative Angiogenesis in Moyamoya Disease.","authors":"Jing-Yi Chen, Shun-Fei Xu, Zi-Qing Wang, Wen-Xin Jin, Ri-Sheng Liang, Xian-Kun Tu","doi":"10.1111/jcmm.71267","DOIUrl":"10.1111/jcmm.71267","url":null,"abstract":"Indirect revascularization is an effective treatment for moyamoya disease (MMD), but the surgery effect depends on the collateral vessel formation. This study aimed to explore the molecular mechanisms associated with angiogenesis in the temporal muscle post-surgery. We employed a single-centre, prospective sampling, retrospective cohort design. Temporal muscle tissues were harvested during surgery, and comprehensive transcriptome-wide RNA sequencing was performed. Patients were categorized into Good (Matsushima Grade A, n = 13) and Poor (Matsushima Grade C, n = 12) collateralization groups based on postoperative angiography. Differentially expressed genes (DEGs) were analysed, and key findings were validated via quantitative real-time PCR (qPCR). A total of 25 patients were enrolled. Transcriptomic profiling revealed that pathways related to the extracellular matrix (ECM) and collagen family were significantly enriched in the Good group, suggesting a pivotal role for collagens in promoting postoperative angiogenesis. Subgroup analysis revealed distinct transcriptional profiles: paediatric patients exhibited a cluster characterized by high collagen expression alongside altered expression of genes related to mitochondrial electron transport. qPCR validation confirmed the upregulation of the core ECM component COL1A1 and the downregulation of the matrix-degrading enzyme MMP3 in the Good group, indicating active ECM remodelling within the temporal muscle. Collectively, these findings suggest that a collagen-rich ECM signature and the balance between collagen deposition and remodelling may modulate surgical efficacy in MMD.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 16","pages":"e71267"},"PeriodicalIF":4.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13520919/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148828586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Myeloid-Derived Growth Factor Improves Endothelial Progenitor Cell Function and Angiogenesis in Mice With Diabetic Hindlimb Ischemia by Activating Akt/HIF-1α Signalling Pathway. 髓源性生长因子通过激活Akt/HIF-1α信号通路改善糖尿病后肢缺血小鼠内皮祖细胞功能和血管生成

IF 4.2 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2026-07-01 DOI: 10.1111/jcmm.71287

Wen Mei, Biying Meng, Bilin Zhang, Yi Shu, Haizhao Luo, Jingwen Ye, Yijiang Hou, Biao Zhu, Jiajia Zhang

引用次数: 0

Dual PARP/Tankyrase Inhibition Enhances Antitumor Efficacy in PTEN-Deficient Endometrial Cancer. 双抑制PARP/ tankyase增强pten缺陷子宫内膜癌的抗肿瘤效果。

IF 4.2 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2026-06-01 DOI: 10.1111/jcmm.71242

Sung Wan Kang, Hyerim Eum, Ji-Young Lee, Min-Seo Lee, Yong-Man Kim, Tae Won Kim, Shin-Wha Lee

{"title":"Dual PARP/Tankyrase Inhibition Enhances Antitumor Efficacy in PTEN-Deficient Endometrial Cancer.","authors":"Sung Wan Kang, Hyerim Eum, Ji-Young Lee, Min-Seo Lee, Yong-Man Kim, Tae Won Kim, Shin-Wha Lee","doi":"10.1111/jcmm.71242","DOIUrl":"10.1111/jcmm.71242","url":null,"abstract":"Endometrial cancer (EC) incidence continues to rise, underscoring the need for effective therapies beyond BRCA-mutant disease. Although PTEN loss, a frequent alteration in EC, has been implicated in impaired homologous recombination and increased sensitivity to PARP inhibitors, responses to PARP inhibitor monotherapy remain variable and are often limited by resistance mechanisms in PTEN-deficient tumours. Here, we show that the dual PARP/tankyrase (TNKS) inhibitor JPI-547 exerts potent antitumor activity, particularly in PTEN-deficient Ishikawa tumours. In vitro, JPI-547 and olaparib more effectively reduced cell survival in PTEN-deficient cells, and combined treatment with olaparib and the TNKS inhibitor XAV-939 induced synergistic cytotoxicity with elevated DNA double-strand breaks. Dual PARP/TNKS inhibition did not further suppress RAD51 but modulated non-homologous end joining and attenuated Wnt/β-catenin signalling in a PTEN-dependent manner. PTEN knockdown further showed enhanced vulnerability to combined targeting. These findings show that JPI-547 enhances antitumor efficacy in PTEN-deficient EC by disrupting DNA repair pathways and Wnt signalling, supporting dual PARP/TNKS inhibition as a potential therapeutic strategy and providing a rationale for further clinical evaluation.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 11","pages":"e71242"},"PeriodicalIF":4.2,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13263240/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148239410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0