Journal of Cellular and Molecular Medicine最新文献

{"title":"A Network Pharmacology and Experimental Validation Strategy for Hypoglycemic Study of Lonicerae Japonicae Flos on Diabetes.","authors":"Zhang Nan, Liu Xiaolong, Li Chunyan, Ren Lu, Guo Chao, Xue Jintao","doi":"10.1111/jcmm.71167","DOIUrl":"10.1111/jcmm.71167","url":null,"abstract":"<p><p>As diabetes has become an important public health issue, Lonicerae Japonicae Flos (LJF) had gradually attracted increasing attention on diabetes. This study aimed to investigate the hypoglycemic ingredients and underlying mechanisms of LJF in diabetes using an integrated strategy of network pharmacology, molecular docking and experimental validation. Network pharmacology screened 73 active ingredients, 65 targets and 20 main signalling pathways. The results of molecular docking, protein-protein interaction and ingredient-target-pathway network indicated that four targets (PPARG, PPARD, MGAM, GAA) and three signalling pathways (PPAR signalling pathway, Starch and sucrose metabolism, Galactose metabolism) played essential roles. Subsequently, animal experiments and in vitro tests were performed to evaluate the anti-diabetic effect, antioxidant capacity and α-amylase inhibitory activity for the LJF extract. Animal studies indicated the LJF alcohol extract could significantly decrease blood glucose level and mitigate the weight loss compared to the model group (p < 0.05), respectively. Furthermore, both in vitro and in vivo tests confirmed that the LJF alcohol extract exhibited strong antioxidant capacity (p < 0.05 for MDA and SOD) and α-amylase inhibitory activity (maximum efficacy: 66.6% ± 4.6%). This strategy provided a promising approach to further elucidate the active ingredients and underlying mechanisms of LJF and other herbs.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 9","pages":"e71167"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135239/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147815067","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}

{"title":"SORBS2: A Molecular Nexus in Multisystem Diseases Through Scaffold-Mediated Regulation.","authors":"Qiwei Jia, Yong Zhang","doi":"10.1111/jcmm.71160","DOIUrl":"10.1111/jcmm.71160","url":null,"abstract":"<p><p>Sorbin and SH3 Domain Containing 2 (SORBS2), a multifunctional scaffold protein harbouring Sorbin homology (SoHo) and Src homology 3 (SH3) domains, serves as a molecular hub in human diseases by integrating cytoskeletal remodelling, signal transduction and RNA metabolic regulation. This study systematically analyses SORBS2's molecular features, expression regulatory mechanism and disease associations. In oncology, it suppresses metastasis via enhancing the stability of certain mRNAs and immunomodulation yet exhibits oncogenic properties in triple-negative breast cancer. Cardiovascular manifestations demonstrate dose-sensitive pathology: deficiency causes arrhythmogenic cytoskeletal disorganization, while overexpression induces β-tubulin hyper polymerization and ventricular maldevelopment. Epigenetic silencing by miR-484 exacerbates metabolic liver disease, whereas defective interaction with the large-conductance Ca²⁺-activated K⁺ (BK) channel drives diabetic vasculopathy. Neurologically, it modulates synaptic remodelling and neuroinflammatory pathways. Functioning as a signalling nexus, SORBS2 interconnects chronic inflammation, oxidative stress and metabolic dysfunction, supporting 'one target for multiple diseases' strategy. Future research requires integration of single-cell omics, Artificial intelligence (AI)-based drug design and epigenetic editing for clinical translation.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 9","pages":"e71160"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13121097/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772489","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}

{"title":"From Adipose Tissue to Cardiac Repair: Extracellular Vesicles in Cardiovascular Regeneration.","authors":"Karolina Ignaczak, Pola Ochocka, Karol Sadowski, Weronika Ploch, Dominika Tomkiel, Mariusz Tomaniak, Wioletta Olejarz","doi":"10.1111/jcmm.71148","DOIUrl":"10.1111/jcmm.71148","url":null,"abstract":"<p><p>Adipose-derived extracellular vesicles (ADEVs) secreted by adipose tissue have gained increasing attention due to their regenerative and immunomodulatory properties in cardiovascular diseases. They carry proteins, lipids, and nucleic acids that mediate intercellular communication and influence cardiac pathophysiology. In atherosclerosis, ADEVs promote vascular regeneration, protect endothelial integrity, modulate macrophage polarization, foam cell formation, and regulate lipid homeostasis. In myocardial infarction, they limit apoptosis, reduce fibrosis, stimulate angiogenesis, and regulate inflammation through miRNA-dependent paracrine mechanisms. While preclinical studies support their therapeutic relevance, clinical translation remains at an early stage due to fragmented evidence and lack of standardization in isolation methods, dosing, and safety assessment. This review synthesizes current pathophysiological and translational evidence on the role of ADEVs in cardiovascular repair and provides a structured perspective to guide the development of ADEV-based therapies toward clinical application.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 9","pages":"e71148"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13129225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772302","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}

{"title":"Research Progress of Cuproptosis in Orthopaedics: Opportunities and Challenges.","authors":"Chaoshuai Wang, Pengfei An","doi":"10.1111/jcmm.71175","DOIUrl":"10.1111/jcmm.71175","url":null,"abstract":"<p><p>Cuproptosis, a recently identified and copper-dependent form of regulated cell death, has emerged as a potential therapeutic target for a variety of diseases. This review synthesizes current evidence from PubMed to elucidate the mechanisms of cuproptosis and its implications in common orthopaedic disorders, including arthritis, bone tumours and osteoporosis. We systematically explore the dual role of copper homeostasis-highlighting how its dysregulation contributes to disease pathogenesis and how its targeted modulation may offer novel therapeutic strategies. Finally, we discuss the associated challenges and future directions for translating cuproptosis research into clinical orthopaedics practice.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 9","pages":"e71175"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13158165/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147868496","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}

{"title":"Exosomal Non-Coding RNAs in Gastrointestinal Cancer Drug Resistance: A Systematic Review of Emerging Mechanisms and Clinical Implications.","authors":"Mohsen Sharif-Zak, Zahra Sadeghloo, Fateme Binayi, Stefania Nobili, Sara Ashtari, Amir Sadeghi, Nayeralsadat Fatemi","doi":"10.1111/jcmm.71137","DOIUrl":"10.1111/jcmm.71137","url":null,"abstract":"<p><p>Gastrointestinal (GI) tumours are one of the most prevalent cancers globally. Even with normal GI function, individuals may develop neoplasms, highlighting the need to better understand the underlying causes of tumorigenesis. The emergence of tumour drug resistance represents the main reason for the failure of drug treatment; thus, it is imperative to investigate all the potential mechanisms of this very complex phenomenon. It is significant that exosomes and noncoding RNAs, such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), originating from tumour cells, are linked to both GI drug resistance and the carcinogenesis and development of GI disease. Thus, we propose a systematic review of the literature to provide an overview of the current landscape concerning exosomal ncRNAs as diagnostic and prognostic biomarker resources in resistant GI cancer. We performed the current systematic review according to PRISMA guidelines and comprehensively explored PubMed, Web of Science, Scopus and Google Scholar databases to achieve the article search. Seventy-six studies were included in the investigation, comprising 50 cohort studies and 26 nested case-control studies (between 1994 and 2025). Among all systematically reviewed exosomal ncRNAs, we primarily found molecules with prognostic significance and predictive relevance, and those that serve both purposes have been identified. Furthermore, among all analysed ncRNAs isolated from exosomes, miRNAs, lncRNAs and circRNAs have emerged as the most extensively studied and are proposed as potential tools for predicting resistance or sensitivity to GI cancer treatments. Our analysis offers a comprehensive overview of the current landscape concerning exosomal ncRNAs as potential clinical biomarkers for resistant GI tumours. However, despite extensive research efforts, the application of exosomal biomarkers in GI cancers is still in its infancy. None of the identified exosomal biomarkers have advanced beyond preclinical studies, and their applicability in clinical settings remains limited, largely due to challenges in clinical validation, standardisation and biomarker specificity.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 9","pages":"e71137"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13156249/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856491","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}

{"title":"Preliminary Clinical Outcomes of Human Umbilical Cord Mesenchymal Stem Cell-Derived Exosomes in Chronic Rhinosinusitis With Nasal Polyps: A Case Report.","authors":"Manoochehr Avatef-Fazeli, Gelavizh Rostaminasab, Iman Janghorban Esfahani, Amir Barimani, Kamran Mansouri","doi":"10.1111/jcmm.71166","DOIUrl":"10.1111/jcmm.71166","url":null,"abstract":"<p><p>Chronic Rhinosinusitis with Nasal Polyps (CRSwNP) is a persistent inflammatory disease that may be resistant to medical management and recurs with traditional surgery. We report a 28-year-old male with a history of CRSwNP with comorbid asthma, who was resistant to all medical management, including saline irrigation, intranasal corticosteroids (INCS), and multiple courses of antibiotics, and elected against surgical intervention. Nasal endoscopy and imaging studies demonstrated bilateral polyposis and opacification of the ostia of all sinuses (Meltzer score 5 and Lund-Mackay score of 18). Serum IgE level remained significantly high. The patient declined surgical intervention but consented to treatment with human umbilical cord MSC-Exo (hUCMSC-Exo) intramucosal and intrapolyp injections while continuing his standard regimen of saline irrigation and INCS. The treatment was well tolerated, with only reported mild and transient epistaxis. At follow-up after two months, the patient experienced a rapid decrease in SNOT-22 score (56-6). However, the symptomatic relief had abated, and the symptoms returned gradually but did not reach baseline (SNOT-22 increased to 41). Conversely, asthma control remained stable during this time, and the serum IgE level showed an overall negative trend. Given the single-patient, uncontrolled design with concurrent INCS and short follow-up, causality cannot be inferred. This case supports feasibility/tolerability and generates hypotheses for larger controlled studies of this cell-free approach.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 9","pages":"e71166"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13161984/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147874316","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}

{"title":"Longchai Decoction Treated the Fibrosis of Liver Induced by CCl₄ Regulates Nrf2/GPX4 Pathway to Suppress Ferroptosis.","authors":"Hui Wang, Liang Wang, Fangshi Zhu, Siru Chen","doi":"10.1111/jcmm.71151","DOIUrl":"10.1111/jcmm.71151","url":null,"abstract":"<p><p>The aim of the study is to evaluate the therapeutic efficacy of Longchai Decoction (LCD), an empirical traditional Chinese medicine formula for liver disorders, on liver fibrosis (LF) and to elucidate its molecular mechanisms. A mouse model of LF and an erastin-induced ferroptosis model was established in LX-2 cells, which were then treated with silybin and LCD. The therapeutic function of LCD on liver fibrosis was evaluated using biochemical assays, histopathological staining, transmission electron microscopy, transcriptome sequencing, and immunohistochemistry. The mechanisms by which LCD alleviated LF were investigated using western blotting and immunofluorescence. LCD treatment significantly decreased the serum concentrations of IL-1β, IL-6, and TNF-α. It also effectively suppressed lipid peroxidation, diminished iron accumulation, and preserved mitochondrial integrity within hepatic tissues. Transcriptome sequencing analysis revealed that LCD significantly increased the levels of genes including NRF2, GPX4, and HO-1, thereby modulating the Nrf2/GPX4 pathway both in vivo and in vitro, thereby inhibiting lipid peroxidation and ferroptosis. Our findings suggest that LCD plays a protective role against hepatocyte ferroptosis and mitigates CCl4-induced liver damage and fibrosis through the activation of the Nrf2/GPX4 pathway.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 8","pages":"e71151"},"PeriodicalIF":4.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13109816/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147771835","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}

{"title":"The Crosstalk Mechanisms Between Ferroptosis and Pyroptosis and Their Applications in Diseases: From Molecular Networks to Clinical Strategies.","authors":"Wei-Yi Zhao, Lu-Yao Li, Fang-Wang Ye, Jin-Wei Zhao","doi":"10.1111/jcmm.71138","DOIUrl":"10.1111/jcmm.71138","url":null,"abstract":"<p><p>Ferroptosis and pyroptosis are two distinct forms of regulated cell death that play crucial roles in cancer, neurodegeneration, and inflammatory diseases. Ferroptosis is characterised by iron-dependent lipid peroxidation, while pyroptosis is an inflammatory cell death mediated by gasdermin proteins. Recent studies reveal extensive crosstalk between these pathways. This review establishes the first hierarchical framework coupling the autophagy bridge function (ferritinophagy-mitophagy-cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) axis) with the p53/signal transducer and activator of transcription 3 (STAT3)/Nuclear factor erythroid 2-related factor 2 (NRF2) transcriptional hub, creating a unified decision-making network absent in prior reviews. Crosstalk mechanisms include the reactive oxygen species (ROS)-NOD-like receptor protein 3 (NLRP3) positive feedback loop, caspase cross-activation, and iron metabolism-inflammasome integration. Preclinically, the transferrin-targeted nanosystem Tf-LipoMof@PL increased intratumoral iron/ROS 3-5-fold, inducing robust antitumour immunity, while Ginsenoside Rh3 suppressed colorectal cancer growth in vivo via STAT3/p53/NRF2-mediated dual death induction. We critically address STAT3's paradoxical roles-promoting Gasdermin E (GSDME)-mediated pyroptosis in oesophageal cancer while suppressing NLRP3 via suppressor of cytokine signalling 3 (SOCS3) feedback in acute respiratory distress syndrome (ARDS)-highlighting cell type-specific feedback architectures that dictate phenotypic outcomes. For therapeutic translation, we propose a Translational Priority Matrix ranking nanodelivery systems (Tf-LipoMof@PL) and dual-function small molecules (N6F11) as the highest priority for intrahepatic cholangiocarcinoma (iCCA)/triple-negative breast cancer (TNBC), while deprioritising metal photosensitizers pending resolution of cardiac retention toxicity (0.8 μg/g myocardium in Good Laboratory Practice (GLP) studies). The \"registration gap\" stems from iron burst-release (> 80% within 30 min) and species-specific biomarker failures. We advocate replacing murine malondialdehyde (MDA)/glutathione (GSH) ratios with human-anchored metrics (ferritin heavy chain 1 (FTH1)/solute carrier family 40 member 1 (SLC40A1) expression, serum ferritin) and propose a \"Cross-Death AI Platform\" integrating network pharmacology (OmniPath/STRING), GraphSAGE deep learning (AlphaFold2 structures), and organoid validation to stratify patients and predict optimal drug combinations. By resolving spatiotemporal heterogeneity and implementing AI-guided precision medicine, we can transform multi-target interventions from empirical strategies into rational, patient-specific regimens, bridging the gap between preclinical promise and clinical success in cancers and neurodegenerative diseases.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 8","pages":"e71138"},"PeriodicalIF":4.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13099587/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147771813","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}

{"title":"Correction to 'Cul4A is an oncogene in malignant pleural mesothelioma'.","authors":"","doi":"10.1111/jcmm.71156","DOIUrl":"https://doi.org/10.1111/jcmm.71156","url":null,"abstract":"","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 8","pages":"e71156"},"PeriodicalIF":4.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098534/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772738","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}

{"title":"Exploration of the Potential Mechanism of Metal Ion Transport-Related Genes in Myocardial Infarction Based on Transcriptomics.","authors":"Xiaowei Zhou, Fanyan Luo, Meihong Yu, Yao Deng, Kaixuan Li","doi":"10.1111/jcmm.71134","DOIUrl":"10.1111/jcmm.71134","url":null,"abstract":"<p><p>Myocardial infarction (MI), a severe coronary artery disease manifestation, is a top global cause of death. Abnormal metal ion transport (MIT) is key to MI pathological progression, and this study explores MIT's molecular characteristics/regulatory mechanisms in MI via transcriptome and bioinformatics data. Differentially expressed genes (DEGs) in MI were screened, and their intersection with MIT-related genes (MITRGs) identified candidate genes. Protein-protein interaction (PPI) network analysis, expression validation, gene set enrichment, immune infiltration analyses, and regulatory network construction were used to find hub genes and mechanisms. Through algorithmic analysis combined with gene expression validation, Ace, Igf1, Lgals3, and Serpine1 were identified as hub genes. These hub genes are mainly involved in metabolic pathways such as the TCA cycle and lysosomes. In the MI group, the infiltration of innate immune cells was increased, while that of adaptive immune cells was decreased. Additionally, Serpine1, Lgals3, Ace, and Igf1 showed a significant positive correlation with macrophages and monocytes. Various potential drugs were predicted for these hub genes. Molecular docking revealed strong binding capacities between these human hub genes and their corresponding drugs. Through bioinformatics analysis, this study identified four hub genes closely associated with MIT in MI, providing a new research basis for the mechanism of MI.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 7","pages":"e71134"},"PeriodicalIF":4.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13066501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147645570","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}