JOURNAL OF CELLULAR AND MOLECULAR MEDICINE最新文献

{"title":"Correction to “The Effects of Simvastatin-Loaded Nanoliposomes on Human Multilineage Liver Fibrosis Microtissue”","authors":"","doi":"10.1111/jcmm.71360","DOIUrl":"10.1111/jcmm.71360","url":null,"abstract":"<p>\u0000 <span>S. Parsa</span>, <span>M. Dousti</span>, <span>N. Mohammadi</span>, <span>M. Abedanzadeh</span>, <span>N. Dehdari Ebrahimi</span>, <span>M. Dara</span>, <span>M. Sani</span>, <span>M. Nekouee</span>, <span>S. S. Abolmaali</span>, <span>F. Sani</span>, and <span>N. Azarpira</span>, “ <span>The Effects of Simvastatin-Loaded Nanoliposomes on Human Multilineage Liver Fibrosis Microtissue</span>,” <i>Journal of Cellular and Molecular Medicine</i> <span>28</span>, no. <span>13</span> (<span>2024</span>): e18529. https://doi.org/10.1111/jcmm.18529.\u0000 </p><p>We apologize for this error.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 19","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13625814/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of Calcium-Sensing Receptor Suppresses Malignant Behaviours of Human Hepatocellular Carcinoma","authors":"Tingting Liu,&nbsp;Wei Xu,&nbsp;Qianqian Gao,&nbsp;N. Ngwa Adeline,&nbsp;Qi Yang,&nbsp;Dawei He,&nbsp;Yukai Tao,&nbsp;Jun Sun,&nbsp;Jie Gu,&nbsp;Haifeng Shi,&nbsp;Michael Aschner,&nbsp;Yang Ye,&nbsp;Jian Chen,&nbsp;Rongzhu Lu","doi":"10.1111/jcmm.71389","DOIUrl":"10.1111/jcmm.71389","url":null,"abstract":"<p>Hepatocellular carcinoma (HCC) continues to pose significant worldwide health burdens due to restricted treatment alternatives and unfavourable prognosis. This investigation reveals the pivotal involvement of calcium-sensing receptor (CaSR) in HCC advancement and its potential as a promising therapeutic target. Through pharmacological blockade with NPS-2143 and genetic knockdown using siRNA, we found that CaSR inhibition substantially reduced HCC cell proliferation, migration, and invasion, while promoting apoptotic cell death in HepG2 and SMMC-7721 cells. At the molecular level, CaSR interference triggered p38 MAPK activation, while inhibiting the ERK1/2 cascade, resulting in diminished expression of proliferation indicators (PCNA), metastatic markers (MMP-2/9), and cell survival proteins (Bcl-2), concurrent with elevated levels of apoptosis mediators (Bax, cleaved caspase-3). In vivo, NPS-2143 significantly suppressed xenograft tumour growth. Western blotting of xenograft tumour tissues further showed increased p-p38/p38 and Bax levels and decreased p-ERK/ERK, MMP-9, and Bcl-2 levels, consistent with the in vitro findings. Additional validation in a male nude mouse xenograft model using Huh7 cells further supported the anti-tumour effect of NPS-2143 in another independent HCC model. These findings suggest that CaSR facilitates malignant HCC cebehaviours through MAPK signalling and may represent a potential therapeutic target for HCC treatment.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 19","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ya-Jie-Sha-Ba Decoction Regulates Arachidonic Acid Metabolism to Treat Alcohol-Associated Liver Disease by Activating PPARα–CYP4A14 Axis: Insights From Multi-Omics Analysis and Experimental Validations","authors":"Dehong Ma,&nbsp;Xia Chen,&nbsp;Huixian Dao,&nbsp;Hongyu Deng,&nbsp;Yingcheng Guo,&nbsp;Hui Yang,&nbsp;Yuanyuan Chen,&nbsp;Congmei Zhang,&nbsp;Yuan Long,&nbsp;Weibo Wen,&nbsp;Yinghong Zhao,&nbsp;Huantian Cui","doi":"10.1111/jcmm.71385","DOIUrl":"10.1111/jcmm.71385","url":null,"abstract":"<p>Ya-Jie-Sha-Ba decoction (YJSB), a traditional Dai medicinal formulation, has been widely used by the Dai ethnic group and has shown efficacy in alleviating alcohol-associated liver disease (ALD). However, the molecular mechanism of YJSB in the management of ALD remains unclear. Building on evidence that YJSB ameliorates ALD, we combined transcriptomics and untargeted metabolomics to elucidate the molecular mechanisms responsible for its anti-ALD effects. We established an ALD mouse model and treated animals with YJSB to evaluate its therapeutic effects. We then performed integrated transcriptomic and untargeted metabolomic analyses to identify pathways and molecules associated with YJSB treatment. Using UPLC-Q-TOF-MS, we identified YJSB prototype components present in plasma. We screened the major plasma-detected constituent for hepatoprotective activity in an in vitro model of alcohol-induced hepatocyte injury. Finally, we validated the molecular target of this active component using molecular docking, cellular thermal shift assay (CETSA), drug affinity responsive target stability (DARTS), and pharmacological inhibition assays. The results showed that YJSB markedly reduced hepatic injury and lipid accumulation in ALD mice and simultaneously decreased oxidative stress and inflammation. Integrated multi-omics analysis identified arachidonic acid metabolism as a potential pathway mediating YJSB's protective effects. In particular, YJSB robustly increased the expression of CYP4A14, a key enzyme in this pathway. We identified methyl palmitate as the major active component of YJSB that mitigated alcohol-induced hepatocyte injury in vitro. Methyl palmitate decreased oxidative stress and enhanced CYP4A14 expression in injured hepatocytes. Molecular docking demonstrated a preferable binding affinity between methyl palmitate and PPARα. CETSA and DARTS further validated this interaction by showing that methyl palmitate increased the thermal stability and proteolytic resistance of PPARα. Importantly, pharmacological inhibition of PPARα completely abolished the hepatoprotective effects of methyl palmitate in vitro. In conclusion, YJSB effectively reduces liver injury in ALD mice. Mechanistically, its active component methyl palmitate activates PPARα, thereby upregulating CYP4A14, reshaping arachidonic acid metabolism, and attenuating alcohol-induced oxidative stress in hepatocytes.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 19","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Traditional Chinese Medicine Formulas in Delaying Aging: From Theoretical Foundations to Molecular Mechanisms and Translational Perspectives","authors":"Chenrong Jin,&nbsp;Ding Du,&nbsp;Xiaorui Yu,&nbsp;Xiaoyan Ji,&nbsp;Xiuyun Zhang,&nbsp;Anning Li,&nbsp;Shuang Zu,&nbsp;Bo Qu,&nbsp;Daqing Zhao,&nbsp;Dianpeng Wu,&nbsp;Meichen Liu","doi":"10.1111/jcmm.71371","DOIUrl":"10.1111/jcmm.71371","url":null,"abstract":"<p>Aging is a systemic decline in physiological integrity, driving chronic diseases such as neurodegeneration, cardiovascular disorders, and metabolic syndromes. Rapid global population aging urgently demands effective interventions. Traditional Chinese medicine (TCM) formulas, characterized by multi-component, multi-target, and multi-pathway synergy, offer a promising paradigm for delaying aging. This review systematically integrates recent advances in TCM formula-based anti-aging research, bridging classical TCM gerontology with the 14 modern hallmarks of aging. We categorize representative formulas into four mechanistic groups targeting mitochondrial homeostasis and autophagy, cellular senescence and inflammatory microenvironment, stem cell maintenance and epigenetic reprogramming, and gut microbiota and systemic metabolism, and explore their holistic efficacy, key bioactive constituents, and multi-component synergy. In terms of methodological innovations, we introduced network pharmacology combined with AI-driven target screening and proteomic aging clocks to assess biological age. We discussed challenges in chemical complexity, mechanistic completeness, and clinical translation, and proposed a roadmap for development. This review establishes an integrative model that integrates TCM principles with modern aging biology, offering insights for translational research toward healthy longevity.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 19","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620404/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149074740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Huangqi Guizhi Wuwu Decoction Ameliorates Cachexia in Lung Cancer Mice Through Regulating Amino Acid Metabolism: Insights From Transcriptomics, Metabolomics and Experimental Validation","authors":"Yingjia Zhou,&nbsp;Shaoli Zhao,&nbsp;Hongmei Shen,&nbsp;Jia Wu,&nbsp;Mei Li,&nbsp;Shan Liu,&nbsp;Jian Yang,&nbsp;Xiaowei Jin,&nbsp;Fan Li,&nbsp;Huantian Cui","doi":"10.1111/jcmm.71387","DOIUrl":"10.1111/jcmm.71387","url":null,"abstract":"<p>The effects and mechanisms of Huangqi Guizhi Wuwu Decoction (HGWD) in cancer cachexia remain unclear. We generated an in vivo cachexia model by implanting Lewis lung carcinoma cells into mice and treated animals with HGWD. We evaluated muscle function using grip strength and wire-grip tests. We also assayed markers of muscle synthesis and oxidative stress, and assessed tumour growth to evaluate any antitumor effects of HGWD. Finally, we performed transcriptomic and untargeted metabolomic analyses. HGWD increased muscle strength and restored muscle mass in cachectic mice. HGWD improved levels of proteins associated with muscle anabolism and altered oxidative stress–related factors. Treated mice showed modest tumour inhibition and greater food and water intake. Transcriptomic profiling of gastrocnemius muscle revealed significant enrichment of amino acid–related metabolic pathways after HGWD treatment. Untargeted metabolomics indicated that most branched-chain amino acids were upregulated following HGWD intervention. Further validation showed that HGWD increased both gene and protein expression of adenosylmethionine decarboxylase 1 (AMD1) and spermine oxidase (SMOX), while decreasing gene and protein expression of glycine N-methyltransferase (GNMT) in the gastrocnemius of cachectic mice. The anti-cancer cachexia effect of HGWD appears to be associated with promoting the conversion of S-adenosylmethionine (SAM) to spermidine, thereby correcting amino acid metabolic disturbances.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 19","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13616822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149069664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Injectable Hydrogel Loaded With Umbilical Cord Blood-Derived Exosomes Promotes Periodontal Bone Regeneration via the TLR4/NF-κB Signalling Pathway","authors":"Dongao Zhu,&nbsp;Mingkun Liu,&nbsp;Yue Fan,&nbsp;Lv Lang,&nbsp;Xin Luo,&nbsp;Zhihong Zhang,&nbsp;Zuojun Shen,&nbsp;Honghong Liu","doi":"10.1111/jcmm.71347","DOIUrl":"10.1111/jcmm.71347","url":null,"abstract":"<p>Periodontitis is an immune-mediated inflammatory disease characterised by progressive alveolar bone loss, which can lead to tooth loss in severe cases. Existing therapeutic agents have limited efficacy in reversing the associated inflammatory bone defects. Exosomes (Exos), enriched with bioactive molecules, exhibit significant potential in anti-inflammation and osteogenic regeneration. In this study, an injectable and photocurable composite hydrogel sustained-release system (GA-Exos) loaded with human umbilical cord blood-derived exosomes (UCB-Exos) was constructed. In vitro and in vivo experiments demonstrated that GA-Exos possesses excellent performance, enabling sustained release of exosomes for approximately 21 days. It significantly promotes the proliferation and differentiation of osteoblasts, upregulates the expression of osteogenic markers (e.g., RUNX2, ALP, and OPN), reduces the levels of pro-inflammatory cytokines (e.g., TNF-α and IL-1β), and inhibits inflammatory cell infiltration and osteoclast differentiation. mRNA sequencing and validation experiments confirmed that UCB-Exos inhibits the activation of the TLR4/NF-κB pathway by downregulating the expression of TLR4, LBP, and CD14, as well as the phosphorylation of P65. In conclusion, GA-Exos enhances periodontal bone regeneration through the regulation of the TLR4/NF-κB pathway, providing a novel and effective strategy for periodontitis treatment. This system is expected to break through the limitations of existing therapies and bring new insights for clinical applications.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 19","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13616824/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149069626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SUN11602 Accelerates Early Peripheral Nerve Regeneration in an Experimental Median Nerve Transection Model","authors":"Giovanna Casili,&nbsp;Igor Papalia,&nbsp;Alessio Ardizzone,&nbsp;Rossella Basilotta,&nbsp;Alfio Luca Costa,&nbsp;Paolo Titolo,&nbsp;Emanuela Esposito,&nbsp;Michele Rosario Colonna,&nbsp;Mariarosaria Galeano","doi":"10.1111/jcmm.71375","DOIUrl":"https://doi.org/10.1111/jcmm.71375","url":null,"abstract":"<p>Peripheral nerve injury (PNI) is one of the common life-altering disabilities resulting in various degrees of impairment in movement and sensation alongside apraxia and long-lasting pain. The gold standard for restoring the transected nerves is bridging the distal and proximal ends of disrupted autologous nerve using neurosurgical sutures. This approach is helpful, however nerve bridging is valid in pay of consuming healthy nerves and scarring phenomena in damaged site besides difficult donor nerve accessibility and extra surgery is required. Many studies have demonstrated that bFGF plays a pivotal role in the regeneration of PNI and severe spinal cord injury, exerting neuroprotective activity by binding to fibroblast growth factor receptors (FGFRs). Particularly, bFGF exhibits a high affinity for the receptor FGFR1, serving as its specific ligand. The novel synthetic compound SUN11602 exhibited neuroprotective activities like bFGF. Therefore, this study aimed to evaluate the effect of SUN11602 treatment in a rat experimental model of peripheral median nerve transection (MNT) and end-to-end suture. MNT was performed on rats, starting from 24 h following the surgical procedure, to orally treat, daily for 7 days, with SUN11602 at the dose of 2.5 mg/kg. The results showed that SUN11602 administration significantly reduced the alteration of PNI, promoting median nerve regeneration, suppressed mast cell accumulation, and resident macrophages. Also, SUN11602 reduced pro-inflammatory response of M1 macrophages, stimulated Schwann cell proliferation, and slowed down median nerve demyelination and fibrosis. Therefore, SUN11602 could be considered a valuable pharmacological strategy for MNT.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 19","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71375","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149048487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of a Lactylation-Related Gene Signature and Candidate Biomarkers for Dilated Cardiomyopathy","authors":"Xiaoyan Zhi,&nbsp;Miao Zhang,&nbsp;Luyao Xu,&nbsp;Yajing Zhang,&nbsp;Zhijun Zhang,&nbsp;Xiaohui Wang,&nbsp;Li Wang","doi":"10.1111/jcmm.71379","DOIUrl":"https://doi.org/10.1111/jcmm.71379","url":null,"abstract":"&lt;p&gt;Dilated cardiomyopathy (DCM) is a leading cause of heart failure. Due to its complex pathogenesis, effective treatment strategies remain limited. Therefore, it is particularly important to identify novel candidate biomarkers from the pathogenesis level. In recent years, lactylation modification plays an important role in various cardiovascular diseases; however, its specific involvement in DCM remains unclear. Therefore, it is of great significance to identify lactylation-related biomarkers associated with DCM to provide insights for future mechanistic investigations. The DCM gene expression datasets were obtained from the Gene Expression Omnibus (GEO) database. Differentially expressed genes and co-expression modules were identified using differential expression analysis and weighted gene co-expression network analysis (WGCNA). Lactylation-related gene sets (LRGs) were obtained from the MSigDB database. The intersection of these results was further analysed using machine learning algorithms: Least Absolute Shrinkage and Selection Operator (LASSO), Random Forest (RF), and Support Vector Machine (SVM). CIBERSORT algorithm was used to analyse the immune infiltration characteristics of DCM, and DCM was divided into two subtypes by unsupervised consensus clustering. Mendelian randomization (MR) analysis was employed to evaluate potential causal associations between the candidate genes and DCM or heart failure progression. Finally, the candidate genes were verified by the GSE57338 database and β&lt;sub&gt;1&lt;/sub&gt;-AA-induced heart failure model with DCM characteristics. Through comprehensive transcriptomic analysis integrating WGCNA and LRGs, 38 characteristic genes associated with DCM and lactylation were finally identified. Subsequently, 18 key genes were selected by machine learning. The risk prediction model based on these genes demonstrated good predictive performance for DCM. Immune infiltration analysis revealed dysregulated inflammatory responses in DCM patients, and 18 key genes were significantly related to CD8&lt;sup&gt;+&lt;/sup&gt; T cells, CD4&lt;sup&gt;+&lt;/sup&gt; T cells, neutrophils, and Natural killer T cell infiltration. Unsupervised consensus clustering divided DCM patients into two distinct subtypes (C1 and C2), with marked differences in gene expression. Subtype C1 was characterized by activation of CD8&lt;sup&gt;+&lt;/sup&gt; T cells and Natural Killer T cells, whereas C2 mainly exhibited CD4&lt;sup&gt;+&lt;/sup&gt; T cells and neutrophils activation. Furthermore, Mendelian randomization analysis suggested that &lt;i&gt;EXT1&lt;/i&gt; may be associated with heart failure, while &lt;i&gt;IER3&lt;/i&gt; was potentially associated with DCM. Finally, the external validation set GSE57338 and the heart failure model with DCM characteristics were used to verify the two genes identified. The results showed that &lt;i&gt;EXT1&lt;/i&gt; was up-regulated and &lt;i&gt;IER3&lt;/i&gt; was down-regulated. Based on the deep excavation of public database, combined with machine learning algorithm and Mendelian randomization, this study identi","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 18","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71379","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149048516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From Mechanical Cues to Lung Injury: Mapping the Global Landscape and Frontiers of Mechanoregulation Through Bibliometrics and LDA Analysis","authors":"Liyan Luo,&nbsp;Bin Yao,&nbsp;Qiqi Ruan,&nbsp;Yu He,&nbsp;Meiyu Zhang,&nbsp;Qing Ai,&nbsp;Qiuju Wu,&nbsp;Sile Hu,&nbsp;Ying Zhang,&nbsp;Feng Jiang,&nbsp;Yuan Shi","doi":"10.1111/jcmm.71377","DOIUrl":"https://doi.org/10.1111/jcmm.71377","url":null,"abstract":"<p>Pulmonary cells continuously experience mechanical forces, yet the rapid expansion of mechanotransduction research has fragmented the knowledge base and obscured how research priorities have shifted over time. We therefore mapped the intellectual structure and thematic evolution of pulmonary mechanoregulation using bibliometric analysis and latent Dirichlet allocation (LDA). A total of 1896 articles and reviews published during 2000–2025 were retrieved from the Web of Science Core Collection and analysed with CiteSpace and LDA. Annual output increased from fewer than 60 publications per year before 2012 to more than 160 in 2024. Citation, co-occurrence, clustering and burst analyses showed a transition from macroscopic injury paradigms, including cyclic stretch and alveolar overdistension, towards matrix stiffness. Yes-associated protein/transcriptional coactivator with PDZ-binding motif (YAP/TAZ) signalling, mechanosensitive ion channels and mechano-immunology. LDA resolved 15 latent topics; idiopathic pulmonary fibrosis and macrophage activation was the largest topic (254 documents), while temporal modelling showed increasing prominence of macrophage-centred fibrosis and viral-associated lung injury and declining emphasis on classical mechanical stretch. These findings define major knowledge gaps at the biomechanics–immunology interface and provide a quantitative roadmap for prioritizing biomimetic models, multi-omics integration and selective mechanotherapeutic strategies.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 18","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71377","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149048517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of CAR-T-Cell-Based Immunotherapies in Patients With Glioma: A Systematic Review and Meta-Analysis","authors":"Seyed Mostafa Mostafavi Zadeh,&nbsp;Sima Kalantari,&nbsp;Shaghayegh Shafiee Dastgerdi,&nbsp;Hossein Sharifi,&nbsp;Mahdi Mohammadi,&nbsp;Raheleh Roudi,&nbsp;Ahmad Shariftabrizi,&nbsp;Abolfazl Kalantari,&nbsp;Davoud Ahmadvand,&nbsp;Maryam Yazdi,&nbsp;Reza Nedaeinia","doi":"10.1111/jcmm.71358","DOIUrl":"https://doi.org/10.1111/jcmm.71358","url":null,"abstract":"<p>Glioma is an aggressive intracranial malignancy associated with a poor prognosis and high mortality. Chimeric antigen receptor (CAR) T-cell therapy has emerged as a promising immunotherapeutic approach for solid tumours; however, its application in glioma is constrained by several significant challenges. This study conducted a systematic review and meta-analysis to synthesise current methodologies and critically evaluate the clinical efficacy of CAR-T-cell-based immunotherapies in patients with glioma. A comprehensive literature search was performed across PubMed, Scopus, Web of Science and Embase using MeSH terms along with relevant keywords. The review process adhered to the PRISMA framework, applying clearly defined inclusion and exclusion criteria. Standard and augmented meta-analyses were employed to evaluate clinical outcomes, associated complications and potential publication bias. The study protocol was prospectively registered in PROSPERO under registration number CRD42022373297. Of 7723 retrieved records, 23 studies encompassing 306 patients with glioma met inclusion criteria. Efficacy analysis of 12 studies (<i>n</i> = 153 evaluable patients) demonstrated a pooled overall response rate of 16.9% (95% confidence interval [CI], 8.0%–32.2%), driven by complete responses in 8.1% (95% CI, 3.5%–17.8%) and partial responses in 13.1% (95% CI, 6.3%–25.5%) of patients. Stable disease was achieved in 46.6% (95% CI, 34.3%–59.3%); progressive disease was observed in 43.9% (95% CI, 27.7%–61.5%). Safety evaluation revealed grade ≥ 3 adverse events in 18.6% (95% CI, 10.0%–33.0%) of treated patients (<i>n</i> = 69 across 9 studies). Cytokine release syndrome affected 29.7% (95% CI, 9.3%–63.3%) (<i>n</i> = 80 across 9 studies), while immune effector cell-associated neurotoxicity syndrome developed in 12.9% (95% CI, 3.6%–37.0%) (<i>n</i> = 59 across 7 studies). This review demonstrated CAR-T-cell therapy to have promise in glioma, but evidence remains limited by heterogeneity and small samples. Larger standardised trials, systematic adverse-event reporting and mechanistic studies on constructs, dosing and combinations are needed. Biomarker discovery will refine patient selection, reduce risk and clarify the therapeutic role of CAR-T cells in glioma.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 18","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71358","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149048536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}