Cell Biology International最新文献

{"title":"B Cell Deficiency Protects Against the Development of c-MET and Beta-Catenin Driven Hepatocellular Carcinoma in Mice","authors":"Fang Wang,&nbsp;Eun Bi Lim,&nbsp;Rehan Mehta,&nbsp;Yee Ling Wu","doi":"10.1002/cbin.70227","DOIUrl":"https://doi.org/10.1002/cbin.70227","url":null,"abstract":"<p>Hepatocellular carcinoma (HCC), a lethal form of liver cancer, continues to show rising mortality rates despite advancements in immunotherapies. This highlights the need for more effective treatments. Recent studies linked the presence of B cells within human tumors, including HCC, to improved responses to immunotherapy and better prognoses. Specifically, tumor-infiltrating B cells have been associated with reduced cancer cell proliferation, suggesting that B cell-mediated responses may be harnessed as a potential therapeutic strategy against HCC. However, in advanced HCC, IL-10-producing regulatory B cells accumulate and promote tumor growth. These paradoxical findings on B cells in human HCC highlight the necessity for clarifying the specific functions of B cells in HCC development to develop B cell-targeted therapies. To investigate the role of B cells in HCC, we used B cell-deficient (muMT) mice and anti-CD20 antibodies to deplete B cells in WT mice. In both systems, we observed a strong protection against liver tumor formation upon HCC induction, indicating the presence of a potent anti-tumor effect in the absence of B cells before HCC induction. Additionally, depletion of B cells after tumor foci have formed in the liver at later stage of HCC also potently suppressed tumor growth. Functionally, depletion of CD4⁺ and CD8⁺ T cells partially restored susceptibility to tumor growth, suggesting that B cell depletion suppresses HCC development partly through enhanced T cell-mediated immunity. These findings reveal an underappreciated tumor-suppressing effect of B cells in HCC and suggest that targeting the mechanisms of B cell suppression may boost anti-tumor responses in HCC.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 11","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.70227","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149206052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SIRT6 Inhibits Glycolysis and Cementogenesis via Targeting IRS2","authors":"Liyuan Huang,&nbsp;Jie Shen,&nbsp;Zhebin Cheng,&nbsp;Jian Yuan,&nbsp;Peng Deng,&nbsp;Lijie Fan,&nbsp;Qianming Chen","doi":"10.1002/cbin.70226","DOIUrl":"10.1002/cbin.70226","url":null,"abstract":"<div>\u0000 \u0000 <p>Cementum shares similar characteristics with bone in terms of biochemical composition. Recent studies have reported that glycolysis is the main energy source driving osteoblast differentiation, but the role of glycolysis in cementoblast differentiation remains elusive. Previously, we found Sirtuin 6 (SIRT6) suppressed cementoblast differentiation and mineralization via inhibiting glucose transporter 1 (GLUT1), indicating that glycolysis may also be required for cementogenesis. However, the underlying mechanisms remain largely unknown. In this study, we observed that the expression of glycolytic enzymes increased progressively during cementoblast differentiation. Measurements of extracellular acidification rate, glucose uptake, lactate release, and gain-and-loss of function demonstrated that overexpressing SIRT6 in immortalized mouse cementoblasts (OCCM-30) suppressed cementoblast glycolysis. Mechanistically, chromatin immunoprecipitation assay results revealed that SIRT6 inhibits insulin receptor substrate 2 (IRS2) transcription by deacetylating histone H3 at lysine K9 (H3K9). Overexpression of IRS2 promoted OCCM-30 glycolysis and mineralization through phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway, whereas SIRT6 significantly inhibited PI3K/AKT pathway activity. Overall, our results demonstrate that SIRT6 inhibits IRS2 transcription by deacetylating histone H3K9, thereby reducing PI3K/AKT signaling-induced glycolysis and suppressing cementoblast mineralization.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bromodomain-Containing Protein 4 in Ischemia-Reperfusion Injury: Mechanisms, Preclinical Evidence, and Translational Challenges","authors":"Namrata Vadak,&nbsp;Lokesh Kumar Bhatt","doi":"10.1002/cbin.70223","DOIUrl":"10.1002/cbin.70223","url":null,"abstract":"<div>\u0000 \u0000 <p>Ischemia reperfusion (IR) injury is a major contributor to tissue damage and organ dysfunction following ischemic events and clinical interventions such as thrombolysis, revascularization, and transplantation, yet effective pharmacological strategies to limit this injury remain limited. Bromodomain-containing protein 4 (BRD4), an epigenetic reader that recognizes acetylated lysine residues to drive super-enhancer-associated transcription. Upregulated BRD4 has emerged as a key regulator of the inflammatory, endothelial, and cell death pathways underlying post-IR injury pathophysiology. Preclinical evidence across cerebral, cardiac, renal, and hepatic IR injury models indicates that BRD4 hyperactivation amplifies NFκB-dependent inflammatory signaling, while its pharmacological or genetic inhibition confers substantial tissue protection. This review synthesizes current mechanistic understanding of BRD4 in IR injury pathogenesis, evaluates emerging BET/BRD4-targeted therapeutic strategies, and outlines key translational challenges for advancing epigenetic pharmacology toward clinical application in IR-associated disorders.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"circCDR1as/miR-671-5p Axis Modulates Chondrocyte Ferroptosis and Macrophage Reprogramming via Targeting NCOA4 and TLR4 in Legg-Calvé-Perthes Disease","authors":"Quan Liu,&nbsp;Tao Luo,&nbsp;Jiachao Xiong,&nbsp;Xiaohua Jiang,&nbsp;Tonghua Zhou,&nbsp;Shiding Jiang,&nbsp;Gangan Liu,&nbsp;Xia Lan","doi":"10.1002/cbin.70207","DOIUrl":"10.1002/cbin.70207","url":null,"abstract":"<div>\u0000 \u0000 <p>Legg-Calvé-Perthes disease (LCPD) causes malformations of femoral head in children, which presents as a treatment challenge due to its unclear pathogenesis. This study aimed to investigate the influence of circCDR1as on LCPD and its related mechanisms. An in vivo LCPD model was established in spontaneously hypertensive rats (SHRs) and HMGB1-stimulated chondrocytes were used to mimic LCPD in vitro. We found that circCDR1as was up-regulated, while miR-671-5p was down-regulated in LCPD patients, which exhibited a negative correlation. Depletion of circCDR1as restored the proliferation and inhibited -ferroptosis of HMGB1-exposed chondrocytes, Mechanistically, circCDR1as silencing increased miR-671-5p expression that targeted NCOA4 mRNA to disrupt the NCOA4-FTH1 interaction-mediated ferritinophagy. Moreover, treatment with conditioned medium (CM) of circCDR1as-silenced chondrocytes repressed M1 macrophage polarization via enhancing miR-671-5p expression that subsequently targeted TLR4 mRNA to inactivate TLR4/NF-κB pathway. FUS was responsible for circCDR1as biogenesis via the direct binding to pre-CDR1as mRNA. Collectively, chondrocyte ferroptosis was triggered by FUS-activated circCDR1as via sponging miR-671-5p to enhance NCOA4-FTH1 interaction-mediated ferritinophagy, which resulted in M1 macrophage reprogramming via activating the TLR4/NF-κB pathway, thus promoting LCPD development.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tomatidine Exposure During Early Myogenesis Promotes Hypertrophy of C2C12 Muscle Cells Through Increased Nuclei Accretion","authors":"Marissa K. Caldow,&nbsp;Kristy Swiderski,&nbsp;John H. V. Nguyen,&nbsp;Emily S. Haber,&nbsp;Kyla J. H. Fritz,&nbsp;Gordon S. Lynch","doi":"10.1002/cbin.70224","DOIUrl":"10.1002/cbin.70224","url":null,"abstract":"<p>During myogenesis or myofiber regeneration, a proliferating muscle cell must leave the cell cycle, commit to differentiate, and fuse to neighboring myoblasts to create multinucleated myotubes, and eventually mature myofibers. These stages can be manipulated by exogenous factors including signaling molecules, mechanical cues, and nutrient supplementation. Supplementation with bioactives, such as tomatidine, can improve aspects of skeletal muscle health when evaluated using in vitro and in vivo models. In this study, a phenotypic characterization of the effects of tomatidine supplementation during proliferation, early maturation and differentiation, was undertaken in C2C12 muscle cells, cultured in growth medium, or alternatively induced to differentiate in medium supplemented with 10 µM tomatidine, for up to 4 days. Real-time impedance assays indicated tomatidine slowed C2C12 proliferation after 3 days of supplementation. Tomatidine supplementation from the onset of differentiation induced myotube hypertrophy within the first 48 h of maturation. Tomatidine-induced hypertrophy was driven by increased myonuclei fusion in developing myotubes with a concomitant increase in protein synthesis. Taken together, tomatidine's growth promoting effects on skeletal muscle cells identify its therapeutic potential for enhancing muscle regeneration and repair, by mechanisms that improve myofiber maturation and function.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.70224","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AI-Assisted Micronucleus Detection: A Critical Systematic Review With Quantitative Synthesis","authors":"Somnath Paul","doi":"10.1002/cbin.70225","DOIUrl":"10.1002/cbin.70225","url":null,"abstract":"<div>\u0000 \u0000 <p>Automated micronucleus (MN) scoring is increasingly proposed as a remedy for the subjectivity and labour burden of manual scoring yet reported performance has not been appraised systematically. This critical systematic review with quantitative synthesis follows PRISMA 2020. PubMed was searched for studies applying computer-vision, machine-learning, or deep-learning methods to MN determination against expert or expert-derived reference standards. Twenty-four records were screened and eight (2020–2025) met eligibility, spanning fluorescence microscopy, brightfield/Giemsa preparations, imaging flow cytometry, and whole-slide imaging. Because no study reported a reconstructable 2 × 2 table, bivariate diagnostic-accuracy meta-analysis was not possible; reported scalar metrics were instead logit-transformed and combined by DerSimonian–Laird random effects as explicitly descriptive summaries, with correlations combined on the Fisher-z scale. Summarized recall was 0.924 (95% CI 0.845–0.965) and precision 0.874 (0.790–0.927), both with near-total heterogeneity (I² ≈ 97%), whereas agreement between automated and reference counts was high and homogeneous (Pearson r = 0.920, 0.911–0.929; I² = 0%). Metric definition was the dominant moderator of heterogeneity; residual variation in precision tracked imaging modality rather than network architecture. Although there are bias regarding choice of staining or systems used for analysis as discussed here, current evidence supports a future of automated MN frequency estimation for regulatory and biomonitoring endpoints; but not object-level equivalence with expert scoring.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunometabolic Reprogramming in the Bone Marrow Niche: Mechanisms, Plasticity, and Precision Therapeutic Targeting","authors":"Adrian Khu,&nbsp;Alexander P Marpaung,&nbsp;Princella Halim,&nbsp;Amama Rani,&nbsp;Putri Cahaya Situmorang,&nbsp;Alexander Patera Nugraha,&nbsp;Fahrul Nurkolis,&nbsp;Rosy Iara Maciel de Azambuja Ribeiro,&nbsp;Bonglee Kim,&nbsp;Rony Abdi Syahputra","doi":"10.1002/cbin.70217","DOIUrl":"10.1002/cbin.70217","url":null,"abstract":"<div>\u0000 \u0000 <p>The bone marrow (BM) microenvironment is increasingly recognized as a dynamic immunometabolic niche that critically governs hematologic malignancies and BM-associated disorders, including acute myeloid leukemia (AML), multiple myeloma, myelodysplastic syndromes (MDS), metastatic infiltration, and aplastic anemia. At the core of this ecosystem, hematopoietic and leukemic stem cells (HSCs/LSCs) undergo profound immunometabolic reprogramming driven by complex interactions with stromal and immune components. Mesenchymal stromal cells (MSCs) enhance mitochondrial fitness and oxidative phosphorylation (OXPHOS) in malignant cells via cysteine supply and mitochondrial transfer, while endothelial cells regulate niche retention and survival through CXCL12 and adhesion molecules such as E-selectin. Adipocytes further support tumor bioenergetics by supplying free fatty acids (FFAs) that fuel fatty acid oxidation (FAO), whereas M2-polarized macrophages reinforce immunosuppressive and metabolic adaptations through arginase-1 activity and FAO-dependent pathways. These coordinated interactions promote a metabolically flexible phenotype characterized by shifts between OXPHOS and glycolysis, activation of FAO and glutamine metabolism, and engagement of one-carbon metabolism, collectively sustaining malignant progression. Concurrently, the BM niche establishes a profoundly immunosuppressive milieu mediated by myeloid-derived suppressor cells (MDSCs), regulatory T cells (Tregs), indoleamine 2,3-dioxygenase 1 (IDO1)-driven kynurenine signaling, lactate-induced acidosis, and HIF-1α-mediated pseudo-hypoxia, which together impair anti-tumor immunity and facilitate disease persistence. Importantly, these immunometabolic dependencies provide actionable therapeutic vulnerabilities. Targeted strategies, including IDH1/2 inhibitors (ivosidenib and enasidenib), BCL-2 inhibition (venetoclax), niche-disrupting agents (plerixafor and uproleselan), OXPHOS inhibitors (IACS-010759 and metformin), and immunometabolic interventions such as IDO1 inhibitors and CAR-T therapies represent emerging precision approaches. Collectively, this integrative framework highlights the BM microenvironment as a central regulator of cancer cell metabolism and immune evasion, underscoring the potential of immunometabolic targeting to overcome therapeutic resistance and enable next-generation precision medicine in hematologic diseases.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149104539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Curcumin-Loaded Nanospheres Attenuate Fine Dust (PM10)-Induced Cellular Toxicity by Suppressing Reactive Oxygen Species-Dependent Signaling in Human Keratinocytes","authors":"Ju-Yeon Lee,&nbsp;Ji-Yeon Park,&nbsp;Seo-Young Ju,&nbsp;Yong Li,&nbsp;Won-Kyo Jung,&nbsp;Jae-Young Je,&nbsp;Sei-Jung Lee","doi":"10.1002/cbin.70222","DOIUrl":"10.1002/cbin.70222","url":null,"abstract":"<div>\u0000 \u0000 <p>Curcumin has various biological effects, but its poor aqueous solubility limits its practical use. This study investigated the effects of curcumin-loaded nanospheres (CN) on cellular injury induced by fine dust (PM₁₀) in HaCaT human keratinocytes and examined the signaling mechanisms involved. PM₁₀ exposure significantly decreased cell viability, whereas CN at 10⁻⁴ μg/mL significantly restored cell viability and showed a protective effect at a lower concentration than unformulated curcumin. PM₁₀ rapidly increased intracellular reactive oxygen species (ROS) levels, followed by activation of extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase (MAPK), and nuclear factor-kappa B (NF-κB). CN reduced ROS generation and inhibited activation of these signaling molecules. CN also restored the altered Bax/Bcl-2 balance, decreased caspase-3 cleavage, and reduced caspase-1-dependent IL-1β processing in PM₁₀-exposed cells. Treatment with NAC and inhibitors of ERK, p38 MAPK, NF-κB, and caspase-1 further reduced PM₁₀-induced cytotoxic and inflammatory responses, supporting the involvement of these pathways. Overall, CN attenuated fine dust-induced cellular toxicity in keratinocytes by suppressing ROS-dependent MAPK/NF-κB signaling and downstream apoptotic and inflammatory responses.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149104560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sister Chromatid Cohesion: A Multilayered Regulatory Network Beyond the Cohesin Ring","authors":"Jianing Fan,&nbsp;Jinghan Gao,&nbsp;Mengjie Chen,&nbsp;Limin Deng,&nbsp;Siyu Yuan,&nbsp;Longyuan Bu,&nbsp;Guoshuang Li,&nbsp;Lingluo Chu","doi":"10.1002/cbin.70220","DOIUrl":"10.1002/cbin.70220","url":null,"abstract":"<div>\u0000 \u0000 <p>Sister chromatid cohesion, mediated by the cohesin complex, ensures faithful chromosome segregation by providing the mechanical resistance required for bipolar spindle attachment. While the cohesin ring serves as the central executor, cohesion is regulated by a remarkably intricate multi-layered network extending far beyond the core complex. This review synthesizes current understanding of cohesion by integrating classical cohesin-centric regulation with emerging evidence implicating diverse non-cohesin factors, including DNA and RNA helicases, spliceosome components, microtubule-associated proteins, and post-translational modifications. We also examine the often-overlooked contribution of DNA catenation to sister chromatid association and discuss how kinase-phosphatase networks, chaperones, and non-coding RNAs coordinate cohesion establishment, maintenance, and dissolution. Throughout this review, we emphasize that the cohesin complex remains the central mediator; the additional layers discussed here modulate, stabilize, or complement its function rather than replacing it. By integrating these diverse layers into a unified framework, we highlight unresolved questions and provide a roadmap for future investigations into the molecular mechanisms that ensure genomic stability.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149104613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proteomic Signatures of Noise-Induced Hearing Loss in the Mouse Cochlea","authors":"Ana Carla Batissoco,&nbsp;Danillo Alencar-Coutinho,&nbsp;Ana Carolina Ferreira-Scatone,&nbsp;Stella Diogo-Cavassana,&nbsp;Jeanne Oiticica,&nbsp;Karina Lezirovitz,&nbsp;Ricardo Ferreira Bento","doi":"10.1002/cbin.70218","DOIUrl":"10.1002/cbin.70218","url":null,"abstract":"<p>Hearing loss affects over 1.5 billion people worldwide and has substantial social, educational, and economic consequences. Although genetic studies have identified numerous hearing-loss-associated genes, the molecular changes accompanying noise-induced hearing loss (NIHL) remain incompletely understood. We characterized the adult mouse cochlear proteome following damaging noise exposure using nano-LC–MS/MS and an integrative bioinformatics workflow. Comparative profiling of normal-hearing and NIHL cochleae identified 1742 proteins and an 80-protein NIHL-associated signature comprising 49 quantitatively defined differentially abundant proteins and 31 condition-specific proteins. These proteins were organized into five functional groups encompassing metabolic and mitochondrial function, protein synthesis and ribonucleoprotein complexes, structural and synaptic organization, cell polarity and cytoskeletal remodeling, and regulatory and stress-responsive functions. Representative alterations included reduced HSPA9, a mitochondrial chaperone involved in protein homeostasis; changes in the RNA-associated proteins PRMT1 and CIRBP; reduced HAPLN1, associated with extracellular matrix organization; and altered MAP2K2, a signaling protein related to cell polarity; and increased SYNJ2. Comparison with an independent cochlear proteomic data set identified 39 of the 80 proteins as dysregulated, with 22 showing concordant directional changes. Single-cell transcriptomic mapping provided cellular context for 74 of the 80 protein-associated genes, while human genetic and disease annotations supported the prioritization of selected proteins associated with hearing or ear phenotypes. Together, these findings define a proteomic landscape of the noise-exposed cochlea and identify molecular candidates and cellular processes for further investigation of NIHL.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13628698/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149104548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}