Cell Biology International最新文献

{"title":"Unlocking Cancer Immunity: Deciphering the Role of Tumor-Associated Macrophages in Modulating Immunosuppressive Tumor Microenvironment","authors":"Durre Aden,&nbsp;Samreen Zaheer,&nbsp;Sufian Zaheer","doi":"10.1002/cbin.70156","DOIUrl":"10.1002/cbin.70156","url":null,"abstract":"<div>\u0000 \u0000 <p>The tumor microenvironment (TME) significantly influences cancer progression, metastasis, and therapeutic resistance. Among the diverse cellular constituents of the TME, tumor-associated macrophages (TAMs) are critical players that support tumor growth, facilitate angiogenesis, and suppress anti-tumor immune responses. Metabolic reprogramming of TAMs has emerged as a pivotal mechanism driving their immunosuppressive and pro-tumourigenic functions. This extensive review delves into the intricate metabolic pathways involved in TAM reprogramming, the underlying molecular mechanisms, and the impact of these metabolic alterations on the TME. We also explore potential therapeutic strategies targeting TAM metabolism to reprogram the TME and enhance cancer immunotherapy efficacy.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147618478","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":"Synergistic Combinations for Improved Therapeutic Outcomes in Triple Negative Breast Cancer.","authors":"Avani Jha, Shashi Kumar Sampangin Venkatesh, Anuradha Singh, Naga Rajiv Lakkaniga","doi":"10.1002/cbin.70157","DOIUrl":"https://doi.org/10.1002/cbin.70157","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is a biologically aggressive and clinically challenging subtype of breast cancer, defined by the absence of hormone receptors and HER2 amplification. This limits the applicability of targeted therapies and contributes to poor prognosis. Emerging evidence underscores the therapeutic importance of rationally designed combination regimens capable of generating synergy by simultaneously engaging complementary oncogenic vulnerabilities. Synergistic combinations, such as dual blockade of PI3K/AKT and MAPK signalling, co-inhibition of DNA repair pathways (PARP with ATR or WEE1), and the integration of immune checkpoint inhibitors with chemotherapy, angiogenesis blockade, or epigenetic modifiers, enhance tumour control by disrupting adaptive resistance, promoting immunogenic cell death and remodelling the tumour microenvironment. These strategies exploit synthetic lethality and reverse immune exclusion, often yielding effects greater than the sum of individual agents. Increasing clinical evidence suggests that synergy-based therapeutic design may improve outcomes in TNBC by converting transient responses into durable remissions. Herein, we review the mechanistic insights and translational data that support synergy-driven polytherapy as a foundational paradigm in the evolving management of TNBC.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 4","pages":"e70157"},"PeriodicalIF":3.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697716","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":"CAR-NK Cell Biology and Engineering for Solid Tumors, With a Focus on Lung Cancer.","authors":"Xiao Lyu, Na Zhu, Ruijuan Guo, Jurbek Yuldasheyv","doi":"10.1002/cbin.70152","DOIUrl":"10.1002/cbin.70152","url":null,"abstract":"<p><p>Over the past decade, chimeric antigen receptor (CAR) T-cell therapy has revolutionized cancer immunotherapy, demonstrating remarkable efficacy in treating relapsed or refractory hematologic malignancies across both pediatric and adult populations. In parallel, CAR-engineered natural killer (CAR-NK) cells have emerged as a complementary and promising alternative to CAR-T therapy, offering several inherent advantages. Unlike CAR-T cells, CAR-NK cells operate independently of major histocompatibility complex (MHC) compatibility and are associated with a lower risk of adverse immune reactions. They also provide practical benefits, such as the potential for standardized, \"off-the-shelf\" therapeutic formulations. Consistent and encouraging outcomes have been reported with CAR-NK cell therapy in hematologic cancers; however, their success against solid tumors remains constrained by multiple challenges, including limited tumor infiltration, suboptimal trafficking, and the immunosuppressive characteristics of the tumor microenvironment. Importantly, lung cancer presents indication-specific barriers to cellular immunotherapy, including profound inter and intratumoral heterogeneity, a highly immunosuppressive pulmonary tumor microenvironment, and a narrow safety margin in a vital organ where inflammation or edema can rapidly impair gas exchange. These factors limit the depth and durability of responses achieved with current systemic modalities in a substantial fraction of patients and also constrain adoptive cell therapy in thoracic malignancies. Therefore, lung cancer represents both a compelling and stringent setting to develop safer and more durable engineered cellular platforms such as CAR-NK cells. Lung cancer, one of the most prevalent and lethal malignancies worldwide, still depends largely on conventional treatment modalities such as surgery, chemotherapy, radiotherapy, and targeted agents. Accordingly, we organize this review around lung cancer-specific design constraints, antigen heterogeneity/escape, impaired trafficking into pulmonary tumors, an immunosuppressive lung microenvironment, and a narrow pulmonary safety window, and map each constraint to actionable CAR-NK engineering and combination strategies.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 4","pages":"e70152"},"PeriodicalIF":3.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688568","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":"ORC6 Exerts Oncogenic Functions in Kidney Renal Clear Cell Carcinoma by Regulating Cell Proliferation and Apoptosis: A Prognostic and Immunological Indicator for Future Clinical Interventions.","authors":"Yang Yu, Jing Zhai, Shiwei Liu, Yi Wang, Guanxiong Ding","doi":"10.1002/cbin.70159","DOIUrl":"https://doi.org/10.1002/cbin.70159","url":null,"abstract":"<p><p>With the application of precise clinical interventions in tumor treatment, it is of great value to explore novel biomarkers and their underlying molecular mechanisms. In this paper, we firstly explored the prognostic, immunological features, functions, and potential mechanisms of ORC6 in kidney renal clear cell carcinoma (KIRC) via single-cell and bulk RNA sequencing. Single-cell and bulk RNA sequencing data related to ORC6 data in KIRC were acquired from shared online databases. Spearman correlation analyses were carried out to investigate the relationships between ORC6 expression and interested targets, including tumor mutation burden (TMB), tumor microenvironment, and immunotherapy responses. Besides, the expression pattern of ORC6 and its role in KIRC were verified in vitro experiments. Also, the potential mechanisms and regulatory upstream of ORC6 in KIRC were explored. ORC6 was up-regulated in KIRC samples compared with normal tissues, validated by PCR analyses of KIRC tissues and cell lines (p < 0.05). Single-cell RNA sequencing analysis showed that ORC6 was mainly expressed in immune T cells. Survival and Cox regression analysis showed ORC6 had prognostic values in KIRC (p < 0.05). Correlation analysis revealed ORC6 was strongly correlated with immunity and immunotherapy sensitivity (p < 0.05). Further experiments in vitro indicated that ORC6 could regulate the cell proliferation/apoptosis of KIRC. Finally, a putative long non-coding RNA (LncRNA)/RNA binding protein (RBP)/ORC6 regulatory network was identified to explore ORC6-related potential upstream regulatory mechanisms in KIRC. In conclusion, ORC6 might play oncogenic roles in KIRC and regulate cell proliferation/apoptosis in KIRC. Furthermore, ORC6 showed significant associations with immunity and potential immunotherapy sensitivity. These findings provided a foundation for future studies evaluating the clinical significance of ORC6 in KIRC.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 4","pages":"e70159"},"PeriodicalIF":3.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697696","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":"TDP43 and hnRNP K Regulate Alternative Splicing of DNAJC5.","authors":"Helder Y Nagasse, Ellen K Okuda, Patricia P Coltri","doi":"10.1002/cbin.70158","DOIUrl":"10.1002/cbin.70158","url":null,"abstract":"<p><p>Alternative splicing is a finely regulated process which defines the final maturation of pre-mRNAs. Modulation of trans-acting spliceosome proteins changes specific patterns of splicing and contributes to the development of diseases. During Amyotrophic Lateral Sclerosis (ALS) disease progression, loss of nuclear trans-acting splicing protein TDP43 leads to accumulation of cryptic exons in mRNAs, which inhibits expression of proteins and aggravates the disease. One of the affected genes is DNAJC5, which codes for a protein responsible for clearance of misfolded proteins in the cytoplasm. We first observed that TDP43 knockdown regulates DNAJC5 transcript splicing. A similar phenotype was observed upon hnRNP K knockdown. We hypothesized canonical splicing of DNAJC5 is dependent on the activity of both TDP43 and hnRNP K. Our results confirmed TDP43 and hnRNP K interaction is dependent on RNA. We also confirmed that DNAJC5 canonical splicing is dependent on its internal TDP43 and hnRNP K binding sites. Taken together, our work enrolls both TDP43 and hnRNP K on splicing regulation of DNAJC5 transcript, affecting activity of the protein encoded by DNAJC5 on endosomal traffic. As a result, activity of both TDP43 and hnRNP K and their association are important for ALS progression.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 4","pages":"e70158"},"PeriodicalIF":3.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13081507/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688535","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":"Mitotic Bookmarking and Chromosomal Coating by Nuclear Receptors: Segregating Myth & Reality","authors":"Sheeba Rizvi,&nbsp;Rakesh K. Tyagi","doi":"10.1002/cbin.70155","DOIUrl":"10.1002/cbin.70155","url":null,"abstract":"<div>\u0000 \u0000 <p>Traditionally viewed as a transcriptionally inert phase, mitosis is now recognized as a critical window during which cells preserve their transcriptional memory. This is executed through selective retention of regulatory proteins on the condensed mitotic chromatin. Two distinct but overlapping mechanisms of mitotic bookmarking and chromosomal coating are proposed to facilitate the faithful transmission of cellular traits and phenotypes across multiple cell divisions. However, their mechanistic boundaries and physiological relevance remain debated. We propose that ‘chromosomal coating’ represents a genome-wide, non-sequence-specific scanning mechanism that increases the probability for ‘mitotic bookmarking’, the site-specific, functional retention of factors at regulatory elements in the chromatin. The current review explores these mechanisms with a specific focus on nuclear receptors (NRs), a family of ligand-modulated transcription factors (TFs) central to development, metabolism, and endocrine regulation. Emerging evidence suggests that NRs associate with mitotic chromatin exhibiting the bookmarking phenomenon and also participate in broader receptor-chromatin interactions <i>via</i> chromosomal coating during mitosis. We also use FOXA1 to draw parallels with nuclear receptors, emphasizing how similar principles may underlie other TF-mediated chromosomal coating and bookmarking events. By integrating current findings from genomics, imaging-based approaches, and chromatin profiling techniques, we aim to segregate myth from reality in the context of NR-chromatin interactions and discuss implications for gene regulation and endocrine-related pathologies.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147510121","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":"Concurrent Ferroptosis and Apoptosis in Resveratrol-Treated Glioblastoma Cells: Relevance With NRF2 Downregulation and Oxidative Stress","authors":"Ali Farman,&nbsp;Xu Zheng,&nbsp;Mo-Li Wu,&nbsp;Li Hong,&nbsp;Wang Qian,&nbsp;Jia Liu","doi":"10.1002/cbin.70153","DOIUrl":"10.1002/cbin.70153","url":null,"abstract":"<div>\u0000 \u0000 <p>Glioblastomas (GBMs) are lethal brain tumors characterized by rapid growth and resistance to standard treatment. Resveratrol (RES) increases the levels of reactive oxygen species (ROS) and induces cell death in sensitive GBM cells. However, the death patterns induced by RES and their relevance to NFE2-related factor 2 (NRF2) remain unclear. The current study aimed to address these issues using RES-sensitive U251 and less-sensitive LN428 GBM cell lines, as well as an orthotopic GBM xenograft rat model. In silico analysis revealed high NRF2 expression in GBM tissues and a strong correlation with tumor progression in the TCGA dataset. After 48 h of 100 µM RES treatment, NRF2 levels remained stable in LN428 cells but significantly decreased by 2.3-fold in U251 cells, accompanied by suppressed growth and NRF2-regulated and ferroptosis-related xCT and GPX4 downregulation. Elevated Fe^2+, ROS levels, lipid peroxidation, and ferroptotic frequency were evidenced in RES-treated U251 cells; meanwhile, apoptosis and reduced NRF2-HO-1 expression were also evident in U251 cells. Combined treatment with Ferrostatin-1 and Z-VAD FMK rescued 60% of U251 cells compared to RES-treated counterparts. In vivo, lumbar puncture (LP) administration of RES induced both ferroptosis and apoptosis in rat orthotopic GBM xenografts. These findings highlight the dual cell death induced by RES in sensitive GBM cells and identify NRF2 signaling status as a novel determinant of cellular response to RES treatment.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 3","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147467270","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":"γδTreg/γδTh17 Cell Imbalance Drives Xanthine-Mediated Metabolic Dysfunction in Restraint Stress-Induced Anxiety-Like Behavior","authors":"Xiang Xue,&nbsp;Chong Tang,&nbsp;Na Yan,&nbsp;Xiaoling Lai,&nbsp;Qianqin Li,&nbsp;Enze Li","doi":"10.1002/cbin.70149","DOIUrl":"10.1002/cbin.70149","url":null,"abstract":"<div>\u0000 \u0000 <p>Anxiety disorder is a highly prevalent psychiatric disorder, yet the role of γδT17/γδTreg-mediated metabolism in its pathogenesis remains unclear. We employed chronic restraint stress (RS) to establish an anxiety-like behavior mouse model and assessed behavioral changes. LC-MS/MS was employed to analyze the serum metabolomics of mice. RS mice were intraperitoneally injected with xanthine and brain tissue was taken for immunofluorescence. Here, Nissl staining and behavioral experiments respectively confirmed the neuronal pathology and behavioral alterations in RS mice. Flow cytometry and immunofluorescence revealed a significant imbalance in γδT17 and γδTreg cell populations in RS mice, characterized by an increase in γδT17 cells accompanied by a decrease in γδTreg cells. Deprivation of γδT17 cells using an αIL-17 antibody significantly ameliorated anxiety-like behavior in RS mice, whereas γδTreg cells deprivation using an αFoxP3 antibody exacerbated anxiety in RS mice. Metabolomic profiling identified profound alterations in the serum metabolic landscape of RS mice, particularly in purine and nucleotide metabolism pathway. Among the differentially abundant metabolites, xanthine and hypoxanthine were significantly increased in RS mice, and γδT17 cell depletion reversed these elevations. Exogenous xanthine administration exacerbated neuronal damage in RS mice, while immunofluorescence confirmed that xanthine primarily affects neurons rather than astrocytes. ELISA demonstrated that xanthine crosses the blood–brain barrier and accumulates in the brains of RS mice. Collectively, this study identifies a novel γδT17/γδTreg–xanthine axis linking immune dysregulation and metabolic reprogramming to anxiety-like behavior, providing new mechanistic insights and potential therapeutic targets for anxiety disorders.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 3","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147456026","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":"Sex Hormones Regulate T-Cell Responses Associated With Rheumatoid Arthritis","authors":"Soham Chowdhury,&nbsp;Debajyoti Ghosh,&nbsp;Sougata Roy Chowdhury","doi":"10.1002/cbin.70150","DOIUrl":"10.1002/cbin.70150","url":null,"abstract":"<div>\u0000 \u0000 <p>Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by sustained synovial inflammation contributing to bone erosion and loss of joint function. The pathological response of infiltrated T cell subsets, followed by the formation of ectopic lymphoid microstructures in the synovial tissue, promotes RA progression and exacerbates disease severity. Two major hallmarks of RA pathogenesis are dysregulated peripheral tolerance and aberrant pro-inflammatory responses due to the secretion of pro-inflammatory cytokines within the RA synovium. Interestingly, regulatory T cells (Tregs) and Th2, which play a vital role in maintaining immune homeostasis and peripheral tolerance, are reduced in numbers or become functionally impaired within the RA synovium, resulting in Th1/Th2 and Th17/Treg imbalance. Additionally, CD8+ T cells have also emerged as major mediators of synovial inflammation and autoantibody production in RA. Women display higher susceptibility to developing RA, and the chances of disease pathogenesis increase steadily from menarche to menopause, possibly due to a decline in sex-hormone levels. Although the decline in female sex hormones has been implicated in aberrant T cell responses and RA progression, the impact of hormone levels on the molecular signaling pathways regulating T cell differentiation and homeostasis, and subsequently the disease pathogenesis in premenopausal and postmenopausal women, remains incompletely understood. Hence, this review aims to provide a comprehensive understanding of the differential control of sex hormone levels in regulating T cell responses, including T cell plasticity and functions associated with RA progression. We further discuss the underlying signaling mechanisms where declining postmenopausal sex-hormone levels promote aberrant T-cell activation and effector functions within the RA synovium, thereby disrupting peripheral tolerance and immune homeostasis, and contributing to RA pathogenesis. A critical understanding of sex hormone-mediated regulation of T cell responses associated with RA may unveil novel hormone-targeted therapeutic strategies to limit disease progression.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 3","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147376080","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":"AJUBA Attenuates Pathological Cardiac Hypertrophy by Enhancing NEDD4-Mediated Ubiquitination and Degradation of DVL2","authors":"Liqin Zhuang,&nbsp;Jun Xiong,&nbsp;Wei Zhou,&nbsp;Yaxin Gong,&nbsp;Huihong Zeng,&nbsp;Jinying Tong","doi":"10.1002/cbin.70151","DOIUrl":"10.1002/cbin.70151","url":null,"abstract":"<div>\u0000 \u0000 <p>Cardiac hypertrophy, a response to pathological stimuli, eventually progresses to heart failure (HF). AJUBA is a multifunctional protein expressed in various human tissues, serving as a critical modulator of cellular processes and signalling pathways involved in cardiac hypertrophy and remodelling. It plays significant roles in cellular signalling, gene transcription, and cytoskeletal organisation, modulating cardiac growth, inflammation, and cell survival. However, the precise function of AJUBA in cardiac hypertrophy remains unclear. In the present study, we examined its function as a novel regulator of HF and pathological cardiac hypertrophy. AJUBA expression was significantly decreased in patients with HF and in mouse models subjected to pressure overload. Using AJUBA knockout mice, we found that compromised echocardiographic function and increased heart weight-to-body weight ratios are signs of worsened cardiac hypertrophy and dysfunction due to AJUBA deficiency. Mechanistic studies revealed that AJUBA acts as a co-activator of C/EBPβ, enhancing the transcription of NEDD4, which promotes the ubiquitin-mediated degradation of DVL2. This prevents the activation of the Ca²⁺/calmodulin-dependent protein kinase II/histone deacetylase 4 signalling pathway, which is essential for heart hypertrophy. Furthermore, during in vitro experiments, AJUBA overexpression reduced hypertrophic responses in cardiomyocytes, whereas AJUBA silencing intensified these changes. Therefore, these findings underscore the protective role of AJUBA in maintaining cardiac homeostasis. Targeting AJUBA or its associated pathways may offer viable therapeutic strategies for regulating HF and cardiac hypertrophy.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 3","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147372247","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}