Cell Biology International最新文献

{"title":"SET Interacts With CENP-A and HJURP to Ensure Proper Mitotic Progression in Human Cells","authors":"Ying Wang,&nbsp;Chengcheng Hu,&nbsp;Xinyang Wang,&nbsp;Fangyuan Xiong,&nbsp;Xuebiao Yao,&nbsp;Zhikai Wang","doi":"10.1002/cbin.70221","DOIUrl":"10.1002/cbin.70221","url":null,"abstract":"<div>\u0000 \u0000 <p>Centromeres are specialized chromosomal loci that ensure faithful chromosome segregation during mitosis, a function that depends on the precise localization of the histone H3 variant centromere protein A (CENP-A) within centromeric chromatin. CENP-A deposition is tightly regulated by assembly factors, including HJURP; however, the complete regulatory network remains incompletely defined. Using CENP-A immunoprecipitation coupled with mass spectrometry, we identified SET, a multifunctional chromatin-associated protein involved in transcription and nucleosome assembly, as one of the most enriched proteins in CENP-A immunoprecipitates, suggesting an association between SET and CENP-A. Here, we investigated this association and its functional significance. Reciprocal co-immunoprecipitation assays showed that SET associates with both CENP-A and HJURP. Immunofluorescence analysis revealed that SET localizes to centromeres and that SET depletion reduces centromeric CENP-A enrichment. Live-cell imaging further showed that SET depletion causes chromosome alignment defects and prolonged mitotic arrest. Together, these findings identify SET as a previously unrecognized regulator of the CENP-A-HJURP axis and suggest that SET supports proper CENP-A localization at centromeres and faithful mitotic progression. This study expands our understanding of the regulatory network that maintains centromere identity.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079890","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":"Fisetin Attenuates Human Macrophage Polarization and Pro-Inflammatory Responses via NLRP3 and NF-κB/MAPK Suppression","authors":"Nattaya Onpan,&nbsp;Chanchao Lorthongpanich,&nbsp;Pakpoom Kheolamai,&nbsp;Pimjai Chingsuwanrote,&nbsp;Napachai Rodboon,&nbsp;Sudjit Luanpitpong,&nbsp;Chonticha Saisawang,&nbsp;Surapol Issaragrisil","doi":"10.1002/cbin.70216","DOIUrl":"10.1002/cbin.70216","url":null,"abstract":"<p>Natural compounds with anti-inflammatory properties are increasingly explored as therapeutic agents due to their lower risk of side effects compared with conventional drugs. Fisetin, a dietary bioflavonol abundant in fruits and vegetables, exhibits anti-inflammatory activity in several cell types, including murine macrophages. However, its effects on human macrophages remain unclear. In this study, human pro-inflammatory M1 macrophages were generated from THP-1 monocytes using PMA, LPS, and IFN-γ. The effects of fisetin on cytokine and chemokine secretion, reactive oxygen species (ROS) production, apoptosis, and phagocytic activity were evaluated. In addition, the NF-κB, MAPK, and NLRP3 inflammasome pathways were analyzed. This study shows that fisetin pre-treatment significantly suppressed LPS/IFN-γ-induced secretion of pro-inflammatory cytokines (IL-6, TNF-α, IL-1β, IL-8) and chemokines (MCP-1, CCL5, CXCL9, CXCL10). It also reduced ROS generation, NLRP3 inflammasome activation, and phagocytic activity. Mechanistically, fisetin inhibited NF-κB activation as well as JNK/MAPK and p38/MAPK signaling, indicating that its anti-inflammatory actions are mediated through multiple pathways. Importantly, fisetin did not affect the viability or proliferation of THP-1-derived macrophages, suggesting that reduced cytokine release was primarily due to attenuation of macrophage polarization rather than cytotoxicity. Fisetin attenuates inflammatory responses in human M1 macrophages through suppression of NF-κB, MAPK, and NLRP3 inflammasome signaling. By limiting cytokine release, ROS production, and phagocytic activity without impairing cell survival, fisetin emerges as a promising natural candidate for managing chronic inflammatory disorders, including atherosclerosis, neurodegenerative diseases, and inflammatory bowel disease.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13621920/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149073636","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":"Mechanobiology of Osteoarthritis: Interactions Between Mechanical Stress, Inflammation, and Joint Remodeling","authors":"Jiawei Shen,&nbsp;Zelin Zhou,&nbsp;Yu Hang Yiu,&nbsp;Zhifei Xie,&nbsp;Na Liu,&nbsp;Shawn He","doi":"10.1002/cbin.70219","DOIUrl":"10.1002/cbin.70219","url":null,"abstract":"<div>\u0000 \u0000 <p>Osteoarthritis (OA) is a multifactorial whole joint disease characterized by cartilage degeneration, subchondral bone remodeling, synovial inflammation, and progressive functional impairment. Increasing evidence suggests that OA is not simply a wear and tear disorder, but a mechanobiological disease in which abnormal mechanical stress interacts with inflammatory and metabolic pathways to drive joint degeneration. This review summarizes recent advances in the mechanobiology of OA, focusing on the interplay between mechanical stress, inflammation, and joint remodeling. We discuss the major mechanosensing and mechanotransduction mechanisms in chondrocytes, including primary cilia, integrins, the cytoskeleton, the LINC complex, and mechanosensitive ion channels such as TRPV4, TRPM7, and PIEZO channels. We further examine how these pathways regulate extracellular matrix homeostasis, chondrocyte fate, and the transition from anabolic maintenance to catabolic degeneration, as well as how altered joint loading affects subchondral bone remodeling through osteocyte responses, the RANK/RANKL/OPG axis, and Wnt/β-catenin signaling. Particular attention is given to the crosstalk between mechanotransduction and inflammatory signaling, including NF-κB, MAPK, and macrophage polarization pathways, which together amplify structural damage under pathological loading. Finally, we highlight emerging therapeutic strategies based on biomechanical modulation and mechano-inflammatory targeting. A better understanding of these integrated mechanisms may provide new insight into OA pathogenesis and support the development of disease-modifying therapies.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149073643","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":"Polymyxin B Attenuates Sepsis-Induced Acute Kidney Injury by Activating a SUMO1-p65 “Molecular Brake” in Kidney Organoids","authors":"Qing Wang,&nbsp;Na Xue,&nbsp;Tian Yu,&nbsp;Yanxia Li,&nbsp;Xiyun Bian,&nbsp;Xiaoming Hou,&nbsp;Lin Dou,&nbsp;Qingguo Feng,&nbsp;Xiaozhi Liu","doi":"10.1002/cbin.70209","DOIUrl":"10.1002/cbin.70209","url":null,"abstract":"<div>\u0000 \u0000 <p>Sepsis-induced acute kidney injury (SAKI) is a deadly complication in critical care, driven by a devastating inflammatory surge and loss of renal parenchymal integrity. While polymyxin B (PMB) is traditionally utilized as a last-resort antibiotic, emerging evidence suggests it possesses non-canonical immunomodulatory properties that remain mechanistically elusive. This study investigated the intracellular post-translational modification (PTM) pathways through which PMB mitigates renal inflammation. We employed a dual-model approach utilizing 3D mouse kidney organoids and SUMO1^−/− mouse models to examine the genetic dependency of PMB-mediated renoprotection. Transcriptomic profiling revealed that PMB robustly suppresses NF-κB -driven inflammatory programs in wild-type (WT) organoids, specifically reducing the expression of <i>Cxcl1</i> and <i>Il6</i>. In contrast, this anti-inflammatory efficacy was abrogated in SUMO1-deficient models, where the pharmacological response shifted toward metabolic pathways, such as cholesterol metabolism. Mechanistically, PMB promotes SUMO1 conjugation to the NF-κB p65 subunit, functioning as a “molecular brake” that limits p65 hyperphosphorylation and transcriptional activation. Together, these results identify the SUMO1-p65 axis constitutes a pivotal regulatory checkpoint for PMB-mediated immunomodulation. This study establishes a novel therapeutic paradigm by underscoring the promise of targeting PTM pathways to alleviate septic organ dysfunction.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149069243","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 Antitumor Effects and Reduced Systemic Toxicity of Berberine Chloride Combined With Cisplatin in a Female BALB/c Mouse Xenograft Model","authors":"Abir Salek,&nbsp;Haifa Messai,&nbsp;Mouna Selmi,&nbsp;Aida Lahmer,&nbsp;Maram Selmi,&nbsp;Fedia Jaber,&nbsp;Refka Hassine,&nbsp;Sihem Safta,&nbsp;Asma Omezzine,&nbsp;Leila Chekir-Ghedira","doi":"10.1002/cbin.70211","DOIUrl":"10.1002/cbin.70211","url":null,"abstract":"<div>\u0000 \u0000 <p>Breast cancer, especially triple-negative breast cancer (TNBC), remains a significant clinical challenge due to limited treatment options, chemoresistance, and the toxic side effects of standard chemotherapy. Cisplatin (Cis) is commonly used but faces limitations from resistance and dose-related toxicity. Berberine chloride (BRB), a natural alkaloid derived from Berberis vulgaris, shows promising anticancer effects. This study examined the antitumor activity and chemosensitizing potential of BRB combined with Cis. We initially examined the effects of BRB and Cis on murine 4T1 breast cancer cells. The results showed that both treatments inhibited cell viability, with IC50 values around 10 µM for BRB and 2.5 µM for Cis. Subsequently, we tested the synergistic effects using the Chou–Talalay method, which indicated that most of the 16 drug combinations exhibited synergy (CI &lt; 1). The most effective combination (IC₅₀/8) had a CI of 0.12 and a Fa of 0.8, greatly reducing cell viability compared to individual treatments. The combined BRB and Cis therapy was then tested in a BALB/c mouse xenograft model via intraperitoneal injection. Cis alone at 1 mg/kg weekly lowered tumor growth by 43.13% but caused notable systemic toxicity, including body weight loss and kidney and liver damage. BRB alone at 10 mg/kg every 2 days resulted in greater tumor suppression (61.17%) with fewer side effects. The BRB/Cis combo achieved the highest tumor growth inhibition (87.05%) and markedly reduced Cis-related toxicity, evidenced by weight recovery and improved kidney and liver biochemical markers. These results indicate that BRB enhances cisplatin's antitumor effects while decreasing systemic toxicity, positioning BRB as a promising chemosensitizer for TNBC therapy.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149069286","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":"β2 Adrenoceptor Signaling Modulates Myoblast Differentiation via miR-374b-5p/GSK3β and miR-326-3p/Tnfrsf11a Axes","authors":"Tatiana E. Koike,&nbsp;Cesar S. Fuziwara,&nbsp;Audrei R. Santos,&nbsp;Fernanda V. B. Delpupo,&nbsp;Tábata L. Nascimento,&nbsp;Andrei Rozanski,&nbsp;Marcelo G. Pereira,&nbsp;Patrícia C. Brum,&nbsp;Edna T. Kimura,&nbsp;Thomas A. Rando,&nbsp;Elen H. Miyabara","doi":"10.1002/cbin.70214","DOIUrl":"https://doi.org/10.1002/cbin.70214","url":null,"abstract":"<p>Myoblast differentiation is a crucial step of skeletal muscle regeneration and is impaired in the absence of the β2 adrenoceptor (ADRβ2). Since miR-374b and miR-326 regulate cell differentiation, this study investigated if ADRβ2 regulates myoblast differentiation via miR-374b-5p and miR-326-3p. Primary myoblasts from ADRβ2 knockout (β2KO) mice were cultured in proliferation and differentiation media. In silico, cellular and molecular analyses were performed to evaluate NF-κB signaling activation and validate mRNAs as miR-374b-5p and miR-326-3p targets in β2KO differentiating myoblasts. Differentiating myoblasts from β2KO mice had decreased mRNA levels of <i>Nr4a1, Myog, Myh3, Cdkn1c,</i> and <i>Tnni2</i> and expression of miR-374b-5p and miR-326-3p. Overexpression of these miRs increased fusion index and gene expression of myogenic markers of these cells. In silico analyses indicated that GSK-3β and receptor activator of NF-kB (Tnfrsf11a) had potential binding sites for miR-374b-5p and miR-326-3p, respectively. The dual-luciferase reporter assay showed that <i>GSK-3β</i> and <i>Tnfrsf11a</i> were targets of miR-374b-5p and miR-326-3p, respectively. Regarding miR-326-3p, there was a reduction of NF-κB signaling and <i>NF-κB</i> mRNA levels in differentiating myoblasts from β2KO mice, and an upregulation of <i>Tnfrsf11a</i> and a downregulation of <i>Tnfrsf11</i>. In summary, ADRβ2 modulates myoblast differentiation via miR-374b-5p/<i>GSK-3β</i> and miR-326-3p/<i>Tnfrsf11a</i> axes.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.70214","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149048399","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":"IGK Suppresses Keloid Fibroblast Activation Through Modulation of MDM2 Expression and p53 Signaling","authors":"Ziqing Ye,&nbsp;Feng Liu,&nbsp;Huancheng Tang,&nbsp;Xiaoshuang Wang,&nbsp;Shuhua Liu,&nbsp;Qiongfang Ruan,&nbsp;Junhui Xu,&nbsp;Maolong Dong,&nbsp;Weiguo Xie,&nbsp;Siyu Zhang","doi":"10.1002/cbin.70213","DOIUrl":"10.1002/cbin.70213","url":null,"abstract":"<div>\u0000 \u0000 <p>Keloids are intricate fibroproliferative disorders characterized by sustained fibroblast activation, excessive deposition of extracellular matrix, and dysregulated wound-healing responses. This study explored the therapeutic effects and underlying mechanisms of Isoginkgetin (IGK) in keloid fibroblasts (KFbs) and a human keloid xenograft model. Our findings indicated that MDM2 expression was elevated in clinical keloid specimens, and IGK treatment inhibited KFbs proliferation and migration while inducing cell cycle arrest and apoptosis. Mechanistically, IGK downregulated MDM2 expression at the transcriptional level and was associated with the modulation of the MDM2/p53 signaling axis. LiP-MS and molecular docking analyses identified eukaryotic translation elongation factor 1 alpha 1 (EEF1A1) as a potential IGK-associated protein, suggesting that EEF1A1 may play a role in IGK-mediated regulation of MDM2 expression. Moreover, transcriptomic analysis of xenograft tissues combined with serum multicytokine profiling demonstrated that IGK treatment modulated inflammation-associated signatures, including those related to TNF signaling pathways, within the xenograft model. In vivo, administration of IGK resulted in a reduction in volume, collagen deposition, and α-SMA expression in established human keloid xenografts. Taken together, these findings indicate that IGK exerts anti-keloid effects by modulating the MDM2/p53 signaling axis and inflammation-associated pathways, underscoring its potential as a therapeutic candidate for keloid treatment.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149036313","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":"The Role of Ferroptosis Induced by Iron Overload in Osteoblast and Osteoclast Function","authors":"Supagarn Sooksawanwit,&nbsp;Kornkamon Lertsuwan,&nbsp;Natnicha Tannop,&nbsp;Ploypapus Lapatkeattisukul,&nbsp;Thanayuth Jenpichitkulchai,&nbsp;Nittiyaporn Sotapong,&nbsp;Jarinthorn Teerapornpuntakit,&nbsp;Tueanjai Khunluck,&nbsp;Siriwan Punvilai,&nbsp;Narattaphol Charoenphandhu","doi":"10.1002/cbin.70210","DOIUrl":"10.1002/cbin.70210","url":null,"abstract":"<p>Iron overload disrupts bone homeostasis by suppressing osteoblast survival and mineralization, while promoting osteoclastogenesis. As a programmed cell death driven by iron-dependent lipid peroxidation and glutathione peroxidase 4 (GPX4) downregulation. This study investigated the role of ferroptosis in bone cells under iron overload. Exposure to ferric ammonium citrate (FAC) led to decreased osteoblast viability, downregulation of GPX4 and nuclear factor erythroid 2-related factor 2 (Nrf2) protein expression and osteoblastic markers. It also increased ROS production and lipid peroxidation in osteoblasts. In addition, intracellular reduced glutathione (GSH) levels showed a decreasing trend in osteoblasts exposed to FAC. Ferrostatin-1 (Fer-1), a ferroptosis inhibitor, significantly restored osteoblast viability and reduced lipid peroxidation, confirming the involvement of ferroptosis in iron-induced cytotoxicity. Additionally, iron overload increased the receptor activator of nuclear factor-κB ligand (RANKL)/osteoprotegerin (OPG) ratio, thereby promoting osteoclast differentiation. Interestingly, Fer-1 effectively attenuated these osteoclastogenic effects. On the other hand, FAC increased RAW264.7 osteoclast precursor cells viability, ROS production and lipid peroxidation; while, Fer-1 suppressed lipid peroxidation without affecting cell viability and ROS levels. Furthermore, we examined the role of cystine, an essential precursor for GSH synthesis and critical antioxidant cofactor for GPX4, in bone cells under iron-overload conditions. Cystine enhanced osteoblast viability and reduced osteoclast viability under iron overload, but it did not exhibit a synergistic effect with Fer-1. These findings highlight ferroptosis as an underlying mechanism for iron-induced osteoporosis and may represent a promising therapeutic strategy for managing iron overload-associated bone disorders.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13596065/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015809","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":"Hydrogel-Based Mechano-Immunomodulation in Bone Fracture Healing: Mechanical Regulation of Macrophage Phenotypes, Osteoimmune Interactions, and Regeneration","authors":"Praveen Ramakrishnan,&nbsp;Nooruddin Thajuddin,&nbsp;S. B. Mohamed,&nbsp;Saranya Vinayagam,&nbsp;Lalitha Gnanasekaran,&nbsp;Shanmugapriya D,&nbsp;Rajaram Rajamohan,&nbsp;Abdulkadhar Mohamed Jalaludeen,&nbsp;Thanigaivel Sundaram","doi":"10.1002/cbin.70208","DOIUrl":"https://doi.org/10.1002/cbin.70208","url":null,"abstract":"<div>\u0000 \u0000 <p>Bone fracture healing is a meticulously regulated process encompassing the inflammatory, reparative, and remodelling phases. Macrophages serve as pivotal coordinators within this cascade, with their polarisation from pro-inflammatory M1 to proregenerative M2 phenotypes, which play a crucial role in determining the repair outcome. Emerging evidence underscores the significant influence of mechanical cues such as strain, stiffness, vibration, and scaffold topography on macrophage behaviour, thereby linking mechanobiology with immunology. This review summarises the current knowledge on mechano-immunomodulation in fracture repair, emphasising how mechanotransduction pathways, including Piezo1, YAP/TAZ, and PI3K/AKT, affect macrophage polarisation and their interactions with mesenchymal stem cells, osteoblasts, and endothelial cells. This review examined biomaterial strategies that leverage mechanical properties ranging from ceramic scaffolds and calcium phosphate coatings to hydrogels and advanced magnetic/electrical interfaces to shape the osteoimmune niche. Translational perspectives highlight mechanobiologics, immunometabolic reprogramming, and personalised loading regimens as next-generation approaches for fracture care. The remaining challenges include context-dependent macrophage responses, limited bone-specific mechanosensing data, and the need for standardised models and regulatory-compliant biomaterials. Collectively, these insights establish mechano-immunomodulation as a promising paradigm for enhancing bone regeneration and addressing the limitations of the current fixation-centric therapies.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149007473","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":"Potential Protective Effects of Mitochondria-Related Gene EHHADH on Diabetic Cardiomyopathy","authors":"Han Sun,&nbsp;Mengchen Sun,&nbsp;Yonghao Sheng,&nbsp;Hua Wang,&nbsp;Xiaoyan Jiang,&nbsp;Chunxiao Wang,&nbsp;Lin Zhong","doi":"10.1002/cbin.70212","DOIUrl":"https://doi.org/10.1002/cbin.70212","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 <p>Diabetic cardiomyopathy (DCM) induces myocardial lipotoxicity, mitochondria are essential for lipid metabolism. This study explored the role of mitochondria-related gene Enoyl-CoA hydratase and 3-hydroxyacyl CoA dehydrogenase (EHHADH) in DCM. Mitochondria-related differentially expressed genes(Mito DEGs) were screened from DCM and mitochondrial datasets. Protein-protein interaction (PPI) network and CytoHubba were applied to identify hub Mito DEGs. Hub gene expression in vivo and vitro DCM models was verified by western blot and RT-qPCR. H9C2 cell apoptosis was detected by Tunel and flow cytometry, lipid accumulation was clarified by oil red O staining, oxidative stress was assessed by detecting ROS, BODIPY-C11 and malondialdehyde(MDA). Mitochondrial function was determined by JC-1 staining and ATP levels. After adding Fenofibrate(FNB), apoptosis proteins were detected by western blot. DCM genes are enriched in fatty acid metabolism pathway. EHHADH is the most critical hub gene in all hub Mito DEGs and upregulated in vivo and vitro DCM models. EHHADH knockdown aggravate high glucose and palmitic acid (HGHP)-treated H9C2 cell apoptosis, oxidative stress, lipid peroxidation, and lipid accumulation, which are associated with mitochondrial functional damage. FNB promoted EHHADH expression, thereby reducing apoptosis, lipid accumulation, and mitochondrial damage in myocardial cells. EHHADH exerts a protective effect in DCM by reducing mitochondrial damage, oxidative stress, lipid accumulation, and cardiomyocyte apoptosis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149007472","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}