Cell Biology International最新文献

{"title":"Cyclophosphamide Induces Glioblastoma Tumor Cell Death and Oxidative Stress Through the Increase of TRPM2 Channel Stimulation: The Role of Carvacrol.","authors":"Kemal Ertilav, Mustafa Nazıroğlu","doi":"10.1002/cbin.70039","DOIUrl":"https://doi.org/10.1002/cbin.70039","url":null,"abstract":"<p><p>Cyclophosphamide (CP) damages glioblastoma cells by producing an excessive amount of intracellular (iROS) and mitochondrial (mROS) reactive oxygen species. Both iROS and mROS are produced when TRPM2 is activated, but they are decreased when carvacrol (CAR) and N-(p-amylcinnamoyl) anthranilic acid (ACA) inhibit it. Therefore, iROS, and mROS via upregulating Ca²⁺ influx and apoptosis in glioblastoma (DBTRG-05MG) cells, CP-mediated TRPM2 stimulation may cause oxidant and apoptotic activities. We investigated how TRPM2 activation not only promotes DBTRG-05MG death but also modifies oxidative damage and apoptosis to counteract the effects of ACA and CAR. The groups of control (CN), CAR (200 μM for 24 h), CP (2 mM for 24 h), and CP + CAR were induced in the DBTRG-05MG. While cytosolic free Ca²⁺ levels decreased in the cells as a result of the CAR and ACA treatments, they were further elevated in the CP group by the stimulation of TRPM2 (H₂O₂). The cells in the CP group had higher levels of dead cell percentage, apoptosis, mitochondrial membrane dysfunction, mROS, iROS, and caspases -3, -8, and -9 than the CN and CAR cells, although their levels were lower in the CP + CAR than in the CP only. CAR incubation increased the CP-induced glutathione concentration and cell viability percentage declines. In summary, the anticancer effect of CP was enhanced by TRPM2 stimulation, while CP-induced oxidative stress and DBTRG-05MG death were reduced by TRPM2 suppression when CAR was treated. TRPM2 activation may be a possible tumor killer channel due to oxidative glioma damage caused by CP.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144118959","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 Ultrastructure of the Apical Organ of the Goette's Larvae of the Polyclad Flatworm Stylochus pilidium Indicates Homology Between Polyclad Larvae","authors":"Davina Düngler,&nbsp;Clemens Gotsis,&nbsp;Isabel L. Dittmann,&nbsp;Stefan Redl,&nbsp;Michael W. Hess,&nbsp;Bernhard Egger","doi":"10.1002/cbin.70034","DOIUrl":"10.1002/cbin.70034","url":null,"abstract":"<p>Polyclad flatworms exhibit both direct and indirect development, with various larval types observed, including Müller's larva, Kato's larva, Goette's larva and Curini-Galletti's larva. The different larval types are distinguished by shape, number of eyes and number of lobes. The Goette's larva of <i>Stylochus pilidium</i> exhibits a distinct six-lobed morphology, with one cerebral and one epidermal eye. The posterior half of the larva features a posterior tuft and four lobes, two of which are ventrolateral and two of which are lateral. Anteriorly, a larger lobe called the oral hood is situated ventrally, opposite a smaller dorsal lobe. The larval types share a distinct feature, known as the apical organ, which is located at the anterior tip of the larvae. Here, we investigated the ultrastructure of the apical organ in Goette's larvae of the polyclad <i>S. pilidium</i>. Six apical tuft sensory (ATS) cells are at the centre of the apical organ, encircled by a ring of apical tuft gland (ATG) cell type 1 necks. These cell necks merge into two distinct gland cells that extend dorsoposteriorly and terminate posterior to the brain. Two epidermal apical tuft anchor (ATAn) cells encircle the ATS cells and the central gland cell necks. Additionally, four ATG cell type 2 necks, which are distributed symmetrically around the ATAn cells, merge into a single cell and extend ventrally to the level of the cerebral eye. The third type of ATG cells is in a circular pattern around the anchor cells, with necks in the epidermal layer. The ultrastructural arrangements of the apical organ in Goette's larva of <i>S. pilidium</i> are very similar to those of previously studied polyclad larvae, supporting the hypothesis of a common origin of larvae within Polycladida.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 8","pages":"989-1002"},"PeriodicalIF":3.3,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.70034","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076293","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":"Regulatory T Cells in Tumor Microenvironment: Therapeutic Approaches and Clinical Implications","authors":"Niti Sureka,&nbsp;Sufian Zaheer","doi":"10.1002/cbin.70031","DOIUrl":"10.1002/cbin.70031","url":null,"abstract":"<div>\u0000 \u0000 <p>Regulatory T cells (Tregs), previously referred to as suppressor T cells, represent a distinct subset of CD4+ T cells that are uniquely specialized for immune suppression. They are characterized by the constitutive expression of the transcription factor FoxP3 in their nuclei, along with CD25 (the IL-2 receptor α-chain) and CTLA-4 on their cell surface. Tregs not only restrict natural killer cell-mediated cytotoxicity but also inhibit the proliferation of CD4+ and CD8+ T-cells and suppress interferon-γ secretion by immune cells, ultimately impairing an effective antitumor immune response. Treg cells are widely recognized as a significant barrier to the effectiveness of tumor immunotherapy in clinical settings. Extensive research has consistently shown that Treg cells play a pivotal role in facilitating tumor initiation and progression. Conversely, the depletion of Treg cells has been linked to a marked delay in tumor growth and development.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 8","pages":"897-928"},"PeriodicalIF":3.3,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143954567","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":"ω-3 PUFAs Alleviate GJ-Cx43 Uncoupling Induced by Long-Term Isoflurane Exposure by Activating the Wnt/β-catenin Signaling Pathway in Astrocytes","authors":"Zimo Wang,&nbsp;Rui Dong,&nbsp;Yuqiang Han,&nbsp;Liangyu Peng,&nbsp;Shuai Liu,&nbsp;Zhengliang Ma,&nbsp;Tianjiao Xia,&nbsp;Xiaoping Gu","doi":"10.1002/cbin.70028","DOIUrl":"10.1002/cbin.70028","url":null,"abstract":"<div>\u0000 \u0000 <p>Isoflurane, a widely used anesthetic, has raised concerns due to its potential neurotoxic effects, including oxidative stress and astrocytic gap junction (GJ) dysfunction. This study investigates whether ω-3 polyunsaturated fatty acids (PUFAs), particularly docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), can mitigate these effects by activating the Wnt/β-catenin signaling pathway. Using primary astrocytes, we found that long-term isoflurane exposure uncoupled GJ-Cx43, increased reactive oxygen species (ROS), and inhibited Wnt/β-catenin signaling. ω-3 PUFA treatment restored GJ-Cx43 coupling, reduced ROS levels, and partially reactivated the Wnt/β-catenin pathway. These findings suggest that ω-3 PUFAs protect against isoflurane-induced neurotoxicity by enhancing GJ-Cx43 coupling and reducing oxidative stress, offering a potential therapeutic strategy for perioperative neurocognitive disorders.”</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 7","pages":"865-877"},"PeriodicalIF":3.3,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144062395","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":"Ishophloroglucin A Isolated From Ishige okamurae Stimulates Osteoblast Differentiation Through Activation of the Bone Morphogenetic Protein and Wnt/β-Catenin Signaling Pathways in MC3T3-E1 Cells","authors":"Seung-Hong Lee,&nbsp;Mihyang Kim,&nbsp;Kyung Im Jung,&nbsp;Sang-Jae Lee,&nbsp;Mi Hwa Park","doi":"10.1002/cbin.70030","DOIUrl":"10.1002/cbin.70030","url":null,"abstract":"<div>\u0000 \u0000 <p>Current osteoporosis treatments are insufficient as they cause a relatively small increase in bone mass and are unable to recover lost bone structures, in addition to having severe side effects. The bone morphogenetic protein (BMP) and Wnt/β-catenin signaling pathways cooperatively modulate bone formation and osteoblast differentiation and therefore may play a role in treating osteoporosis. This study aimed to investigate the effects of Ishophloroglucin A (IPA), a novel phenolic compound isolated from <i>Ishige okamurae</i>, on osteoblast differentiation by activating the BMP and Wnt/β-catenin signaling pathways. According to our findings, IPA significantly promoted the osteogenic proliferation of MC3T3-E1 osteoblastic cells and increased alkaline phosphatase (ALP) activity and calcium nodule formation in MC3T3-E1 cells compared to the untreated control. IPA also upregulated osteogenesis markers such as type 1 collagen, ALP, p-Smad1/5/8, osterix, osteopontin, runt-related transcription factors (Runx2), and BMP2 in MC3T3-E1 cells in a dose-dependent manner. Moreover, IPA activated Wnt3a, LRP5, DVL2, and β-catenin in MC3T3-E1 cells. Overall, our results demonstrate that IPA promotes the differentiation of MC3T3-E1 osteoblastic cells by activating the BMP and Wnt/β-catenin signaling pathways, suggesting that it may be a potential candidate target for treating or preventing osteoporosis.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 8","pages":"965-974"},"PeriodicalIF":3.3,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143974004","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":"Isoquercetin Alleviates Diabetic Retinopathy Via Inhibiting p53-Mediated Ferroptosis","authors":"Yu Cai,&nbsp;Shijing Peng,&nbsp;Bingfen Duan,&nbsp;Yinan Shao,&nbsp;Xiaonan Li,&nbsp;Hua Zou,&nbsp;Huimin Fan,&nbsp;Zhipeng You","doi":"10.1002/cbin.70027","DOIUrl":"10.1002/cbin.70027","url":null,"abstract":"<div>\u0000 \u0000 <p>Diabetic retinopathy (DR) is a retinal vasculopathy stemming from diabetes mellitus, characterized by microvascular changes in the retina that can lead to visual impairment or even blindness. Ferroptosis, a form of regulated cell death driven by iron accumulation and lipid peroxidation, has been implicated in the progression of DR. Isoquercetin (IQC), a flavonoid compound, has been shown to inhibit cellular ferroptosis and apoptosis, yet its specific role and underlying mechanisms in DR remain to be elucidated. The present study aimed to investigate the effects of IQC on DR and to delineate its protective mechanisms, particularly focusing on whether these effects are mediated through p53. We employed streptozotocin-induced diabetic C57BL/J mouse models and high glucose (HG)-induced human retinal capillary endothelial cells (HRCECs) models for both in vivo and in vitro experiments. Pathological damage was assessed using hematoxylin and eosin staining, while cell apoptosis rates was detected by TUNEL staining and FITC/PI flow cytometry. Mitochondrial damage was evaluated using transmission electron microscopy. Additionally, we measured levels of reactive oxygen species (ROS) and glutathione (GSH) to assess lipid peroxidation and quantified ferrous ions (Fe²⁺). Protein expression was detected by immunofluorescence and western blot analysis, and mRNA levels were determined by real-time quantitative PCR. Our findings revealed that IQC mitigated retinal damage in diabetic mice, and in vitro studies further demonstrated that this effect was mediated by the inhibition of p53. In HG-induced HRCECs, we observed decreased cell viability, lipid peroxidation, and ferroptosis. IQC alleviated HG-induced ferroptosis in HRCECs by modulating the p53 pathway, which exhibited varying responses following p53 inhibition or activation. In summary, IQC downregulated the p53 signaling pathway, thereby reducing ferroptosis and apoptosis, and effectively ameliorated the damage associated with DR. These discoveries offer novel insights into the protective mechanisms of IQC in DR.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 7","pages":"852-864"},"PeriodicalIF":3.3,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143973960","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":"SERP1 Alleviates Cerebral Ischemia/Reperfusion Injury by Inhibiting ER Stress-Mediated Apoptosis","authors":"Le Yin,&nbsp;Dan Wang,&nbsp;Xinyue Zhang,&nbsp;Xiao Wang,&nbsp;Hong Jiao,&nbsp;Xiaodan Liu,&nbsp;Jiaolin Zheng","doi":"10.1002/cbin.70029","DOIUrl":"10.1002/cbin.70029","url":null,"abstract":"<div>\u0000 \u0000 <p>Ischemic stroke is a common disease of the central nervous system, and endoplasmic reticulum (ER) stress-induced apoptosis plays a key role in brain damage following ischemic stroke. Stress-associated endoplasmic reticulum protein 1 (SERP1) is a Sec. 61-associated polypeptide induced by ER stress, which is implicated in stabilizing membrane proteins during ER stress. However, the precise molecular mechanism of SERP1 in ischemic stroke is still unknown. This study aimed to explore the protective effect of SERP1 against cerebral ischemia/reperfusion (I/R) injury. Male Sprague-Dawley rats with transient middle cerebral artery occlusion/reperfusion (tMCAO/R) were used to simulate cerebral I/R injury in vivo. To mimic the cerebral I/R injury in vitro, PC12 cells were treated with oxygen glucose deprivation/reperfusion (OGD/R). The results revealed that the SERP1 expression was increased during cerebral I/R injury in vivo and in vitro. SERP1 knockdown promoted apoptosis and ER stress as well as aggravated I/R-induced brain injury in rats with tMCAO/R, but SERP1 overexpression presented the opposite effects. SERP1 also alleviated OGD/R-induced cell damage in PC12 cells. Mechanically, SERP1 inhibited the ER stress-induced neuronal apoptosis through the PERK-EIF2α-ATF4-CHOP pathway. In conclusion, these results suggest that SERP1 may be a novel candidate gene for therapies against cerebral I/R injury.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 7","pages":"878-894"},"PeriodicalIF":3.3,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143955172","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":"Exploring Ferroptosis in Allergic Inflammatory Diseases: Emerging Mechanisms and Therapeutic Perspectives","authors":"Henry Sutanto,&nbsp;Laras Pratiwi,&nbsp;Deasy Fetarayani","doi":"10.1002/cbin.70026","DOIUrl":"10.1002/cbin.70026","url":null,"abstract":"<div>\u0000 \u0000 <p>Ferroptosis, a unique form of regulated cell death driven by iron accumulation and lipid peroxidation, has emerged as a critical process in various diseases. Recent evidence suggests its involvement in the pathogenesis of allergic diseases, including asthma, allergic rhinitis, and atopic dermatitis. These conditions are characterized by chronic inflammation, oxidative stress, and immune dysregulation, all of which intersect with the molecular mechanisms of ferroptosis. Key regulators, such as glutathione peroxidase 4 (GPX4), the cystine/glutamate antiporter system Xc-, and iron metabolism pathways, play pivotal roles in ferroptotic processes and their contribution to allergic disease progression. This review explores the mechanistic link between ferroptosis and allergic diseases, emphasizing how oxidative damage and iron overload exacerbate inflammation and tissue injury. We also highlight emerging diagnostic biomarkers, including lipid peroxidation products and iron regulators, which could improve disease monitoring and stratification. Therapeutic strategies targeting ferroptosis, such as GPX4 activators, iron chelators, and lipid peroxidation inhibitors, show promise in preclinical studies, offering potential new avenues for treating allergic diseases. However, challenges remain in translating these findings into clinical applications. By integrating current knowledge, this review underscores the need for further research into ferroptosis as both a biomarker and therapeutic target in allergic diseases.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 7","pages":"739-756"},"PeriodicalIF":3.3,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967272","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":"NEIL3 Deficiency Enhances HCC Cell Sensitivity to Oxaliplatin by Inhibiting the Fanconi Anaemia Pathway","authors":"Jialiang Wang,&nbsp;Chunhong Liao,&nbsp;Jing Luo,&nbsp;Mingna Li,&nbsp;Lin Gu,&nbsp;Xiaoyan Li,&nbsp;Lubiao Chen","doi":"10.1002/cbin.70023","DOIUrl":"10.1002/cbin.70023","url":null,"abstract":"<div>\u0000 \u0000 <p>Despite some achievements in oxaliplatin-based chemotherapy for the treatment of advanced hepatocellular carcinoma (HCC), the abnormal activation of DNA damage repair pathways in HCC cells remains a major problem, limiting the efficacy of oxaliplatin-based chemotherapy. In a previous study, we found that endonuclease VIII-like protein 3 (NEIL3) is expressed in a high proportion of patients with HCC and associated with an unfavourable prognosis. However, the role of NEIL3 in chemoresistance is still unclear. The aim of this study was to evaluate whether and how NEIL3 regulates oxaliplatin anti-tumour efficacy. Gene expression after oxaliplatin treatment in HCC cell lines was assessed by real-time quantitative PCR, western blot analysis and bioinformatics analysis. The effect of NEIL3 on regulating oxaliplatin efficacy was assessed using cell counting kit-8 assays, colony formation assays, flow cytometry and an in vivo nude mice study. Mechanistic insights into the sensitivity to oxaliplatin mediated by the inhibition of NEIL3 were obtained through immunofluorescence and RNA sequencing analyses. Our findings demonstrated that NEIL3 expression was markedly downregulated after oxaliplatin administration. NEIL3 knockdown impaired cell viability and colony formation and increased apoptosis in HCC cells exposed to oxaliplatin. In addition, NEIL3 inhibition reduced tumour progression and enhanced oxaliplatin efficacy in xenograft nude mice models. Furthermore, knocking down NEIL3 significantly increased the oxaliplatin-mediated inhibition of the Fanconi anaemia pathway. Our results revealed that NEIL3 may be a promising therapeutic target for improving oxaliplatin efficacy in the treatment of HCC.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 7","pages":"824-835"},"PeriodicalIF":3.3,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983098","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 Polarization of Macrophages Regulated by KCNG3 via the Activation of ASK1 Mediated by Potassium Ion Efflux","authors":"Shuting Zhang,&nbsp;Yanlong Xin,&nbsp;Yu Yang,&nbsp;Yan Zhang,&nbsp;Jing Geng","doi":"10.1002/cbin.70022","DOIUrl":"10.1002/cbin.70022","url":null,"abstract":"<div>\u0000 \u0000 <p>Inflammatory diseases burden the human body and their pathogenesis remains unclear. Macrophages, with plasticity to polarize into M1/M2 phenotypes, play crucial roles in inflammation. The impact of diverse ion channels on macrophage functions and their underlying mechanisms still requires further investigation. In this research, we observed that the expression magnitudes of some ion channels increased under the stimulation of LPS by transcriptomics analysis. Among them, KCNG3 has drawn our attention as it represents a potassium channel subunit with an undefined role in macrophages. To investigate its role, we knocked down KCNG3, resulting in an enhancement of phagocytosis, bactericidal ability, and the expression of pro-inflammatory cytokines, thereby facilitating M1 polarization. Knockdown of KCNG3 led to an increase in potassium ion efflux, an effect that was recapitulated under low potassium conditions, which in turn activated ASK1 and promoted M1 polarization. Through administering inhibitors NQDI-1, ASK1 was blocked and reversed the M1 phenotype caused by KCNG3 knockdown. In summary, KCNG3 regulates macrophage polarization via potassium ion flux and ASK1, offering potential for inflammatory disease treatment.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 7","pages":"810-823"},"PeriodicalIF":3.3,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143987236","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}