IF 5.1 2区生物学

Cells Pub Date : 2025-05-18 DOI: 10.3390/cells14100738

Vadim Genkel, Yana Zaripova, Alla Kuznetsova, Alena Sluchanko, Anna Minasova, Maria Zotova, Anna Saenko, Albina Savochkina, Anastasiya Dolgushina

{"title":"Neutrophils at the Crossroads of Inflammatory Bowel Disease and Atherosclerosis: A State-of-the-Art Review.","authors":"Vadim Genkel, Yana Zaripova, Alla Kuznetsova, Alena Sluchanko, Anna Minasova, Maria Zotova, Anna Saenko, Albina Savochkina, Anastasiya Dolgushina","doi":"10.3390/cells14100738","DOIUrl":"10.3390/cells14100738","url":null,"abstract":"Inflammatory bowel disease (IBD) is a growing global problem, particularly in regions with low sociodemographic indices and growing populations. IBD incidence is increasing among children and adolescents, leading to a growing economic burden. The prevalence of atherosclerotic cardiovascular diseases among patients with IBD is also higher than in the general population. While mortality rates have decreased, cardiovascular disease (CVD) remains a significant contributor to mortality and disability in IBD patients. According to the current understanding, neutrophils play an important role in both the atherogenesis and pathogenesis of IBD. This review addresses the state of the art of neutrophil involvement in the development of atherosclerosis and IBD. In the present review, we summarize the currently available evidence regarding neutrophils as a possible key driver of extraintestinal manifestations of IBD and cardiovascular complications. We provide a discussion on the potential role of neutrophil-derived markers in the development of new approaches for the precise diagnosis of atherosclerosis in patients with IBD, as well as new therapeutic targets.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Modeling Tumor Microenvironment Complexity In Vitro: Spheroids as Physiologically Relevant Tumor Models and Strategies for Their Analysis. 体外肿瘤微环境复杂性建模：球体作为生理相关肿瘤模型及其分析策略。

IF 5.1 2区生物学

Cells Pub Date : 2025-05-17 DOI: 10.3390/cells14100732

Shrey Shah, Gerard G M D'Souza

{"title":"Modeling Tumor Microenvironment Complexity In Vitro: Spheroids as Physiologically Relevant Tumor Models and Strategies for Their Analysis.","authors":"Shrey Shah, Gerard G M D'Souza","doi":"10.3390/cells14100732","DOIUrl":"10.3390/cells14100732","url":null,"abstract":"Drug delivery to solid tumors is challenged by multiple physiological barriers arising from the tumor microenvironment, including dense extracellular matrix, cellular heterogeneity, hypoxic gradients, and elevated interstitial fluid pressure. These features hinder the uniform distribution and accumulation of therapeutics, reducing treatment efficacy. Despite their widespread use, conventional two-dimensional monolayer cultures fail to reproduce these complexities, contributing to the poor translational predictability of many preclinical candidates. Three-dimensional multicellular tumor spheroids have emerged as more representative in vitro models that capture essential features of tumor architecture, stromal interactions, and microenvironmental resistance mechanisms. Spheroids exhibit spatially organized regions of proliferation, quiescence, and hypoxia, and can incorporate non-tumor cells to mimic tumor-stroma crosstalk. Advances in spheroid analysis now enable detailed evaluation of drug penetration, cellular migration, cytotoxic response, and molecular gradients using techniques such as optical and confocal imaging, large-particle flow cytometry, biochemical viability assays, and microfluidic integration. By combining physiological relevance with analytical accessibility, spheroid models support mechanistic studies of drug transport and efficacy under tumor-like conditions. Their adoption into routine preclinical workflows has the potential to improve translational accuracy while reducing reliance on animal models.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Competitive Loss of Cerebellar Granule and Purkinje Cells Driven by X-Linked Mosaicism in a Female Mouse Model of CASK-Related Disorders. 在雌性小鼠cask相关疾病模型中，x -连锁嵌合体驱动的小脑颗粒和浦肯野细胞竞争性损失

IF 5.1 2区生物学

Cells Pub Date : 2025-05-17 DOI: 10.3390/cells14100735

Takuma Mori, Mengyun Zhou, Ken Kunugitani, Taichi Akatsuka, Yukina Yoshida, Emi Kouyama-Suzuki, Shin Kobayashi, Yoshinori Shirai, Katsuhiko Tabuchi

{"title":"The Competitive Loss of Cerebellar Granule and Purkinje Cells Driven by X-Linked Mosaicism in a Female Mouse Model of CASK-Related Disorders.","authors":"Takuma Mori, Mengyun Zhou, Ken Kunugitani, Taichi Akatsuka, Yukina Yoshida, Emi Kouyama-Suzuki, Shin Kobayashi, Yoshinori Shirai, Katsuhiko Tabuchi","doi":"10.3390/cells14100735","DOIUrl":"10.3390/cells14100735","url":null,"abstract":"CASK-related disorders are a form of female-restricted intellectual disabilities associated with cerebellar and pontine hypoplasia. The CASK gene is regulated by X-chromosome inactivation, which results in a mosaic distribution of CASK-expressing and CASK-deficient neurons in the female brain. This mosaic distribution is believed to play a key role in the pathophysiology of X-linked neurological disorders; however, the detailed brain structure has not been extensively characterized. In this study, we used CASK heterozygous knockout (CASK-hKO) mice combined with X-linked GFP reporter mice to investigate motor abilities and the distribution of CASK-expressing cells in the brains of female CASK-hKO mice. The CASK-hKO mice exhibited motor deficits and cerebellar hypoplasia similar to those observed in patients with CASK-related disorders. Interestingly, although half of the cerebellar granule cells were CASK-negative during early postnatal development, almost all Purkinje cells and cerebellar granule cells were CASK-positive in adulthood, suggesting that CASK expression may determine the survival of cerebellar granule cells during postnatal development. We also analyzed CASK-hypomorphic mice, which express 50% less CASK than wild-type mice, and compared hemizygous males and heterozygous females. The CASK-hypomorphic heterozygous females displayed a thinner cerebellar cortex and a higher probability of CASK-positive granule cells in CASK-hKO females, suggesting that the survival of cerebellar granule cells is regulated by a combination of cell-autonomous and cell-competitive mechanisms between CASK-expressing and CASK-deficient cells, which are generated by X-chromosome inactivation. These findings provide new insights into the relationship between the mosaic distribution of cells established by X-chromosome inactivation and the pathophysiology of CASK-related disorders.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Accumulation of Small-Size, Highly Dispersive Mesoporous Silica Nanoparticles in a Tumor in Both Chorioallantoic Membrane and Mouse Models. 小尺寸、高分散的介孔二氧化硅纳米颗粒在绒毛膜和小鼠模型肿瘤中的积累。

IF 5.1 2区生物学

Cells Pub Date : 2025-05-17 DOI: 10.3390/cells14100734

Aoi Komatsu, Yuya Higashi, Cong-Kai Lin, Yi-Ping Chen, Si-Han Wu, Minoru Suzuki, Kotaro Matsumoto, Fuyuhiko Tamanoi

{"title":"Accumulation of Small-Size, Highly Dispersive Mesoporous Silica Nanoparticles in a Tumor in Both Chorioallantoic Membrane and Mouse Models.","authors":"Aoi Komatsu, Yuya Higashi, Cong-Kai Lin, Yi-Ping Chen, Si-Han Wu, Minoru Suzuki, Kotaro Matsumoto, Fuyuhiko Tamanoi","doi":"10.3390/cells14100734","DOIUrl":"10.3390/cells14100734","url":null,"abstract":"(1) Background: The chorioallantoic membrane (CAM) model has the potential to contribute to the development of personalized medicine based on individual cancer patients. We previously established the CAM model using patient-derived CIC-DUX4 sarcoma cells. We also used the CAM model for characterization and a comparison with the mouse model by examining the tumor accumulation of small-size, highly dispersive mesoporous silica nanoparticles (MSNs). (2) Method: In this study, we transplanted a variety of cancer cell lines, including patient-derived osteosarcoma (OS) and extraskeletal osteosarcoma (ESOS) cells. Patient-derived OS, ESOS and other cell lines were transplanted onto CAMs. The proliferation of cancer cells within CAM tumors was confirmed using H&E staining. For the comparison of the CAM and mouse models, rhodamine B-labeled MSNs were administered intravenously to CAMs and to xenograft mice. Tumor accumulation was evaluated by examining fluorescence and by confocal microscopy. The biodistribution of MSNs was examined by measuring the Si content by ICP. (3) Results: H&E staining demonstrated the proliferation of cancer cells of OS, ESOS and others on CAMs. While growth patterns and morphologies varied among different cancer types, H&E staining confirmed the establishment of tumors. As for the tumor accumulation, both the CAM and mouse models showed that MSNs were selectively accumulated in the tumors in both the CAM and mouse models. (4) Conclusions: We have expanded the range of CAM models by using a variety of cancer cells, including patient-derived cell lines. We also report that the small-size, highly dispersive MSNs exhibit excellent tumor accumulation in both the CAM and mouse models. These results point to the usefulness of the CAM model for patient-derived cancer cells as well as for evaluating drug carriers for tumor targeting.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Coupling of Intracellular Calcium Homeostasis and Formation and Secretion of Matrix Vesicles: Their Role in the Mechanism of Biomineralization. 细胞内钙稳态与基质囊泡形成和分泌的耦合：它们在生物矿化机制中的作用。

IF 5.1 2区生物学

Cells Pub Date : 2025-05-17 DOI: 10.3390/cells14100733

Azzurra Margiotta

引用次数: 0

Genetic Predisposition and Mitochondrial Dysfunction in Sudden Cardiac Death: Role of MCU Complex Genetic Variations. 心源性猝死的遗传易感性和线粒体功能障碍：MCU复杂遗传变异的作用。

IF 5.1 2区生物学

Cells Pub Date : 2025-05-16 DOI: 10.3390/cells14100728

Haoliang Meng, Yan He, Yukun Rui, Mengqi Cai, Dongke Fu, Wanli Bi, Bin Luo, Yuzhen Gao

{"title":"Genetic Predisposition and Mitochondrial Dysfunction in Sudden Cardiac Death: Role of MCU Complex Genetic Variations.","authors":"Haoliang Meng, Yan He, Yukun Rui, Mengqi Cai, Dongke Fu, Wanli Bi, Bin Luo, Yuzhen Gao","doi":"10.3390/cells14100728","DOIUrl":"10.3390/cells14100728","url":null,"abstract":"Sudden cardiac death (SCD) is a major cause of cardiovascular mortality, with coronary artery disease-related SCD (SCD-CAD) being the most prevalent form. Genetic factors and mitochondrial dysfunction, particularly in calcium homeostasis, are critical in SCD-CAD. However, the specific genetic factors linked to mitochondrial dysfunction in SCD-CAD remain poorly understood. In this case-control study, we analyzed 229 SCD-CAD cases and 598 controls from a Southern Han Chinese population, focusing on 12 insertion-deletion (indel) variants across six mitochondrial calcium uniporter (MCU) complex genes. We used capillary electrophoresis-based multiplex genotyping and performed logistic regression and haplotype analyses to assess the association of these variants with SCD-CAD susceptibility. Four significant indel variants and three risk-associated haplotypes were identified. Two of these indels were previously validated in the GWAS catalog as strongly linked to cardiac disorders. Additionally, Mendelian randomization (MR) analysis revealed a causal relationship between elevated levels of the SMDT1-encoded MCU regulator and increased risks of cardiovascular diseases, including coronary atherosclerosis, myocardial infarction, and cardiomyopathy. These findings highlight the role of MCU complex variants in SCD-CAD susceptibility and suggest their potential as biomarkers for cardiovascular risk stratification. Further research with larger cohorts is needed to confirm these results and explore underlying mechanisms.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Taurine Prevents Impairments in Skin Barrier Function and Dermal Collagen Synthesis Triggered by Sleep Deprivation-Induced Estrogen Circadian Rhythm Disruption. 牛磺酸防止睡眠不足引起的雌激素昼夜节律紊乱引起的皮肤屏障功能和真皮胶原合成损伤。

IF 5.1 2区生物学

Cells Pub Date : 2025-05-16 DOI: 10.3390/cells14100727

Qi Shao, Zhaoyang Wang, Yifang Li, Xun Tang, Ziyi Li, Huan Xia, Qihong Wu, Ruxue Chang, Chunna Wu, Tao Meng, Yufei Fan, Yadong Huang, Yan Yang

{"title":"Taurine Prevents Impairments in Skin Barrier Function and Dermal Collagen Synthesis Triggered by Sleep Deprivation-Induced Estrogen Circadian Rhythm Disruption.","authors":"Qi Shao, Zhaoyang Wang, Yifang Li, Xun Tang, Ziyi Li, Huan Xia, Qihong Wu, Ruxue Chang, Chunna Wu, Tao Meng, Yufei Fan, Yadong Huang, Yan Yang","doi":"10.3390/cells14100727","DOIUrl":"10.3390/cells14100727","url":null,"abstract":"Sleep deprivation is a prevalent issue that disrupts the circadian rhythm of estrogen, particularly estradiol, thereby significantly affecting women's skin health and appearance. These disruptions can impair skin barrier functionality and decrease dermal collagen synthesis. In this study, our results demonstrate that topical taurine supplementation promotes the expression of tight junction (TJ)-related proteins and enhances collagen production, effectively restoring skin homeostasis in sleep-deprived female mice. Mechanistically, taurine upregulates the expression of TMEM38B, a gene encoding the TRIC-B trimeric cation channel, resulting in increased intracellular calcium ion levels. This, in turn, promotes the upregulation of TJ-related proteins, such as ZO-1, occludin, and claudin-11 in epidermal cells, while also enhancing the expression of type III collagen in fibroblasts, thus restoring skin homeostasis. These findings suggest that taurine may serve as an alternative to estradiol, effectively improving skin homeostasis disrupted by sleep deprivation while mitigating the potential risks associated with exogenous estrogen supplementation. Collectively, these results provide preliminary insights into the protective mechanisms of taurine against sleep deprivation-induced skin impairments and establish a foundation for its potential application in treating skin conditions related to estrogen imbalances, such as skin aging in menopausal women.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

G-Protein-Coupled Receptors in Chronic Kidney Disease Induced by Hypertension and Diabetes. 高血压和糖尿病所致慢性肾病的g蛋白偶联受体

IF 5.1 2区生物学

Cells Pub Date : 2025-05-16 DOI: 10.3390/cells14100729

Huidi Tang, Kang Li, Zhan Shi, Jichao Wu

{"title":"G-Protein-Coupled Receptors in Chronic Kidney Disease Induced by Hypertension and Diabetes.","authors":"Huidi Tang, Kang Li, Zhan Shi, Jichao Wu","doi":"10.3390/cells14100729","DOIUrl":"10.3390/cells14100729","url":null,"abstract":"Hypertension and diabetes are two common causes of chronic kidney disease. Hypertension can induce renal vascular injury, glomerular damage, podocyte loss, and tubular injury, leading to tubulointerstitial fibrosis. A number of factors influence the regulation of hypertension, among which G-protein-coupled receptors (GPCRs) have been studied extensively because they are desirable targets for drug development. Compared to hypertension, the regulatory effects of GPCRs on hypertensive kidney disease (HKD) are less generalized. In this review, we discussed the GPCRs involved in hypertensive kidney disease, such as angiotensin II receptors (AT1R and AT2R), Mas receptor (MasR), Mas-related G-protein-coupled receptor member D (MrgD), relaxin family receptor 1 (RXFP1), adenosine receptors (A1, A2A, A2B, and A3), purinergic P2Y receptors, and endothelin receptors (ETA and ETB). The progression of HKD is rarely reversed but can be retarded by ameliorating the hypertensive microenvironment in the kidneys. However, simply reducing blood pressure cannot stop the progression of HKD. Diabetic nephropathy (DN) is the most common cause of end-stage renal disease (ESRD), which is a major cause of morbidity and mortality in diabetes. Many GPCRs are involved in DN. Here, we select some well-studied GPCRs that are directly associated with the pathogenesis of DN to illustrate their mechanisms. The main purpose of this review is to provide an overview of the GPCRs involved in the occurrence and progression of HKD and DN and their probable pathophysiological mechanisms, which we hope will help in developing new therapeutic strategies.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PANoptosis as a Two-Edged Sword in Colorectal Cancer: A Pathogenic Mechanism and Therapeutic Opportunity. PANoptosis是结直肠癌的双刃剑：致病机制和治疗机会。

IF 5.1 2区生物学

Cells Pub Date : 2025-05-16 DOI: 10.3390/cells14100730

Györgyi Műzes, Ferenc Sipos

{"title":"PANoptosis as a Two-Edged Sword in Colorectal Cancer: A Pathogenic Mechanism and Therapeutic Opportunity.","authors":"Györgyi Műzes, Ferenc Sipos","doi":"10.3390/cells14100730","DOIUrl":"10.3390/cells14100730","url":null,"abstract":"The examination of PANoptosis in colorectal cancer is particularly important, as many tumor cells can evade apoptotic cell death while continuing to proliferate through inflammatory mediators and creating an immunosuppressive environment. The PANoptosome functions as a regulatory complex that unites proteins governing pyroptotic, apoptotic, and necroptotic pathways, rather than allowing distinct death pathways to compete. The expression and functional status of key molecules within the PANoptosome, such as ZBP1, RIPK1, RIPK3, CASP8, and ASC, may influence tumor viability and immune detection. The tumorigenic impact of PANoptosis is complex and predominantly manifests through chronic inflammation, immune response modulation, and changes in the tumor microenvironment. PANoptosis also aids in the defense against colon cancer by directly eradicating tumor cells and modifying the cellular environment. The expression profile of PANoptosis components may possess prognostic and predictive significance. The therapeutic ramifications of PANoptosis in colorectal cancer are now being investigated through many avenues. It provides an opportunity to develop targeted therapeutic techniques. In contrast, it may also be pertinent in conjunction with immunotherapy, as PANoptosis signifies an immunogenic type of cell death and may consequently enhance the anti-tumor immune response. A thorough comprehension of how these parameters influence PANoptosis is crucial for practical implementation.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Revisiting Pathogen Exploitation of Clathrin-Independent Endocytosis: Mechanisms and Implications. 重新审视病原体对不依赖网格蛋白的内吞作用的利用：机制和意义。

IF 5.1 2区生物学

Cells Pub Date : 2025-05-16 DOI: 10.3390/cells14100731

Oliver Goldmann, Eva Medina

{"title":"Revisiting Pathogen Exploitation of Clathrin-Independent Endocytosis: Mechanisms and Implications.","authors":"Oliver Goldmann, Eva Medina","doi":"10.3390/cells14100731","DOIUrl":"10.3390/cells14100731","url":null,"abstract":"Endocytosis is a specialized transport mechanism in which the cell membrane folds inward to enclose large molecules, fluids, or particles, forming vesicles that are transported within the cell. It plays a crucial role in nutrient uptake, immune responses, and cellular communication. However, many pathogens exploit the endocytic pathway to invade and survive within host cells, allowing them to evade the immune system and establish infection. Endocytosis can be classified as clathrin-mediated (CME) or clathrin-independent (CIE), based on the mechanism of vesicle formation. Unlike CME, which involves the formation of clathrin-coated vesicles that bud from the plasma membrane, CIE does not rely on clathrin-coated vesicles. Instead, other mechanisms facilitate membrane invagination and vesicle formation. CIE encompasses a variety of pathways, including caveolin-mediated, Arf6-dependent, and flotillin-dependent pathways. In this review, we discuss key features of CIE pathways, including cargo selection, vesicle formation, routes taken by internalized cargo, and the regulatory mechanisms governing CIE. Many viruses and bacteria hijack host cell CIE mechanisms to facilitate intracellular trafficking and persistence. We also revisit the exploitation of CIE by bacterial and viral pathogens, highlighting recent discoveries in entry mechanisms, intracellular fate, and host-pathogen interactions. Understanding how pathogens manipulate CIE in host cells can inform the development of novel antimicrobial and immunomodulatory interventions, offering new avenues for disease prevention and treatment.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

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