Frontiers in Cell and Developmental Biology最新文献

{"title":"New insights into tuberous sclerosis complex: from structure to pathogenesis.","authors":"Chao-Sheng Chen, Christopher H S Aylett","doi":"10.3389/fcell.2025.1595867","DOIUrl":"10.3389/fcell.2025.1595867","url":null,"abstract":"<p><p>Tuberous sclerosis complex is a genetic disorder characterised by the formation of benign tumours in multiple organs, primarily due to pathogenic variants in the <i>TSC1</i> and <i>TSC2</i> tumour suppressor genes. These genes encode hamartin and tuberin, respectively, which together with TBC1D7 form a crucial protein complex regulating cell growth and proliferation through mTOR signalling and other pathways. This review provides an overview of recent progress in understanding the molecular structure and function of this key protein complex, its role in cellular processes, pathogenesis, and current and future therapeutic strategies.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1595867"},"PeriodicalIF":4.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12245910/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell analysis reveals the spatiotemporal effects of long-term electromagnetic field exposure on the liver.","authors":"Mingming Zhang, Zhichun Lv, Lingping Zhao, Quan Zeng, Yunqiang Wu, Junnian Zhou, Jiafei Xi, Xuetao Pei, Haiyang Wang, Changyan Li, Wen Yue","doi":"10.3389/fcell.2025.1579121","DOIUrl":"10.3389/fcell.2025.1579121","url":null,"abstract":"<p><strong>Introduction: </strong>Artificial electromagnetic fields (EMFs) can impair the functions of several organs. The impact of long-term artificial EMF on the liver, the synthetic and metabolic center of the body, has become concerning. The aim of this study was to systematically evaluate the effect of long-term EMF exposure on the liver.</p><p><strong>Methods: </strong>Mice were exposed to 2.45 GHz EMF daily for up to 5 months, and serum liver function test, lipidomic analysis, and histological analysis were performed to detect the general impact of EMF on the liver. Furthermore, EMF-induced liver transcriptome variations were investigated using single-cell RNA sequencing and a spatiotemporally resolved analysis.</p><p><strong>Results: </strong>Different hepatic cells exhibited diverse sensitivities and response patterns. Notably, hepatocytes, endothelial cells, and monocytes showed higher sensitivity to electromagnetic radiation, with their lipid metabolic functions, immune regulation functions, and intrinsic functions disturbed, respectively. Moreover, transcriptomic alterations were predominantly observed in the hepatocytes and endothelial cells in peri-portal regions, suggesting a zonation-related sensitivity to EMF within the liver.</p><p><strong>Conclusion: </strong>Our study provided a spatiotemporal visualization of EMF-induced alterations in hepatic cells, which ultimately elucidated the biological effects of EMF exposure.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1579121"},"PeriodicalIF":4.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12245793/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A risk prediction model for neovascular glaucoma secondary to proliferative diabetic retinopathy based on Boruta feature selection and random forest.","authors":"Zihan Huang, Di Gong, Cuicui Tang, Jinghui Wang, Chenchen Zhang, Kuanrong Dang, Xiaoyan Chai, Jiantao Wang, Zhichao Yan","doi":"10.3389/fcell.2025.1604832","DOIUrl":"10.3389/fcell.2025.1604832","url":null,"abstract":"<p><strong>Background: </strong>Neovascular glaucoma (NVG) is one of the most severe complications of proliferative diabetic retinopathy (PDR), carrying a high risk of blindness. Establishing an effective risk prediction model can assist clinicians in early identification of high-risk patients and implementing personalized interventions to reduce the incidence of vision impairment. This study aimed to develop and evaluate a risk prediction model for NVG in PDR patients based on the Boruta feature selection method and random forest algorithm to improve clinical predictive performance.</p><p><strong>Methods: </strong>This retrospective study included 365 PDR patients treated at Shenzhen Eye Hospital between January 2019 and December 2024, comprising 269 controls (non-NVG) and 96 cases (NVG). The Boruta feature selection method was employed to identify key features associated with NVG development in PDR. A risk prediction model was then constructed using the random forest algorithm. Model performance was evaluated based on accuracy, sensitivity, specificity, and area under the curve (AUC). Additionally, calibration curves and decision curve analysis (DCA) were used to assess clinical utility. All data analyses and modeling were performed in R (version 4.2.3).</p><p><strong>Results: </strong>The Boruta algorithm selected 12 significant predictive features. The random forest-based model achieved an accuracy of 90.74%, sensitivity of 82.14%, specificity of 93.75%, and an AUC of 0.87, demonstrating strong predictive performance. Calibration curves indicated reliable prediction probabilities within the 0.4-0.8 range. Decision curve analysis revealed substantial clinical net benefit across threshold probabilities of 0.2-0.8.</p><p><strong>Conclusion: </strong>The Boruta-guided random forest model developed in this study exhibits excellent predictive performance and clinical applicability for assessing NVG risk in PDR patients.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1604832"},"PeriodicalIF":4.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12247303/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic alterations within the primary visual cortex in blind patients with end-stage glaucoma: a proton magnetic resonance spectroscopy study.","authors":"Wenqing Zhu, Linying Guo, Wenwen Chen, Tingting Liu, Xinghuai Sun","doi":"10.3389/fcell.2025.1590460","DOIUrl":"10.3389/fcell.2025.1590460","url":null,"abstract":"<p><strong>Introduction: </strong>Glaucoma, a leading cause of irreversible blindness worldwide, imposes a devastating burden on over 11 million end-stage patients through permanent vision loss. Despite this profound disability, the neurochemical basis of preserved cortical plasticity remains unclear, compounded by the challenge of recruiting this vulnerable population for advanced neuroimaging studies.</p><p><strong>Methods: </strong>We conducted single-voxel proton magnetic resonance spectroscopy (1H-MRS) in 11 blind patients with end-stage primary open-angle glaucoma (POAG) and 11 normal controls to characterize metabolic alterations in the primary visual cortex (V1) and their relationship to residual retinal function.</p><p><strong>Results: </strong>Glutamate-glutamine complex (Glx), N-acetylaspartate (NAA), choline (Cho), and myo-inositol (Ins) ratios relative to creatine (Cr) were quantified, revealing significantly elevated Glx/Cr in POAG (95% CI: 0.09 ∼ 0.63, P = 0.011), while NAA/Cr, Cho/Cr, and Ins/Cr remained stable (P > 0.05). Notably, the Glx/Cr ratio correlated significantly with the N1-wave latency of mfERG (ρ = -0.676, P = 0.022), independent of other clinical parameters.</p><p><strong>Discussion: </strong>These findings demonstrate glutamate hyperactivity coexisting with preserved neuronal and osmotic homeostasis in the V1 of end-stage POAG patients, suggesting adaptive neuroglial compensation. The correlation between Glx/Cr ratios and mfERG responses indicates persistent retinocortical signaling despite blindness, highlighting the potential of 1H-MRS as a valuable tool for assessing cortical plasticity in advanced glaucoma rehabilitation.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1590460"},"PeriodicalIF":4.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12245899/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Zebrafish: bona fide pathophysiological models of human diseases.","authors":"Nicola Facchinello, Antionette L Williams, Natascia Tiso","doi":"10.3389/fcell.2025.1624614","DOIUrl":"https://doi.org/10.3389/fcell.2025.1624614","url":null,"abstract":"","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1624614"},"PeriodicalIF":4.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12246545/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research progress of ECT2 and RhoA-related signaling pathways in gynecological tumors.","authors":"Liying Sheng, Meili Liang, Yueli Wang, Zhimei Zhou, Yajing Xie, Yumin Ke, Zhuna Wu","doi":"10.3389/fcell.2025.1602649","DOIUrl":"10.3389/fcell.2025.1602649","url":null,"abstract":"<p><p>Epithelial Cell Transformation Factor 2 (ECT2) is highly expressed in a variety of cancers, including gynecological tumors. The mislocalization of ECT2 can abnormally activate Ras homolog family member A (RhoA) in the Ras homolog gene family (Rho) Guanine nucleotide Exchange Factor (GEF) family. Activated RhoA binds to Rho-associated protein kinase (ROCK), phosphorylates various target proteins, triggers a cascade reaction, regulates the functions of downstream proteins, and thereby plays an important role in the occurrence and development of tumors. This article reviews the roles of ECT2 and RhoA/ROCK signaling pathways in ovarian cancer, cervical cancer, and endometrial cancer, and summarizes and discusses the research progress of downstream molecules, transduction pathways, and mechanisms related to them. Through comprehensive analysis and summary of the current research results, it is revealed that the ECT2/RhoA/ROCK signaling pathway and related crosstalk pathways play an important role in the occurrence, development, and metastasis of gynecological tumors. This article aims to provide a basis for related research and offer relevant references for the treatment of gynecological tumors in the future.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1602649"},"PeriodicalIF":4.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12246546/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism and regulation of mitophagy in liver diseases: a review.","authors":"Sen Liu, Libo Wang, Liuyang Zhu, Tianyu Zhao, Pinsheng Han, Fengying Yan, Xiaoliang Wang, Chunli Li, Ze Wang, Bao-Feng Yang","doi":"10.3389/fcell.2025.1614940","DOIUrl":"10.3389/fcell.2025.1614940","url":null,"abstract":"<p><p>Mitochondria are vital for the proper operation of healthy eukaryotic cells. Mitophagy, a specialized form of autophagy that targets damaged or surplus mitochondria, plays a key role in both the normal functioning and disease-related processes within the liver. This review aims to explore the main mechanisms underlying the initiation of mitophagy and its importance in various liver conditions, such as alcoholic liver disease, drug-induced liver injury, non-alcoholic fatty liver disease, viral hepatitis, and cancer. Gaining insight into these mechanisms can help overcome the obstacles related to harnessing mitophagy as a therapeutic strategy in clinical practice.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1614940"},"PeriodicalIF":4.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12246547/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding amblyopia from the perspective of neurovascular units: changes in the retina and brain.","authors":"Lin Zhang, Yaqi Zhao, Xiaolu Shi, Fan Wu, Yi Shen","doi":"10.3389/fcell.2025.1590009","DOIUrl":"10.3389/fcell.2025.1590009","url":null,"abstract":"<p><p>As a developmental vision disorder, amblyopia has traditionally been studied with a focus on neurons. However, the neurovascular unit (NVU), a dynamic functional complex of neurons, blood vessels, and glial cells, has recently been implicated in amblyopia. This review systematically discusses the pathological changes and functional interactions of the NVU in retina and brain in amblyopia patients and experimental models, providing a new perspective for clinical intervention.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1590009"},"PeriodicalIF":4.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12245887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interplay between MAPK signaling pathway and autophagy in skin aging: mechanistic insights and therapeutic implications.","authors":"Xu Liu, Bo Chen, Xuefeng Liu, Xiaoqing Zhang, Jingdong Wu","doi":"10.3389/fcell.2025.1625357","DOIUrl":"10.3389/fcell.2025.1625357","url":null,"abstract":"<p><p>Skin aging manifests as structural degradation, functional decline, and heightened disease susceptibility. Central to this process is the overactivation of the mitogen-activated protein kinase (MAPK) signaling pathway triggered by reactive oxygen species (ROS). Autophagy, a lysosomal degradation mechanism essential for maintaining cellular homeostasis, demonstrates context-dependent duality in skin aging by mediating cytoprotective effects and stress-induced dysfunction. Emerging evidence highlights that the interplay between MAPK signaling and autophagy critically modulates skin aging progression. Despite its therapeutic potential, the lack of effective targeting strategies severely hinders clinical translation. Therefore, this review synthesizes current evidence on MAPK-autophagy interplay across key cutaneous cell populations, namely, keratinocytes, fibroblasts, and melanocytes (including melanoma), revealing cell-type-specific regulatory networks that influence skin aging. Subsequently, we explore the therapeutic potential of natural bioactive compounds targeting this interplay to accelerate the translation of evidence into the progression of strategies for combating skin aging.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1625357"},"PeriodicalIF":4.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12245914/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative analysis of small molecule and growth factor-derived human induced pluripotent stem cell-derived hepatocyte-like cells.","authors":"Faizal Z Asumda, Shadia Alzoubi, Kiyasha Padarath, Kimya Jones, Ravindra Kolhe, Ashis Kumar Mondal, Ahmet Alptekin, Wenbo Zhi, Tae Jin Lee, Robert C Huebert, Nathan P Staff, Lewis R Roberts, Lindsey A Kirkeby","doi":"10.3389/fcell.2025.1594340","DOIUrl":"10.3389/fcell.2025.1594340","url":null,"abstract":"<p><p>The growth factor and small molecule protocol are the two primary approaches for generating human induced pluripotent stem cell-derived hepatocyte-like cells (iPSC-HLCs). We compared the efficacy of the growth factor and small molecule protocols across fifteen different human iPSC lines. Morphological assessment, relative quantification of gene expression, protein expression and proteomic studies were carried out. HLCs derived from the growth factor protocol displayed mature hepatocyte morphological features including a raised, polygonal shape with well-defined refractile borders, granular cytoplasm with lipid droplets and/or vacuoles with multiple spherical nuclei or a large centrally located nucleus; significantly elevated hepatocyte gene and protein expression including AFP, HNF4A, ALBUMIN, and proteomic and metabolic features that are more aligned with a mature phenotype. HLCs derived from the small molecule protocol showed a dedifferentiated, proliferative phenotype that is more akin to liver tumor-derived cell lines. These experimental results suggest that HLCs derived from growth factors are better suited for studies of metabolism, biotransformation, and viral infection.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1594340"},"PeriodicalIF":4.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12240953/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}