Frontiers in Cell and Developmental Biology最新文献

{"title":"Chronotherapy and intervertebral disc degeneration: understanding the role of circadian rhythm in degenerative processes.","authors":"Cong Zhang, Rende Zhang, Guanghai Zhao, Zuolong Wu, Wei Song, Rui Ran, Kaisheng Zhou, Haihong Zhang","doi":"10.3389/fcell.2025.1586193","DOIUrl":"10.3389/fcell.2025.1586193","url":null,"abstract":"<p><p>Intervertebral disc degeneration (IDD) and low back pain are prevalent issues globally, affecting a significant portion of the adult population. Recent research has highlighted the crucial role of circadian rhythms in the degenerative processes of intervertebral discs (IVDs). Circadian rhythms are regulated by a coordinated network of oscillators, consisting of a central clock system and various peripheral clock systems. These rhythms are influenced by environmental factors, particularly the light/dark cycle, and disruptions can lead to cumulative stress and imbalances within the body. The IVD tissue contains an autonomous oscillating peripheral clock, and evidence suggests that disruptions in these circadian rhythms can accelerate tissue aging and increase the risk of IDD. Studies have shown that reduced expression of clock genes, such as BMAL1, is an independent risk factor for IDD progression. Furthermore, circadian disruptions can imbalance anabolic and catabolic processes within IVDs, leading to tissue degeneration. Understanding the role of circadian rhythms in IDD may provide valuable insights into potential therapeutic strategies for preventing or mitigating disc degeneration. The review explores the entrainment of circadian rhythms with external physiological signals and their impact on disc physiology. Notably, disruptions in circadian rhythms have been linked to accelerated disc degeneration, with implications for tissue aging, metabolic imbalances, and inflammatory responses. Furthermore, the paper discusses potential therapeutic strategies, including chronotherapy, which aims to synchronize treatment interventions with circadian rhythms to optimize outcomes in IDD management. Understanding the intricate interplay between circadian rhythms and IDD could pave the way for innovative treatment approaches, ultimately improving patient care.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1586193"},"PeriodicalIF":4.6,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12171443/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316297","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":"Deep spatial sequencing revealing differential immune responses in human hepatocellular carcinoma.","authors":"Yan-Ping Yu, Caroline Obert, Bao-Guo Ren, Marielle Krivit, Kyle Metcalfe, Jia-Jun Liu, Tuval Ben-Yehezkel, Silvia Liu, Jian-Hua Luo","doi":"10.3389/fcell.2025.1600129","DOIUrl":"10.3389/fcell.2025.1600129","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is one of the most lethal cancers for humans. HCC is highly heterogeneous. In this study, we performed ultra-depth (∼1 million reads per spot) sequencing of 6,320 spatial transcriptomes on a case of HCC. Sixteen distinct spatial expression clusters were identified. Each of these clusters was spatially contiguous and had distinct gene expression patterns. In contrast, benign liver tissues showed minimal heterogeneity in terms of gene expression. Numerous immune cell-enriched spots were identified in both HCC and benign liver regions. Cells adjacent to these immune cell-enriched spots showed significant alterations in their gene expression patterns. Interestingly, the responses of HCC cells to the nearby immune cells were significantly more intense and broader, while the responses of benign liver cells to immune cells were somewhat narrow and muted, suggesting an innate difference in immune cell activities towards HCC cells in comparison with benign liver cells. However, cell-cell interaction analyses showed significant immune evasion by HCC cancer cells. When standard-depth sequencing was performed, significant numbers of genes and pathways that were associated with these changes disappeared. Qualitative differences in some pathways were also found. These results suggest that deep spatial sequencing may help to uncover previously unidentified mechanisms of liver cancer development.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1600129"},"PeriodicalIF":4.6,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12170511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316347","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":"Induced neural stem cells ameliorate blood-brain barrier injury by modulating the calcium signaling pathway of astrocyte in cerebral ischemia-reperfusion rats.","authors":"Xueyun Liang, Chuanshang Cao, Ningmei Liu, Dongmei Chen, Ting Liu, Haibin Ma, Jiaxin Liu, Taojuan Wu, Jianguo Niu","doi":"10.3389/fcell.2025.1611226","DOIUrl":"10.3389/fcell.2025.1611226","url":null,"abstract":"<p><strong>Background: </strong>Neural stem cells offer new hope for ischemic stroke patients on the basis of their potential to reverse neurological sequelae, but it is still difficult to obtain sufficient neural stem cells in the clinic. We induced human placental mesenchymal stem cells to neural stem cells (iNSCs), the therapeutic effects and possible mechanisms of iNSCs in ischemic stroke were observed in this study.</p><p><strong>Results: </strong>Transplanted iNSCs improved neurological deficits, increased the integrity of blood-brain barrier (BBB) structure and its related proteins expression level in middle cerebral artery occlusion/reperfusion (MCAO/R) rats. The <i>in vitro</i> study demonstrated that iNSCs treatment inhibited Ca²⁺ influx in oxygen-glucose deprived (OGD)-damaged astrocytes. Additionally, iNSCs downregulated the expression level of pCaMK-II, increased the expression level of superoxide dismutase, and inhibited the expression of caspase 9 in both brain of MCAO/R rats and OGD-damaged astrocytes.</p><p><strong>Conclusion: </strong>iNSCs transplantation improved BBB function by modulating calcium signaling pathway of astrocyte in MCAO/R rats, which proved iNSCs may be a new promising neural stem cells origin for the treatment of cerebral ischemia-reperfusion injury.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1611226"},"PeriodicalIF":4.6,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12170639/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316351","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":"Establishment of human periodontal ligament cell lines with <i>ALPL</i> mutations to mimic dental aspects of hypophosphatasia.","authors":"Jana Schiffmaier, Sofia Rehling, Katharina Marnet, Angela Borst, Drenka Trivanović, Denitsa Docheva, Franz Jakob, Stephanie Graser, Marietta Herrmann, Daniel Liedtke","doi":"10.3389/fcell.2025.1572571","DOIUrl":"10.3389/fcell.2025.1572571","url":null,"abstract":"<p><strong>Introduction: </strong>Besides skeletal symptoms, dental abnormalities are a typical feature of the rare inherited disorder hypophosphatasia (HPP), which is caused by loss of function mutations in the <i>ALPL</i> gene (alkaline phosphatase, biomineralization associated) coding for tissue-nonspecific alkaline phosphatase (TNAP). Dental symptoms include premature loss of deciduous teeth, disturbance in dentin and cementum mineralization, and an increased risk for periodontitis. However, the underlying molecular mechanisms are not fully understood and experimental cell lines for <i>in vitro</i> analyses of these processes are missing.</p><p><strong>Methods: </strong>We aimed to develop a physiologically relevant cellular model of dental origin with genetic <i>ALPL</i> variants to investigate the molecular consequences of TNAP deficiencies <i>in vitro</i>. For this purpose, we used immortalized periodontal ligament stem cells (PDL-hTERT cells) to establish five independent clonal cell lines via CRISPR/Cas9, harboring different <i>ALPL</i> genetic variants.</p><p><strong>Results: </strong>Detailed investigation of their genetic properties revealed that four different genotypes were successfully established at two different positions within the <i>ALPL</i> gene locus. The detected variants either result in mis-splicing of <i>ALPL</i> mRNAs or in frameshift mutations. All determined variants implied severe consequences on TNAP function, as indicated by <i>in silico</i> modeling and comparison to reported human pathogenic variants. Subsequent detailed cell culture experiments demonstrated TNAP residual gene expression and altered TNAP activity in the newly established <i>ALPLtg</i> PDL-hTERT lines. Further assessment of cell line features showed significantly reduced cell growth, partly lower levels of intracellular ATP as well as mitochondrial function proteins. TNAP activity was furthermore investigated during <i>in vitro</i> osteogenic differentiation and strong suppression during this process in nearly all newly established lines was observed.</p><p><strong>Discussion: </strong>We report the generation of a new set of immortalized <i>ALPLtg</i> PDL-hTERT cells for investigation of TNAP cellular function in PDL cells, which can be used in subsequent studies for deciphering molecular processes in dental cells affected by reduction of TNAP function.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1572571"},"PeriodicalIF":4.6,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12170583/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316349","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":"Perillaldehyde synergizes with ferroptosis inducers to promote ferroptotic cell death in gastric cancer.","authors":"Rui Wang, Jin-Feng Cui, Jing Lv, Jia-Lin Song, Yang-Yang Lu, Xiao-Juan Huang, Zhong-Kun Lin, Si-Yi Zhang, Sha-Sha Wang, Wen-Sheng Qiu","doi":"10.3389/fcell.2025.1598520","DOIUrl":"10.3389/fcell.2025.1598520","url":null,"abstract":"<p><strong>Introduction: </strong>As a traditional medicine and food homologous plant, Perilla frutescens is widely cultivated in China, Japan, and Korea. According to the <i>Compendium of Materia Medica</i>, the leaves, stems, and seeds of perilla can all be used as medicine. Perilla essential oil has been used in traditional Chinese medicine since ancient times. It has been demonstrated that perillaldehyde (PAH), a primary composition of the essential oil extracted from perilla, can inhibit tumor growth through multiple mechanisms. However, the specific mechanisms by which PAH suppresses gastric cancer remain incompletely understood.</p><p><strong>Methods: </strong>We performed <i>in vitro</i> experiments using three cell lines (AGS, HGC27, and MFC) to assess the effects of PAH on cell viability, proliferation, and migration of gastric cancer cells. Concurrently, we established a subcutaneous gastric tumor model in BALB/c nude mice for <i>in vivo</i> animal studies. Subsequently, oxidative stress was measured via fluorescence staining techniques (H₂DCFDA, DHE, and JC-1). We then evaluated whether PAH induced ferroptosis in gastric cancer cells through FerroOrange staining, quantification of intracellular glutathione (GSH) and lipid peroxidation levels, and Western blotting. Finally, PAH was co-administered with the ferroptosis inhibitor Ferrostatin-1 (Fer-1) or the ferroptosis inducer RSL3, and relevant experiments were re-evaluated.</p><p><strong>Results: </strong>In this study, PAH was proven to inhibit the growth of gastric cancer both <i>in vivo</i> and <i>in vitro</i>. It led to a reduction in mitochondrial membrane potential (MMP), an augmentation of the accumulation of reactive oxygen species (ROS), and an elevation of oxidative stress levels. Moreover, PAH decreased intracellular GSH levels while increasing intracellular lipid peroxidation and Fe²⁺ levels. These effects indicate that PAH induces ferroptosis via inhibiting the system Xc (-)/GSH/GPX4 axis. Furthermore, PAH influenced the expression of proteins related to iron transport and storage and regulated ferroptosis via the P62-Keap1-Nrf2 pathway. When combined with the ferroptosis inducer RSL3, PAH could promote ferroptosis in gastric cancer.</p><p><strong>Discussion: </strong>Our research suggests a potential therapeutic strategy in which PAH could be used to synergize with ferroptosis inducers for treating gastric cancer.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1598520"},"PeriodicalIF":4.6,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12170665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316354","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":"Microbiota dysbiosis impact on the metabolism of T3 and T4 hormones and its association with thyroid cancer.","authors":"Santiago Cadena-Ullauri, Patricia Guevara-Ramírez, Elius Paz-Cruz, Viviana A Ruiz-Pozo, Rafael Tamayo-Trujillo, Ana Karina Zambrano","doi":"10.3389/fcell.2025.1589726","DOIUrl":"10.3389/fcell.2025.1589726","url":null,"abstract":"<p><p>This review explores the impact of gut microbiota dysbiosis on thyroid hormone metabolism and its potential association with thyroid cancer. The analysis highlights specific bacterial genera linked to thyroid dysfunction, the role of gut microbiota in iodine absorption, and mechanisms connecting dysbiosis with thyroid disorders such as hypothyroidism, hyperthyroidism, Hashimoto's thyroiditis, and Graves' disease. Additionally, it examines the potential of gut microbiota as a biomarker for diagnosis and personalized treatment, as well as the prospect of probiotics and microbiota-targeted treatments. The review emphasizes the importance of conducting additional research to fully understand microbiota-thyroid interactions and develop appropriate therapies to improve clinical outcomes and patient quality of life.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1589726"},"PeriodicalIF":4.6,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12171323/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316352","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":"Myosin VI is expressed in developing ovarian follicles in <i>Drosophila</i> but is not essential for effective oogenesis.","authors":"Robert Lenartowski, Jakub Ostrowski, Anna Suwińska, Anna Richert, Przemysław Zakrzewski, Magdalena Izdebska, Wioletta Arendt, Kathryn G Miller, Marta Lenartowska","doi":"10.3389/fcell.2025.1535117","DOIUrl":"10.3389/fcell.2025.1535117","url":null,"abstract":"<p><p>Myosin VI is the only actin-based motor known to move toward the minus end of actin filaments. This protein is involved in many different cellular processes, such as endocytosis, autophagy, secretion, and regulation of actin organization and dynamics. Myosin VI has also been suggested to play an important role in collective migration of border cells and egg chamber development during <i>Drosophila</i> oogenesis. Here we show for the first time that myosin VI is expressed in <i>Drosophila</i> germarium as well as in early ovarian follicles, especially in the developing oocyte. As oogenesis progresses, the level of myosin VI in maturing egg chambers decreases, but this protein is present both in the nascent border cell cluster, during its delamination from the epithelium, and then during the early stages of border cell migration. However, we demonstrate that myosin VI deficiency in border cells, or even complete lack of this protein in myosin VI mutant do not inhibit border cell migration. Moreover, deficiency/lack of myosin VI does not cause any serious defects in ovarian morphology, egg chamber morphogenesis, oogenesis, and egg development. Thus we conclude that myosin VI is not a key player in <i>Drosophila</i> oogenesis.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1535117"},"PeriodicalIF":4.6,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12171261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316353","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":"Review of sensory systems deployed by epidermal keratinocytes.","authors":"Mitsuhiro Denda, Peter M Elias","doi":"10.3389/fcell.2025.1598326","DOIUrl":"10.3389/fcell.2025.1598326","url":null,"abstract":"<p><p>Recent studies have shown that epidermal sensory receptors intercept and direct responses to potentially threatening environmental factors, including shifts in temperature, electric potential, sound, acidity, light, taste, and odor. In addition to stimulating epidermal responses, activation of keratinocytes by these stressors can directly signal the central nervous system. Changes in epidermal permeability barrier homeostasis also depend upon ion dynamics, particularly alterations in intraepidermal gradients of calcium (Ca²⁺) and pH. The purpose of this review is to update readers about recent advances in the field of cutaneous sensory receptors, focusing upon their roles in mediating not only permeability barrier function, but also whole-body physiology and certain aspects of mental status.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1598326"},"PeriodicalIF":4.6,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12171141/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316355","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":"Gonadotropins differentially regulate testicular cell adhesion and junctional complexes during flatfish spermiogenesis through the oxytocin and relaxin signaling pathways.","authors":"Noelia López-Fortún, Jose Vicente Roig-Genovés, Ignacio Giménez, Joan Cerdà, François Chauvigné","doi":"10.3389/fcell.2025.1574690","DOIUrl":"10.3389/fcell.2025.1574690","url":null,"abstract":"<p><strong>Introduction: </strong>The molecular mechanisms regulating teleost semicystic spermatogenesis remain largely unknown. In the flatfish Senegalese sole (<i>Solea senegalensis</i>), haploid round spermatids released into the lumen of the seminiferous tubules resume spermiogenesis (the differentiation of germ cells into spermatozoa) in response to the luteinizing hormone (Lh). However, how the spermatids detach from Sertoli cells and how Lh crosses the blood-testis barrier (BTB) are yet to be determined.</p><p><strong>Methods: </strong>Here, we used an RNA-seq transcriptomic analysis of the testis from sole males treated with recombinant follicle stimulating hormone and Lh (rFsh and rLh, respectively).</p><p><strong>Results: </strong>This analysis reveals that both gonadotropins differentially downregulate a number of transcripts potentially encoding cell-cell junction and adhesion proteins, as well as components of the Oxytocin (Oxt) and Relaxin (Rln) signaling pathways. <i>In situ</i> hybrizidation and immunolocalization experiments confirmed the formation of adherens, gap, and tight junctions between Sertoli cells, and between Sertoli cells and spermatids. Using these methods, we also verified the expression of Oxt and Rln peptides and their cognate receptors in these cells. Further <i>in vitro</i> assays using testicular explants incubated with Oxt, Rln and inhibitors of their receptors, combined with rFsh or rLh, showed that the gonadotropic-induced transcriptional repression of cell junction and adhesion genes in the seminiferous epithelium, particularly by Lh, was largely mediated by the downregulation of Oxt and Rln signaling.</p><p><strong>Discussion: </strong>These data suggest that the Oxt- and Rln-mediated gonadotropic disruption of the BTB and Sertoli cells-spermatid junctions in the sole testis facilitates spermatid release and Lh paracellular transport into the seminiferous lumen during spermiogenesis.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1574690"},"PeriodicalIF":4.6,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12171224/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316350","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":"Automatic detection of optic canal fractures and recognition and segmentation of anatomical structures in the orbital apex based on artificial intelligence.","authors":"Yu-Lin Li, Yu-Hao Li, Mu-Yang Wei, Guang-Yu Li","doi":"10.3389/fcell.2025.1609028","DOIUrl":"10.3389/fcell.2025.1609028","url":null,"abstract":"<p><strong>Background and objectives: </strong>Traumatic optic neuropathy (TON) caused by optic canal fractures (OCF) can result in severe visual impairment, even blindness. Timely and accurate diagnosis and treatment are crucial for preserving visual function. However, diagnosing OCF can be challenging for inexperienced clinicians due to atypical OCF changes in imaging studies and variability in optic canal anatomy. This study aimed to develop an artificial intelligence (AI) image recognition system for OCF to assist in diagnosing OCF and segmenting important anatomical structures in the orbital apex.</p><p><strong>Methods: </strong>Using the YOLOv7 neural network, we implemented OCF localization and assessment in CT images. To achieve more accurate segmentation of key anatomical structures, such as the internal carotid artery, cavernous sinus, and optic canal, we introduced Selective Kernel Convolution and Transformer encoder modules into the original UNet structure.</p><p><strong>Results: </strong>The YOLOv7 model achieved an overall precision of 79.5%, recall of 74.3%, F1 score of 76.8%, and mAP@0.5 of 80.2% in OCF detection. For segmentation tasks, the improved UNet model achieved a mean Intersection over Union (mIoU) of 92.76% and a mean Dice coefficient (mDice) of 90.19%, significantly outperforming the original UNet. Assisted by AI, ophthalmology residents improved their diagnostic AUC-ROC from 0.576 to 0.795 and significantly reduced diagnostic time.</p><p><strong>Conclusion: </strong>This study developed an AI-based system for the diagnosis and treatment of optic canal fractures. The system not only enhanced diagnostic accuracy and reduced surgical collateral damage but also laid a solid foundation for the continuous development of future intelligent surgical robots and advanced smart healthcare systems.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1609028"},"PeriodicalIF":4.6,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12162580/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144301443","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}