Frontiers in Cell and Developmental Biology最新文献

{"title":"Autophagy: regulating the seesaw of bone-fat balance.","authors":"Boya Zhang, Jing Cui, Xu Zhang, Ziyi Pan, Liuyi Du, RongRong Ye, Linlin Wen, Wenhao Zhai, Lei Huang, Daowei Li, Hongchen Sun","doi":"10.3389/fcell.2025.1465092","DOIUrl":"10.3389/fcell.2025.1465092","url":null,"abstract":"<p><p>The interrelationship between bone and fat can be described as a seesaw in bone homeostasis, in which both osteogenesis and adipogenesis occur in a delicate balance. Osteoblasts and adipocytes share a common origin and play key roles in osteogenesis and adipogenesis. Bone-fat balance indicates osteogenesis and adipogenesis keeps a balance for concordant distribution of trabecular bone and bone marrow adipose tissue in bone, thereby leading to the balance between bone metabolism and lipid metabolism. Bone-fat balance is crucial for metabolic health. When disrupted by various factors, this balance can lead to several bone-related metabolic diseases and systemic disorders, such as obesity, osteoporosis, and osteoarthritis. Recent research highlights the role of autophagy dysfunction in these metabolic conditions. Restoring autophagic function can help restore metabolic homeostasis and re-establish the bone-fat balance. The current review explores the factors that regulate bone-fat balance, the consequences of imbalance under pathological conditions, and the potential of autophagy modulation as a therapeutic approach. Overall, it can be concluded that targeting autophagy presents a promising strategy for treating metabolic disorders and restoring bone-fat balance.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1465092"},"PeriodicalIF":4.6,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11891371/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596450","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: Current methods for detecting and diagnosing stem cell pathogenesis: a focus on translational interventions in the contemporary disease and technology landscape.","authors":"Prasad S Koka, Birgitta Sundell-Ranby","doi":"10.3389/fcell.2025.1558476","DOIUrl":"10.3389/fcell.2025.1558476","url":null,"abstract":"","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1558476"},"PeriodicalIF":4.6,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11891188/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596453","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":"Artificial plasticenta: how polystyrene nanoplastics affect <i>in-vitro</i> cultured human trophoblast cells.","authors":"Antonio Ragusa, Loredana Cristiano, Pierluigi Di Vinci, Giuseppe Familiari, Stefania Annarita Nottola, Guido Macchiarelli, Alessandro Svelato, Caterina De Luca, Denise Rinaldo, Isabella Neri, Fabio Facchinetti","doi":"10.3389/fcell.2025.1539600","DOIUrl":"10.3389/fcell.2025.1539600","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;In the human placenta, we have detected the MPs by Raman microspectroscopy analysis and, for the first time, with transmission electron microscopy. MPs fragments have been localized in different compartments of placental tissue, free in the cytoplasm and within organelles like lysosomes. Moreover, their presence has been correlated with ultrastructural alterations of some cell organelles, typical of metabolic stress, mainly dilated rough endoplasmic reticulum and numerous swollen electrodense mitochondria, as well as signs derived from involuting organelles. As a result, we have speculated that microplastics in the placenta could be responsible for pathological traits activation such as oxidative stress, apoptosis, and inflammation causing long-term effects on the health of the mother and child. To demonstrate the cytotoxicity of PS-NPs on the placenta and confirm the &lt;i&gt;in vivo&lt;/i&gt; results, we performed &lt;i&gt;in vitro&lt;/i&gt; experiments on a trophoblast human cell line, the HTR8/SVneo cells.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Materials and methods: &lt;/strong&gt;HTR8/SVneo cells were treated, for 24 h and 48h, with increasing concentrations (10, 25, 50, 75, and 100 μg/mL) of 0.05 µm polystyrene (PS) and cellular viability was evaluated by Counting Kit-8. Fluorescent PS-NPs examined under fluorescence/confocal microscopy were used to investigate the internalization of plastics in the placenta cells. Transmission electron microscopy was used to evaluate possible PS-NPs-dependent ultrastructural alterations of cells and organelles.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Our study shows that starting from 24 h exposure, PS-NPs treatment, at 50 μg/mL dose, has a cytotoxic effect on placental cells, causing the death of 40% of cells and affecting the morphology of the surviving cells. In addition, PS-NPs alter the ultrastructure of some organelles in the surviving cells, like those we have already described &lt;i&gt;in vivo&lt;/i&gt;. We found that NPs enter the cells, affecting the endoplasmic reticulum and mitochondria morphology, accumulating as aggregates within lysosome-like organelles. Interestingly these aggregates become larger as the concentration of NPs increases. We speculated that the accumulation of NPs inside lysosome-like organelles could result from a prolonged and impossible attempt by the cell to remove and destroy PS. This would lead to ER and mitochondrial stress, impairing mitochondria/ER functions and oxidative stress, thus activating the apoptotic pathway and suggesting that PS-NPs could act as a cell stressor, leading to the death of cells. In support of our hypothesis, we also found NPs associated with morphological signs of cellular regression and degeneration, such as the presence of a highly vacuolized cytoplasm, dilatation, and vesiculation of ER, associated with the uncoupling/loss of associated mitochondria, cytoplasmic fragments, and free organelles deriving from cellular lysis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;Based on electron microsc","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1539600"},"PeriodicalIF":4.6,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11891164/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596548","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":"Implications of draxin in neurological disorders.","authors":"Yohei Shinmyo","doi":"10.3389/fcell.2025.1560940","DOIUrl":"10.3389/fcell.2025.1560940","url":null,"abstract":"<p><p>Axon guidance proteins not only play a role in the formation of proper neural circuits but also have other important functions, such as cell survival, migration, and proliferation in the brain. Therefore, mutations in the genes encoding these proteins frequently cause various types of neurological disorders, including psychiatric disorders and neurodegenerative diseases. We previously identified an axon guidance protein, draxin, that is essential for the development of several neural circuits and cell survival in the brain. Recently, the deletion of the <i>draxin</i> gene was identified in an inbred BTBR T⁺ Itpr3^tf/J (BTBR/J) mouse, which is a widely used model of Autism Spectrum Disorder (ASD), suggesting that <i>draxin</i> deletion is a genetic factor for ASD-like characteristics in BTBR/J mice. In this review, I summarize the neuroanatomical abnormalities in <i>draxin</i> knockout mice by comparing them to BTBR/J mice and discuss the possible contributions of draxin to anatomical and behavioral phenotypes in BTBR/J mice.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1560940"},"PeriodicalIF":4.6,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11891372/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596593","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":"Mechanisms underlining R-loop biology and implications for human disease.","authors":"Junzhe Liu, Fengze Li, Yulong Cao, Yonghui Lv, Kunjian Lei, Zewei Tu, Chuandong Gong, Haiyan Wang, Feng Liu, Kai Huang","doi":"10.3389/fcell.2025.1537731","DOIUrl":"10.3389/fcell.2025.1537731","url":null,"abstract":"<p><p>R-loops are three-stranded non-canonical nucleic acid structures composed of nascent RNA hybridized with the template DNA strand, leaving the non-template DNA strand displaced. These structures play crucial roles in regulating gene expression, DNA replication, and transcription processes. However, R-loops have also been increasingly described as highly deleterious, causing genomic instability and DNA damage. To maintain R-loops at a relatively safe level, complex regulatory mechanisms exist to prevent their excessive formation. The growing understanding of R-loop functions has provided valuable insights into their structure and potential clinical applications. Emerging research indicates that R-loops contribute to the pathogenesis of various disorders, including neurodegenerative, immune-related, and neoplastic diseases. This review summarizes R-loop metabolism and its significance in the etiology of associated disorders. By elucidating the regulatory mechanisms governing R-loops, we aim to establish a theoretical foundation for understanding disease pathogenesis and exploring novel therapeutic strategies targeting these hybrid nucleic acid structures.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1537731"},"PeriodicalIF":4.6,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11885306/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585252","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":"Piezo1-related physiological and pathological processes in glioblastoma.","authors":"Weijia Fu, Xue Hou, Lijuan Ding, Jiaying Wei, Wei Hou","doi":"10.3389/fcell.2025.1536320","DOIUrl":"10.3389/fcell.2025.1536320","url":null,"abstract":"<p><strong>Introduction: </strong>Glioblastoma (GBM) is the most malignant of the astrocytomas, primarily involving the cerebral hemispheres and cerebral cortex. It is one of the fatal refractory solid tumors with a 5-year survival rate of only 5% in adults. Cells in biological tissues are subjected to mechanical forces, including hydrostatic pressure, shear stress, compression and tension. Cells can convert mechanomechanical signals into biological or electrical signals, a process known as mechanical signaling. Piezo1 channels, members of the Piezo family of mechanosensitive ion channels, can be directly activated by mechanical stimuli alone, mediating mechanosensitive cation currents that activate subsequent signaling pathways. Studies have shown that Piezo1 is largely unexpressed in normal brain tissues but is expressed at high levels in glioblastoma and can significantly contribute to glioblastoma development and progression, but its role in the pathogenesis of glioblastoma remains unclear.</p><p><strong>Methods: </strong>We reviewed the relevant literature and data in six major databases including PubMed, EMBASE, CINAHL, Scopus, Web of Science and TCGA. Finally, a total of 126 papers were selected for review and analysis (Search terms include: glioblastoma, piezo1, biomechanical, targeted therapy, mechanomechanical, extracellular matrix, radiation therapy and more). The role of piezo1 in the development of glioblastoma was summarized.</p><p><strong>Results: </strong>Piezo1 affects several fundamental pathophysiological processes in glioblastoma, such as tissue sclerosis, angiogenesis, energy supply, and immune cell infiltration, and can be used as an indicator of malignancy and prognosis in patients with glioblastoma, as well as a therapeutic target to control tumor progression.</p><p><strong>Discussion: </strong>The pathological mechanism of piezo1 in glioblastoma is very complex, and the aberrant expression of piezo1 plays a very important role in the development of glioblastoma. Specific mechanistic studies focusing on Piezo1 will help us understand the mechanobiology of glioblastoma and help us develop new therapeutic approaches for glioblastoma patients.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1536320"},"PeriodicalIF":4.6,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11885286/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585258","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":"Advances and challenges in cell therapy for neuropathic pain based on mesenchymal stem cells.","authors":"Wen-Jun Zhang, Xiong-Wei Pi, Dong-Xia Hu, Xiao-Ping Liu, Ming-Ming Wu","doi":"10.3389/fcell.2025.1536566","DOIUrl":"10.3389/fcell.2025.1536566","url":null,"abstract":"<p><p>Neuropathic pain (NPP) is caused by damage to the somatosensory nervous system. Its prominent symptoms are spontaneous pain, hyperalgesia and abnormal pain. This pain is long-lasting and unbearable, seriously affecting the patient's quality of life. At present, the clinical treatment effect of painkillers to relieve NPP is still not ideal, nor can it repair damaged nerves and achieve long-term treatment results. In recent years, the application of cell therapy strategies in the field of pain has yielded encouraging results, including preclinical studies and clinical trials. Mesenchymal stem cells (MSCs) are pluripotent progenitor cells derived from mesogenesis. They have the ability to self-renew and differentiate into multiple cell types and have been widely studied and applied in the field of neuroregenerative medicine. MSCs play an important mechanism functional role in promoting injured nerve regeneration and pain relief by regulating multiple processes in target cells, including immunoregulation, anti-inflammatory properties, promoting axon regeneration and re-myelination, promoting angiogenesis, and secreting neurotrophic factors. Moreover, MSCs can also release exosomes, which may be part of their analgesic effects. Exosomes derived from MSC also have the functional properties of mother cells and have therapeutic potential for treating NPP by promoting cell proliferation, regulating inflammatory responses, reducing cell death, promoting axon regeneration and angiogenesis. Therefore, in this article, we discussed current treatment strategies for NPP and explored the functional role and mechanism of MSCs in the treatment of NPP. We also analyzed the current problems and challenges in the application of MSCs in clinical trials of NPP.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1536566"},"PeriodicalIF":4.6,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11885280/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585108","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":"Notch signaling in cancers: mechanism and potential therapy.","authors":"Chen Chen, Yan Du, Rongzu Nie, Shuangshuang Wang, Hang Wang, Peifeng Li","doi":"10.3389/fcell.2025.1542967","DOIUrl":"10.3389/fcell.2025.1542967","url":null,"abstract":"<p><p>The Notch signaling pathway is an evolutionarily conserved intercellular signaling cascade that regulates a number of cellular processes, including cell development, proliferation, apoptosis, and genome stability. The Notch signaling pathway is pervasive in the human body, affecting tumorigenesis and progression, which is one of the most significant signaling pathways in this regard, influencing various receptors and cellular functions of tumor cells. Aberrant expression or mutation of Notch has been linked to the onset and progression of a variety of malignant tumors. In this review, we discussed the mechanism of Notch signaling in lung, liver and colorectal cancer and explored future strategies and directions for cancer treatment by modifying the Notch signaling pathway.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1542967"},"PeriodicalIF":4.6,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11882598/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572478","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":"Gut microbiota regulates optic nerve fiber myelination.","authors":"Giulia Ronchi, Davide Pellegrino, Marwa El Soury, Olga Amato, Francesco Gaia, Sajjad Farzin, Raffaele Nuzzi, Marijana Basic, Silvia Bolsega, Stefano Geuna, Matilde Cescon, Kirsten Haastert-Talini, Giovanna Gambarotta","doi":"10.3389/fcell.2025.1526855","DOIUrl":"10.3389/fcell.2025.1526855","url":null,"abstract":"<p><strong>Introduction: </strong>Recent evidence supports the hypothesis of an association between gut microbiota and the pathogenesis of retinal and eye diseases, suggesting the existence of a gut-eye axis. However, no data are available on the possible effect of the gut microbiota on the optic nerve fiber maturation and myelin development.</p><p><strong>Methods: </strong>We investigated the impact of gut microbiota on the optic nerves collected from neonatal and young adult germ-free (GF), gnotobiotic (stably colonized with 12 bacteria strains, OMM12) and control (colonized with a complex gut microbiota, CGM) mice, by performing stereological and morphoquantitative analyses with transmission electron microscopy and gene expression analysis by quantitative real-time PCR.</p><p><strong>Results: </strong>Young adult GF and OMM12 optic nerve axons are smaller and hypermyelinated compared to CGM ones, while no such differences were detected in neonatal optic nerves. The transcription factors <i>Olig1</i>, <i>Olig2</i>, and <i>Sox10</i> (oligodendrocyte myelination positive regulators) are downregulated in CGM and OMM12 young adult mice compared to the respective neonates. Such developmental downregulation was not observed in GF optic nerves, suggesting that the absence of the gut microbiota prolongs the stimulation of optic nerve fiber myelination, possibly through mechanisms that are yet to be identified.</p><p><strong>Discussion: </strong>Altogether, these data underscore the gut microbiota pivotal role in driving optic nerve myelination, contributing to our knowledge about both the gut-eye axis and the gut-brain axis, and opening new horizons for further investigations that will explore the role of the microbiota also in pathologies, injuries and regeneration associated with the optic nerve.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1526855"},"PeriodicalIF":4.6,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11904436/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624129","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":"Involvement of SIRT1-mediated aging in liver diseases.","authors":"Yueming Zhang, Chang Gong, Lina Tao, Jinghui Zhai, Fengwei Huang, Sixi Zhang","doi":"10.3389/fcell.2025.1548015","DOIUrl":"10.3389/fcell.2025.1548015","url":null,"abstract":"<p><p>Liver disease is a significant global health issue, responsible for millions of deaths annually. Aging, characterized by the gradual decline in cellular and physiological functions, impairs tissue regeneration, increases susceptibility to liver diseases, and leads to a decline in liver health. Silent information regulator 1 (SIRT1), a NAD⁺-dependent deacetylase, has emerged as a pivotal factor in modulating age-related changes in the liver. SIRT1 preserves liver function by regulating essential aging-related pathways, including telomere maintenance, epigenetic modifications, cellular senescence, intercellular communication, inflammation, and mitochondrial function. Notably, SIRT1 levels naturally decline with age, contributing to liver disease progression and increased vulnerability to injury. This review summarizes the regulatory role of SIRT1 in aging and its impact on liver diseases such as liver fibrosis, alcoholic associated liver disease (ALD), metabolic dysfunction-associated steatotic liver disease (MASLD), and metabolic dysfunction-associated steatohepatitis (MASH), hepatocellular carcinoma (HCC). We also discuss emerging therapeutic approaches, including SIRT1 activators, gene therapy, and nutritional interventions, which are evaluated for their potential to restore SIRT1 function and mitigate liver disease progression. Finally, we highlight future research directions to optimize SIRT1-targeted therapies for clinical applications in age-related liver conditions.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1548015"},"PeriodicalIF":4.6,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11882576/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572390","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}