Frontiers in Cell and Developmental Biology最新文献

{"title":"Harnessing exercise to combat chronic diseases: the role of Drp1-Mediated mitochondrial fission.","authors":"Yingxin Sun, Junchen He, Lei Bao, Xiaoming Shi, Jinghong Wang, Qingwen Li","doi":"10.3389/fcell.2025.1481756","DOIUrl":"10.3389/fcell.2025.1481756","url":null,"abstract":"<p><p>Enhanced Drp1 activity mediates excessive mitochondrial fission, contributing to the onset and progression of various chronic diseases, including neurodegenerative, cardiovascular, and metabolic disorders. Studies indicate that exercise mitigates mitochondrial dysfunction by modulating Drp1-related signaling targets, thereby inhibiting Drp1 activity and reducing excessive mitochondrial fission. This, in turn, enhances mitochondrial function and cellular metabolism. This review synthesizes the current understanding of Drp1 structure and activation mechanisms, and analyzes the effects of exercise interventions on Drp1-mediated mitochondrial fission in different disease models to improve common chronic conditions. This research deepens our insight into the specific mechanisms of Drp1-induced excessive mitochondrial fission in chronic disease pathogenesis, offering new theoretical support and practical guidance for exercise as a non-pharmacological intervention strategy.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1481756"},"PeriodicalIF":4.6,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897009/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614279","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":"Sorting of complex sphingolipids within the cellular endomembrane systems.","authors":"Victor O Svistunov, Kigumbi J Ehrmann, Wayne I Lencer, S S Schmieder","doi":"10.3389/fcell.2024.1490870","DOIUrl":"10.3389/fcell.2024.1490870","url":null,"abstract":"<p><p>Cells contain a plethora of structurally diverse lipid species, which are unevenly distributed across the different cellular membrane compartments. Some of these lipid species require vesicular trafficking to reach their subcellular destinations. Here, we review recent advances made in the field that contribute to understanding lipid sorting during endomembrane trafficking.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"12 ","pages":"1490870"},"PeriodicalIF":4.6,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897003/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614139","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 therapy in gastrointestinal diseases.","authors":"Hanif Ullah, Safia Arbab, Chengting Chang, Saira Bibi, Nehaz Muhammad, Sajid Ur Rehman, Suleman, Irfan Ullah, Inam Ul Hassan, Yali Tian, Ka Li","doi":"10.3389/fcell.2025.1514636","DOIUrl":"10.3389/fcell.2025.1514636","url":null,"abstract":"<p><p>The human gut microbiota, consisting of trillions of microorganisms, plays a crucial role in gastrointestinal (GI) health and disease. Dysbiosis, an imbalance in microbial composition, has been linked to a range of GI disorders, including inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), celiac disease, and colorectal cancer. These conditions are influenced by the interactions between the gut microbiota, the host immune system, and the gut-brain axis. Recent research has highlighted the potential for microbiome-based therapeutic strategies, such as probiotics, prebiotics, fecal microbiota transplantation (FMT), and dietary modifications, to restore microbial balance and alleviate disease symptoms. This review examines the role of gut microbiota in the pathogenesis of common gastrointestinal diseases and explores emerging therapeutic approaches aimed at modulating the microbiome. We discuss the scientific foundations of these interventions, their clinical effectiveness, and the challenges in their implementation. The review underscores the therapeutic potential of microbiome-targeted treatments as a novel approach to managing GI disorders, offering personalized and alternative options to conventional therapies. As research in this field continues to evolve, microbiome-based interventions hold promise for improving the treatment and prevention of gastrointestinal diseases.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1514636"},"PeriodicalIF":4.6,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897527/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614174","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":"Prolactin drives cortical neuron maturation and dendritic development during murine embryonic stem cell differentiation.","authors":"Omar Martinez-Alarcon, Daniela Colin-Lagos, Ximena Ramirez-Meza, Alejandra Castilla, Georgina Hernandez-Montes, Eliezer Flores-Garza, Alejandro Lopez-Saavedra, Daniela Avila-Gonzalez, Alejandro Martinez-Juarez, Anayansi Molina-Hernández, Nestor Emmanuel Diaz-Martinez, Wendy Portillo, Nestor Fabian Diaz","doi":"10.3389/fcell.2025.1551090","DOIUrl":"10.3389/fcell.2025.1551090","url":null,"abstract":"<p><strong>Introduction: </strong>Prolactin (PRL) is a pleiotropic hormone implicated in various physiological processes; however, its contribution to neurodevelopment, particularly early corticogenesis, remains insufficiently characterized. In this study, we investigate PRL's regulatory influence on the initial stages of cortical development, with an emphasis on its effects on neuronal and astrocytic differentiation.</p><p><strong>Methods: </strong>We employed a standardized in vitro differentiation protocol to generate cortical neurons from mouse embryonic stem cells (mESCs). Prolactin receptor (PRLr) expression was evaluated in pluripotent stem cells, neural stem cells (NSCs), immature neurons, and mature neurons using both PCR and immunofluorescence. These analyses revealed dynamic changes in PRLr expression throughout the differentiation process. Additionally, cells were treated with varying concentrations of PRL during early and late differentiation phases, enabling assessment of its impact on neuronal phenotypic distribution and morphological complexity.</p><p><strong>Results: </strong>Early PRL administration significantly enhanced the population of β-tubulin III + immature neurons, promoting neuronal survival without altering NSC proliferation. Furthermore, PRL treatment increased the abundance of Tbr1 + and NeuN + neurons, augmented dendritic complexity, and accelerated neuronal maturation. In contrast, PRL exposure at later stages of neural differentiation did not yield comparable effects. Notably, PRL delayed the maturation of protoplasmic astrocytes, although the total astrocyte population was not affected.</p><p><strong>Discussion: </strong>These findings highlight PRL's pivotal role as a regulator of early corticogenesis by modulating neuronal survival, dendritic development, and astrocyte maturation. PRL thus emerges as a potential key factor in neurodevelopment, underscoring its importance in the hormonal regulation of neural differentiation and maturation. These insights may have broader implications for understanding the molecular and cellular mechanisms underlying normal and pathological neurodevelopment.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1551090"},"PeriodicalIF":4.6,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897521/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614283","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":"Ferroptosis and noncoding RNAs: exploring mechanisms in lung cancer treatment.","authors":"Nadi Rostami Ravari, Farzad Sadri, Mohammad Ali Mahdiabadi, Yaser Mohammadi, Zahra Ourang, Zohreh Rezaei","doi":"10.3389/fcell.2025.1522873","DOIUrl":"10.3389/fcell.2025.1522873","url":null,"abstract":"<p><p>Lung cancer (LC) is a highly prevalent and deadly type of cancer characterized by intricate molecular pathways that drive tumor development, metastasis, and resistance to conventional treatments. Recently, ferroptosis, a controlled mechanism of cell death instigated by iron-dependent lipid peroxidation, has gained attention for its role in LC progression and treatment. Noncoding RNAs (ncRNAs), such as microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), are emerging as key modulators of ferroptosis, significantly influencing LC biology. This review explores how ncRNAs control ferroptotic pathways and affect tumor growth, metastasis, and therapy resistance in LC. By understanding the dual functions of ncRNAs in both activating and inhibiting ferroptosis, we aim to uncover new therapeutic targets and strategies for LC. These insights provide a promising direction for the development of ncRNA-based treatments designed to induce ferroptosis, potentially improving therapeutic outcomes for patients with LC.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1522873"},"PeriodicalIF":4.6,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897296/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614170","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":"Ferritinophagy: multifaceted roles and potential therapeutic strategies in liver diseases.","authors":"Kejia Wu, Wei Zhao, Zeyu Hou, Weigang Zhang, Lei Qin, Junyi Qiu, Daobin Wang, Lin Zhuang, Xiaofeng Xue, Ding Sun","doi":"10.3389/fcell.2025.1551003","DOIUrl":"10.3389/fcell.2025.1551003","url":null,"abstract":"<p><p>Ferritinophagy, the selective autophagic degradation of ferritin to release iron, is emerging as a critical regulator of iron homeostasis and a key player in the pathogenesis of various liver diseases. This review comprehensively examines the mechanisms, regulation, and multifaceted roles of ferritinophagy in liver health and disease. Ferritinophagy is intricately regulated by several factors, including Nuclear Receptor Coactivator 4 (NCOA4), Iron regulatory proteins and signaling pathways such as mTOR and AMPK. These regulatory mechanisms ensure proper iron utilization and prevent iron overload, which can induce oxidative stress and ferroptosis. In liver diseases, ferritinophagy exhibits dual roles. In liver fibrosis, promoting ferritinophagy in hepatic stellate cells (HSCs) can induce cell senescence and reduce fibrosis progression. However, in non-alcoholic fatty liver disease (NAFLD), chronic ferritinophagy may exacerbate liver injury through iron overload and oxidative stress. In hepatocellular carcinoma (HCC), ferritinophagy can be harnessed as a novel therapeutic strategy by inducing ferroptosis in cancer cells. Additionally, ferritinophagy is implicated in drug-induced liver injury and sepsis-associated liver damage, highlighting its broad impact on liver pathology. This review also explores the crosstalk between ferritinophagy and other selective autophagy pathways, such as mitophagy and lipophagy, which collectively influence cellular homeostasis and disease progression. Understanding these interactions is essential for developing comprehensive therapeutic strategies targeting multiple autophagy pathways. In summary, ferritinophagy is a complex and dynamic process with significant implications for liver diseases. This review provides an in-depth analysis of ferritinophagy's regulatory mechanisms and its potential as a therapeutic target, emphasizing the need for further research to elucidate its role in liver health and disease.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1551003"},"PeriodicalIF":4.6,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11893559/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604392","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":"Construction of a novel gene signature linked to ferroptosis in pediatric sepsis.","authors":"Mingyuan Fan, Meiting Chen, Yongqi Gao, Huilin Jiang, Yanling Li, Gongxu Zhu, Shengkuan Chen, Yiming Xu, Xiaohui Chen","doi":"10.3389/fcell.2025.1488904","DOIUrl":"10.3389/fcell.2025.1488904","url":null,"abstract":"<p><strong>Introduction: </strong>Pediatric sepsis is a complex and life-threatening condition characterized by organ failure due to an uncontrolled immune response to infection. Recent studies suggest that ferroptosis, a newly identified form of programmed cell death, may play a role in sepsis progression. However, the specific mechanisms of ferroptosis in pediatric sepsis remain unclear.</p><p><strong>Methods: </strong>In this study, we analyzed microarray datasets from pediatric sepsis and healthy blood samples to identify ferroptosis-associated genes. A protein-protein interaction (PPI) network analysis and histological validation were performed to identify key genes. Additionally, immune infiltration analysis was conducted to explore the correlation between immune cells, immune checkpoint-related genes, and key genes. A competing endogenous RNA (ceRNA) network was constructed to investigate potential regulatory mechanisms involving long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and key ferroptosis-related genes.</p><p><strong>Results: </strong>We identified 74 genes associated with ferroptosis in pediatric sepsis. Among them, five key genes (MAPK3, MAPK8, PPARG, PTEN, and STAT3) were confirmed through PPI network analysis and histological validation. Immune infiltration analysis revealed significant interactions between immune cells and key genes. The ceRNA network provided insights into the regulatory relationships between lncRNAs, miRNAs, and ferroptosis-related genes.</p><p><strong>Discussion: </strong>These findings enhance our understanding of the role of ferroptosis in pediatric sepsis and highlight potential therapeutic targets for future research and clinical interventions.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1488904"},"PeriodicalIF":4.6,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11893615/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604326","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":"Prion protein fragment (106-126) activates NLRP3 inflammasome and promotes platelet-monocyte/neutrophil interactions, potentially contributing to an inflammatory state.","authors":"Rashmi Verma, Jyotsna Kailashiya, Avijit Mukherjee, Rameshwar Nath Chaurasia, Debabrata Dash","doi":"10.3389/fcell.2025.1534235","DOIUrl":"10.3389/fcell.2025.1534235","url":null,"abstract":"<p><strong>Introduction: </strong>Prion diseases are neurodegenerative disorders where infectious prion proteins (PrP) featuring an amyloidogenic amino acid sequence, PrP (106-126), accumulate in the brain leading to neuroinflammation while it can also access circulation by breaching the blood-brain barrier. Platelets are highly sensitive cells in blood, which have been widely employed as \"peripheral\" model for neurons. In addition to their stellar roles in hemostasis and thrombosis, platelets are also known to function as immune cells and possess necessary components of functional inflammasome. This study demonstrates that prion proteins drive inflammasome assembly in platelets and upregulate activity of caspase-1, a critical readout of functional inflammasomes.</p><p><strong>Methods: </strong>Flow cytometric analysis was performed to measure intracellular ROS levels, caspase-1 activity, and platelet-monocyte/neutrophil interactions. Microscopy was used to assess the co-localization of NLRP3 and ASC.</p><p><strong>Results: </strong>Inflammasome activation is fuelled by reactive oxygen species (ROS) generated in prion-stimulated platelets that eventually leads to formation of platelet-monocyte/neutrophil aggregates, which was prohibited by small-molecule inhibitors of either caspase-1 or ROS.</p><p><strong>Discussion: </strong>Thus, in addition to their neurotoxic effects on neuronal cells and stimulation of pro-coagulant activity in platelets, prions also unleash an inflammatory response in the organism.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1534235"},"PeriodicalIF":4.6,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11895701/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604448","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":"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}