Frontiers in Cell and Developmental Biology最新文献

{"title":"Hydrogel systems for spatiotemporal controlled delivery of immunomodulators: engineering the tumor immune microenvironment for enhanced cancer immunotherapy.","authors":"Yanting Liu, Fang Liu, Yan Zeng, Liangbin Lin, Hui Yu, Sunfu Zhang, Wenyong Yang","doi":"10.3389/fcell.2024.1514595","DOIUrl":"10.3389/fcell.2024.1514595","url":null,"abstract":"<p><p>Tumor immunotherapy, modulating innate and adaptive immunity, has become an important therapeutic strategy. However, the tumor immune microenvironment's (TIME) complexity and heterogeneity challenge tumor immunotherapy. Hydrogel is a hydrophilic three-dimensional (3D) mesh structure with good biocompatibility and drug release control, which is widely used in drug delivery, agriculture, industry, etc. Hydrogels loaded with immune cells, cytokines, immune checkpoint inhibitors, and anti-tumor drugs can achieve targeted delivery and ultimately activate the immune response in the TIME. In this review, we will summarize the components of the TIME and their immune effects, the emerging immunomodulatory agents, the characteristics and functions of hydrogels, and how hydrogels regulate innate and adaptive immune cells in the TIME.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"12 ","pages":"1514595"},"PeriodicalIF":4.6,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142902670","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":"Corrigendum: Single nucleotide polymorphisms of porcine lncMGPF regulate meat production traits by affecting RNA stability.","authors":"Wei Lv, Shiyu Zhao, Yunqing Hou, Qian Tong, Yaxin Peng, Jianan Li, Zaiyan Xu, Bo Zuo","doi":"10.3389/fcell.2024.1502304","DOIUrl":"https://doi.org/10.3389/fcell.2024.1502304","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fcell.2021.731712.].</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"12 ","pages":"1502304"},"PeriodicalIF":4.6,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671692/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142902666","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":"Ferrostatin-1 improves acute sepsis-induced cardiomyopathy via inhibiting neutrophil infiltration through impaired chemokine axis.","authors":"Jialin Li, Fang Xiao, Bingsen Lin, Zhilei Huang, Mingyue Wu, Huan Ma, Ruoxu Dou, Xiaodong Song, Zhongxing Wang, Changjie Cai, Xiangdong Guan, Jie Xu, Fu-Li Xiang","doi":"10.3389/fcell.2024.1510232","DOIUrl":"10.3389/fcell.2024.1510232","url":null,"abstract":"<p><strong>Introduction: </strong>Sepsis-induced cardiomyopathy is a common complication of sepsis and is associated with higher mortality. To date, effective diagnostic and management strategies are still lacking. Recent studies suggest that ferroptosis plays a critical role in sepsis-induced cardiomyopathy and ferroptosis inhibitor Ferrostatin-1 (Fer-1) improved cardiac dysfunction and survival in lipopolysaccharide (LPS) induced endotoxemia. However, the effects of Fer-1 in cardiac dysfunction in the early stages of cecal ligation and puncture (CLP) induced sepsis remains unclear. Our study aims to elucidate the role of Fer-1 in the acute phase of peritonitis sepsis induced cardiac injury.</p><p><strong>Methods and results: </strong>CLP was used to induce peritonitis sepsis in mice. Pretreatment of ferroptosis inhibitor ferrostatin-1 (Fer-1) was used in the in vivo models. Survival was monitored for 48h. Cardiac function and histology were analyzed 6h after surgery. We found that ejection fraction (EF) remained normal at 6h after CLP, but the contractility detected by cardiac muscle strain analysis was significantly reduced, along with increased immune cell infiltration. Pretreating the CLP mice with 5 mg/kg Fer-1 significantly reduced mortality. At 6h after CLP, ferroptosis key regulator Gpx4, cardiac iron and malonaldehyde (MDA) did not change, but ferroptosis marker gene expression increased. Fer-1 treatment showed beneficial effects in cardiac function, less myocardial inflammatory cytokine expression and significantly inhibited immune cells, especially neutrophil infiltration in the heart. Consistently, expression of neutrophil associated chemokines (Ccrl2, Cxcl2, Cxcl3 and Cxcl5) as well as extracellular matrix (ECM) degradation enzymes (Adamts1, Adamts4, Adamts9 and Mmp8) significantly decreased in Fer-1 pre-treated CLP heart.</p><p><strong>Conclusion and discussion: </strong>Our findings suggest that Fer-1 inhibits neutrophil infiltration in early sepsis by disrupting the chemokine axis, highlighting its potential as a therapeutic option to manage acute immune overactivation in early stages of sepsis-induced cardiomyopathy.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"12 ","pages":"1510232"},"PeriodicalIF":4.6,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11669711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142893379","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":"Stem cells and bio scaffolds for the treatment of cardiovascular diseases: new insights.","authors":"Zahra Sadat Razavi, Simin Farokhi, Golnaz Mahmoudvand, Arian Karimi-Rouzbahani, Bahareh Farasati-Far, Samaneh Tahmasebi-Ghorabi, Hamidreza Pazoki-Toroudi, Masoud Saadat-Fakhr, Hamed Afkhami","doi":"10.3389/fcell.2024.1472103","DOIUrl":"10.3389/fcell.2024.1472103","url":null,"abstract":"<p><p>Mortality and morbidity from cardiovascular diseases are common worldwide. In order to improve survival and quality of life for this patient population, extensive efforts are being made to establish effective therapeutic modalities. New treatment options are needed, it seems. In addition to treating cardiovascular diseases, cell therapy is one of the most promising medical platforms. One of the most effective therapeutic approaches in this area is stem cell therapy. In stem cell biology, multipotent stem cells and pluripotent stem cells are divided into two types. There is evidence that stem cell therapy could be used as a therapeutic approach for cardiovascular diseases based on multiple lines of evidence. The effectiveness of stem cell therapies in humans has been studied in several clinical trials. In spite of the challenges associated with stem cell therapy, it appears that resolving them may lead to stem cells being used in cardiovascular disease patients. This may be an effective therapeutic approach. By mounting these stem cells on biological scaffolds, their effect can be enhanced.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"12 ","pages":"1472103"},"PeriodicalIF":4.6,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11669526/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142893421","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":"Cell therapy in kidney diseases: advancing treatments for renal regeneration.","authors":"Amankeldi A Salybekov, Aiman Kinzhebay, Shuzo Kobayashi","doi":"10.3389/fcell.2024.1505601","DOIUrl":"10.3389/fcell.2024.1505601","url":null,"abstract":"<p><p>Kidney diseases, including acute kidney injury (AKI) and chronic kidney disease (CKD), pose a significant global health challenge, with high morbidity and mortality rates driven by rising prevalence of risk factors such as diabetes and hypertension. Current therapeutic strategies are often limited, prompting the exploration of advanced cell therapies as potential solutions. This review provides a comprehensive overview of the state of cell therapies in kidney disease, tracing the progression from preclinical studies to clinical applications. Recent studies highlited that cell-based interventions offer kidney-protective properties through mechanisms such as paracrine signaling, immune modulation, and direct tissue integration, demonstrating potential in both AKI and CKD settings. Despite promising results, challenges remain in optimizing cell therapy protocols, including cell sourcing, delivery methods, and long-term outcomes. Finally, the review addresses on efforts to enhance cell function, optimize dosing, and refine delivery techniques to improve clinical outcomes in kidney disease management.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"12 ","pages":"1505601"},"PeriodicalIF":4.6,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11669058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142893376","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":"Anticarcinogenic effects of ursodeoxycholic acid in pancreatic adenocarcinoma cell models.","authors":"Patrik Kovács, Szandra Schwarcz, Petra Nyerges, Tímea Ingrid Bíró, Gyula Ujlaki, Péter Bai, Edit Mikó","doi":"10.3389/fcell.2024.1487685","DOIUrl":"10.3389/fcell.2024.1487685","url":null,"abstract":"<p><p>Changes to the composition of the microbiome in neoplasia, is termed oncobiosis, may affect tumor behavior through the changes to the secretion of bacterial metabolites. In this study we show, that ursodeoxycholic acid (UDCA), a bacterial metabolite, has cytostatic properties in pancreatic adenocarcinoma cell (PDAC) models. UDCA in concentrations corresponding to the human serum reference range suppressed PDAC cell proliferation. UDCA inhibited the expression of epithelial mesenchymal transition (EMT)-related markers and invasion capacity of PDAC cells. UDCA treatment increased oxidative/nitrosative stress by reducing the expression of nuclear factor, erythroid 2-like 2 (NRF2), inducing inducible nitric oxide synthase (iNOS) and nitrotyrosine levels and enhancing lipid peroxidation. Furthermore, UDCA reduced the expression of cancer stem cell markers and the proportion of cancer stem cells. Suppression of oxidative stress by antioxidants, blunted the UDCA-induced reduction in cancer stemness. Finally, we showed that UDCA induced mitochondrial oxidative metabolism. UDCA did not modulate the effectiveness of chemotherapy agents used in the chemotherapy treatment of pancreatic adenocarcinoma. The antineoplastic effects of UDCA, observed here, may contribute to the induction of cytostasis in PDAC cell models by providing a more oxidative/nitrosative environment.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"12 ","pages":"1487685"},"PeriodicalIF":4.6,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11668698/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142893373","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":"The role of sphingolipid rheostat in the adult-type diffuse glioma pathogenesis.","authors":"Ivana Karmelić, Mia Jurilj Sajko, Tomislav Sajko, Krešimir Rotim, Dragana Fabris","doi":"10.3389/fcell.2024.1466141","DOIUrl":"10.3389/fcell.2024.1466141","url":null,"abstract":"<p><p>Gliomas are highly aggressive primary brain tumors, with glioblastoma multiforme being the most severe and the most common one. Aberrations in sphingolipid metabolism are a hallmark of glioma cells. The sphingolipid rheostat represents the balance between the pro-apoptotic ceramide and pro-survival sphingosine-1-phosphate (S1P), and in gliomas it is shifted toward cell survival and proliferation, promoting gliomas' aggressiveness, cellular migration, metastasis, and invasiveness. The sphingolipid rheostat can be altered by targeting enzymes that directly or indirectly affect the ratio of ceramide to S1P, leading to increased ceramide or decreased S1P levels. Targeting the sphingolipid rheostat offers a potential therapeutic pathway for glioma treatment which can be considered through reducing S1P levels or modulating S1P receptors to reduce cell proliferation, as well as through increasing ceramide levels to induce apoptosis in glioma cells. Although the practical translation into clinical therapy is still missing, sphingolipid rheostat targeting in gliomas has been of great research interest in recent years with several interesting achievements in the glioma therapy approach, offering hope for patients suffering from these vicious malignancies.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"12 ","pages":"1466141"},"PeriodicalIF":4.6,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11668798/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142893425","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":"<i>Frataxin</i> is essential for zebrafish embryogenesis and pronephros formation.","authors":"Wesley S Ercanbrack, Austin Dungan, Ella Gaul, Mateo Ramirez, Alexander J DelVecchio, Calvin Grass, Rebecca A Wingert","doi":"10.3389/fcell.2024.1496244","DOIUrl":"10.3389/fcell.2024.1496244","url":null,"abstract":"<p><strong>Background and objectives: </strong>Friedreich's Ataxia (FRDA) is a genetic disease that affects a variety of different tissues. The disease is caused by a mutation in the <i>frataxin</i> gene (<i>FXN)</i> which is important for the synthesis of iron-sulfur clusters. The primary pathologies of FRDA are loss of motor control and cardiomyopathy. These occur due to the accumulation of reactive oxygen species (ROS) in the brain and the heart due to their high metabolic rates. Our research aims to understand how developmental processes and the kidney are impacted by a deficiency of <i>FXN</i>.</p><p><strong>Methods: </strong>We utilized an antisense oligomer, or morpholino, to knockdown the <i>frataxin</i> gene (<i>fxn</i>) in zebrafish embryos. Knockdown was confirmed via RT-PCR, gel electrophoresis, and Sanger sequencing. To investigate phenotypes, we utilized several staining techniques including whole mount <i>in situ</i> hybridization, Alcian blue, and acridine orange, as well as dextran-FITC clearance assays.</p><p><strong>Results: </strong><i>fxn</i> deficient animals displayed otolith malformations, edema, and reduced survival. Alcian blue staining revealed craniofacial defects in <i>fxn</i> deficient animals, and gene expression studies showed that the pronephros, or embryonic kidney, had several morphological defects. We investigated the function of the pronephros through clearance assays and found that the renal function is disrupted in <i>fxn</i> deficient animals in addition to proximal tubule endocytosis. Utilizing acridine orange staining, we found that cell death is a partial contributor to these phenotypes.</p><p><strong>Discussion and conclusion: </strong>This work provides new insights about how <i>fxn</i> deficiency impacts development and kidney morphogenesis. Additionally, this work establishes an additional model system to study FRDA.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"12 ","pages":"1496244"},"PeriodicalIF":4.6,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11669007/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142893354","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":"The pro-fibrotic role of autophagy in renal intrinsic cells: mechanisms and therapeutic potential in chronic kidney disease.","authors":"Ying-Ying Zhang, Xiao-Tao Zhou, Geng-Zhen Huang, Wen-Jun Liao, Xian Chen, Yue-Rong Ma","doi":"10.3389/fcell.2024.1499457","DOIUrl":"10.3389/fcell.2024.1499457","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) represents a significant global public health burden, affecting over 10% of the world's population. Its high morbidity, multifactorial complications, and substantial mortality impose significant burdens on healthcare systems and patients, necessitating considerable investment in healthcare resources. Renal fibrosis (RF) is a key pathological feature and driver of CKD progression. Extensive research indicates that autophagy participates in the complete pathogenesis of RF. Under physiological conditions, autophagy is essential for maintaining renal cellular homeostasis. However, under pathological conditions, perhaps aberrant and sustained activation of autophagy contributes to oxidative stress, apoptosis, inflammation, etc. Ultimately, they accelerate the development of RF. The role of autophagy in RF is currently controversial. This review investigates the molecular mechanisms by which intrinsic renal cell autophagy contributes to RF across diverse disease models, suggesting that autophagy and its associated regulatory pathways represent potential diagnostic and therapeutic targets for CKD.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"12 ","pages":"1499457"},"PeriodicalIF":4.6,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11669005/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142893423","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":"Multi-omics in exploring the pathophysiology of diabetic retinopathy.","authors":"Xinlu Li, XiaoJing Dong, Wen Zhang, Zhizhou Shi, Zhongjian Liu, Yalian Sa, Li Li, Ninghua Ni, Yan Mei","doi":"10.3389/fcell.2024.1500474","DOIUrl":"10.3389/fcell.2024.1500474","url":null,"abstract":"<p><p>Diabetic retinopathy (DR) is a leading global cause of vision impairment, with its prevalence increasing alongside the rising rates of diabetes mellitus (DM). Despite the retina's complex structure, the underlying pathology of DR remains incompletely understood. Single-cell RNA sequencing (scRNA-seq) and recent advancements in multi-omics analyses have revolutionized molecular profiling, enabling high-throughput analysis and comprehensive characterization of complex biological systems. This review highlights the significant contributions of scRNA-seq, in conjunction with other multi-omics technologies, to DR research. Integrated scRNA-seq and transcriptomic analyses have revealed novel insights into DR pathogenesis, including alternative transcription start site events, fluctuations in cell populations, altered gene expression profiles, and critical signaling pathways within retinal cells. Furthermore, by integrating scRNA-seq with genetic association studies and multi-omics analyses, researchers have identified novel biomarkers, susceptibility genes, and potential therapeutic targets for DR, emphasizing the importance of specific retinal cell types in disease progression. The integration of scRNA-seq with metabolomics has also been instrumental in identifying specific metabolites and dysregulated pathways associated with DR. It is highly conceivable that the continued synergy between scRNA-seq and other multi-omics approaches will accelerate the discovery of underlying mechanisms and the development of novel therapeutic interventions for DR.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"12 ","pages":"1500474"},"PeriodicalIF":4.6,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11668801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142893381","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}