Frontiers in Cell and Developmental Biology最新文献

{"title":"Cellular mechanisms of hormone secretion in neuroendocrine tumors: what goes wrong?","authors":"Laura Streit, Emeline Tanguy, Laurent Brunaud, Petra Tóth, Nicolas Vitale, Stéphane Ory, Stéphane Gasman","doi":"10.3389/fcell.2025.1527083","DOIUrl":"10.3389/fcell.2025.1527083","url":null,"abstract":"<p><p>Neuroendocrine tumors (NETs) constitute a heterogeneous group of neoplasms arising from hormone-releasing cells. Secretion of hormones stored in vesicles occurs through calcium-regulated exocytosis, a process that needs to be tightly controlled to avoid unbalanced levels of hormones. A critical feature shared by most of the NETs is a dysfunctional secretory pathway mainly leading to hypersecretion, which often induces clinical complications. In this review, we focus on the cellular process of hormone exocytosis and discuss the potential molecular mechanisms leading to deregulated hormone secretion in various NETs. Particular attention is paid to expression level modifications for genes and proteins involved in the exocytic pathway in NETs.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1527083"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12259560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642230","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":"ELK1 regulates BMPR1B transcriptional activity in ovine granulosa cells.","authors":"Anwar Abdurahman, Yuling Ga, Xuehai Ma","doi":"10.3389/fcell.2025.1623135","DOIUrl":"10.3389/fcell.2025.1623135","url":null,"abstract":"<p><p>BMPR1B, a type I receptor in the BMP/Smad signaling pathway, was the first major gene identified in sheep (<i>Ovis aries</i>) to regulate key reproductive traits such as ovulation rate (OR) and litter size (LS). Despite its critical role in reproductive performance, the transcriptional regulatory mechanisms governing ovine BMPR1B expression remain poorly understood. This study identified the promoter region of the BMPR1B gene and revealed that transcription factor ELK1 regulates its transcriptional activity. Luciferase reporter assays identified the region from -438 bp to -208 bp relative to the essential promoter of the BMPR1B gene as a critical regulatory element. Notably, candidate ELK1-binding elements (EBS) were detected in this promoter region. Interestingly, ELK1 significantly enhances BMPR1B transcriptional activity by binding to specific sites in the promoter region. Further analysis in ovine granulosa cells showed that ELK1 modulates BMPR1B expression and influences granulosa cell apoptosis through the BMPR1B signaling pathway. These findings provide new key targets and mechanistic insights into the molecular regulatory network of ovarin granulosa cell apoptosis, advancing our understanding of reproductive biology in sheep.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1623135"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12259578/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642232","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 in immunotherapy for uveal melanoma: enhancing efficacy and overcoming resistance.","authors":"Jian Song, Pei Mou, Guo-Ge Song, Liang Chen, Yu-Qing Chen, Rui-Li Wei","doi":"10.3389/fcell.2025.1619150","DOIUrl":"10.3389/fcell.2025.1619150","url":null,"abstract":"<p><p>Uveal melanoma (UM) is the most common primary intraocular malignancy in adults, presenting a significant clinical challenge due to its high metastatic potential and limited response to conventional systemic therapies. While immunotherapy has transformed the treatment landscape for numerous cancers, its effectiveness in UM has been substantially limited, primarily due to the tumor's distinct immune-evasive characteristics and a suppressive tumor microenvironment (TME). This review systematically examines the multiple mechanisms underlying immunotherapy resistance in UM, including low tumor mutational burden, immune checkpoint overexpression, metabolic adaptations, and the epigenetic silencing of immune-stimulatory genes. Additionally, we analyze emerging strategies aimed at modifying the TME to enhance immune recognition and response, which include targeting suppressive immune cell populations, addressing metabolic and hypoxic barriers, and utilizing epigenetic modulators to restore immune activation pathways. Furthermore, we highlight recent advances in identifying predictive biomarkers-such as genetic mutations (e.g., <i>BAP1</i>, <i>MBD4</i>), immune gene signatures, circulating tumor DNA, and protein-based blood markers-that may facilitate patient stratification and treatment selection. We also examine novel combination approaches that integrate immune checkpoint inhibitors with targeted therapies, radiation, metabolic interventions, or engineered cellular therapies, several of which have shown promising clinical potential in overcoming UM's inherent resistance mechanisms. Despite persistent challenges, such as toxicity management and limited availability of large-scale trials due to UM's rarity, the integration of multi-omics profiling, precision medicine frameworks, and adaptive trial designs presents new opportunities for therapeutic advancement. This review provides a translational perspective on enhancing immunotherapy efficacy in UM by addressing its unique biology and identifying future directions for clinical innovation.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1619150"},"PeriodicalIF":4.6,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256454/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636584","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":"Interaction networks among miRNA, protein, and metabolite fingerprints identify the regulatory networks and key players in the pathogenesis of diabetic cardiomyopathy.","authors":"Bhaswati Chatterjee, Suman S Thakur","doi":"10.3389/fcell.2025.1602320","DOIUrl":"10.3389/fcell.2025.1602320","url":null,"abstract":"<p><p>Diabetic cardiomyopathy (DCM) is a complication of diabetes and is the main cause of death in diabetic patients. The regulatory networks and key players involved in the pathogenesis of diabetic cardiomyopathy are not clearly known. We selected the miRNA, protein, and metabolite fingerprints that play a significant role in DCM and manually constructed miRNA-protein-metabolite interaction networks from the miRNA-protein and protein-metabolite interaction networks. Furthermore, protein-protein, metabolite-metabolite, and protein-metabolite interaction networks were also constructed. The miRNA-protein interaction included evidence from TarBase and microarrays/HITS-CLIP. The protein-protein, metabolite-metabolite, and protein-metabolite interaction networks were obtained at high confidence scores (≥0.7 or 70%). We proposed that the miRNA-protein-metabolite interaction networks along with their intra- and inter-connected protein-protein, metabolite-metabolite, and protein-metabolite interaction networks formed by miRNA, protein, and metabolite fingerprints such as hsa-mir-122-5p, hsa-mir-30c-5p, hsa-mir-30d-5p, hsa-mir-22-3p, IL6, GSTM2, GPX3, ACADM, GSTM3, LEP, ADIPOQ, INS, CASP1, NLRP3, HADH, ACAT1, PRDX2, PRDX1, TNF, ELAVL1, SERPINA1, A2M, IGFBP7, PRDX6, APOA1, APCS, NPPA, ADAM9, GDF15, ACADVL, ECH1, FGL1, bilirubin, butyric acid (butyrate), octanoylcarnitine (octanoylcarnit.), isoleucine, leucine, alanine, glutamine, L-valine, cytidine triphosphate (ara-CTP), 7-keto-8-aminopelargonic acid (7-keto-8-amino.), creatinine, decanoylcarnitine (decanoylcarnit.), and hexanoylcarnitine (hexanoylcarnit.) are the key players and regulatory networks involved in the pathogenesis of DCM. Notably, we also proposed that the interaction networks formed by miRNA, protein, and metabolite fingerprints involved in the early stage of DCM, such as hsa-mir-122-5p, IL6, FGL1, LEP, ADIPOQ, INS, TNF, IGFBP7, GDF15, GPX3, NPPA, bilirubin, butyric acid (butyrate), and creatinine, are the potential biomarkers and therapeutic targets for the early stage of DCM. To the best of our knowledge, this is the first study of the construction of miRNA-protein-metabolite interactomes in DCM, providing insights into the pathogenesis of DCM.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1602320"},"PeriodicalIF":4.6,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256442/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636587","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":"Influence of secretome from porcine cardiosphere-derived cells on porcine macrophage polarization and their possible implications for cardiac remodeling post-myocardial infarction <i>in vitro</i>.","authors":"M Pulido, M A de Pedro, A M Marchena, V Alvarez, J G Casado, F M Sanchez-Margallo, E López","doi":"10.3389/fcell.2025.1601743","DOIUrl":"10.3389/fcell.2025.1601743","url":null,"abstract":"<p><p>The inflammatory response plays a crucial role in tissue repair following myocardial infarction (MI), with macrophages being central regulators of inflammation and tissue remodeling. Macrophage polarization between pro-inflammatory M1 and anti inflammatory M2 phenotypes significantly influences inflammation and tissue repair. This study evaluates the effect of the secretome from porcine cardio sphere-derived cells (S-CDCs) on macrophage polarization and its downstream impact on endothelial cells (HUVECs) and cardiac fibroblasts (PCF). Macrophages were treated with the secretome from S-CDCs, and their polarization status was assessed. Conditioned media from treated macrophages were applied to HUVECs and PCFs to evaluate effects on migration, wound healing, and fibrotic activity. Additionally, transcriptomic profiling of S-CDCs was performed to identify relevant cytokines. S-CDCs induced a mixed M1/M2 phenotype in macrophages, attenuating M1-associated inflammation without fully promoting M2 characteristics. Conditioned medium from S-CDC-treated M1 macrophages enhanced migration and wound healing in HUVECs, indicating proangiogenic effects. In contrast, medium from M2 macrophages did not show similar activity. Additionally, S-CDC-treated M1 macrophage medium modulated the migratory and fibrotic behavior of PCFs. Transcriptomic analysis revealed a cytokine profile enriched in pro-reparative factors such as VEGFA, TGFB, and CCL2. These findings suggest that S-CDCs modulate macrophage polarization to promote tissue repair and angiogenesis while minimizing excessive inflammation. This highlights their potential as a therapeutic strategy to enhance cardiac regeneration following MI.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1601743"},"PeriodicalIF":4.6,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256530/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636586","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 mitochondria-associated ER membranes in disease pathology: protein complex and therapeutic targets.","authors":"Jin Zhang, Dan Li, Lingjie Zhou, Yanying Li, Qian Xi, Liuyun Zhang, Juan Zhang","doi":"10.3389/fcell.2025.1629568","DOIUrl":"10.3389/fcell.2025.1629568","url":null,"abstract":"<p><p>The dynamic interactions among organelles play a crucial role in facilitating various intercellular functions, with the interaction between the endoplasmic reticulum (ER) and mitochondria being acknowledged as a prominent example of an interorganellar system. Numerous studies have established that the majority of proteins located at the physically tethered regions between the mitochondria and ER, referred to as mitochondria-associated ER membranes (MAMs), play a crucial role in intracellular physiological processes. MAMs are dynamic membrane coupling regions arising from the interaction between the ER and the outer mitochondrial membrane (OMM). MAMs regulate many biological processes, such as Ca²⁺ transport, lipid metabolism, and mitochondrial dynamics. A recent study has demonstrated that the proteins associated with MAMs are crucial for both the structural integrity and functional capabilities of the MAMs. Dysregulations in the MAMs proteins are implicated in the onset and progression of various associated diseases, including cancer, neurodegenerative disorders, diabetes mellitus, and cardiovascular diseases. In this review, we provide a comprehensive overview of the protein complex associated with MAMs. We examine its involvement in the pathological mechanisms underlying these diseases, focusing on its functional roles. Additionally, we evaluate and consider the potential of MAMs as therapeutic targets for these diseases.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1629568"},"PeriodicalIF":4.6,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256456/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636601","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 of natural killer cell-mediated clearance of senescent renal tubular epithelial cells.","authors":"Nils David Funk, Julius Sinning, Patrick Schaser, Inga Soerensen-Zender, Vera Christine Wulfmeyer, Kai Schmidt-Ott, Korbinian Brand, Stephan Halle, Roland Schmitt","doi":"10.3389/fcell.2025.1597230","DOIUrl":"10.3389/fcell.2025.1597230","url":null,"abstract":"<p><strong>Introduction: </strong>Intact kidney function is essential for fluid and electrolyte homeostasis, with renal tubular epithelial cells providing critical functions in the reabsorption or secretion of numerous metabolites. Cellular senescence of the renal epithelial cells can lead to functional deficits. Therefore, immune-cell-mediated clearance of senescent epithelial cells can be an important factor for the maintenance of kidney function.</p><p><strong>Methods: </strong>In this study, we established a model to directly monitor natural killer (NK) cell-mediated clearance of senescent renal tubular cells. To this end we used primary cell co-cultures with different read-outs and life cell imaging.</p><p><strong>Results and discussion: </strong>We observed that the clustering of NK cells on senescent renal epithelial cells could be used to detect senescence-triggered NK cell activation. Also, we found that NKG2D signaling and perforin-dependent lysis of senescent renal epithelial cells were crucial steps in the lysis of senescent cells. In addition, NK cell-mediated attack of senescent renal epithelial cells could be dampened by the addition of cyclosporine A and was augmented by the addition of interleukin 7. Together, these data show that NK cells can efficiently mediate the clearance of senescent renal tubular epithelial cells involving NK cell activation by NKG2D signaling.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1597230"},"PeriodicalIF":4.6,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636588","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":"Nanopathways modulating postoperative cognitive dysfunction: extracellular vesicles.","authors":"Yunmeng Zhang, Zengsheng Yin, Zhiyong Zou, Shangzhi Feng, Huayang Xu","doi":"10.3389/fcell.2025.1613378","DOIUrl":"10.3389/fcell.2025.1613378","url":null,"abstract":"<p><p>Postoperative cognitive dysfunction is a common central nervous system complication after general anesthesia in the elderly, and when it occurs, it will seriously affect the patient's postoperative recovery and quality of life, which puts elderly postoperative general anesthesia patients at an extremely uncertain risk of postoperative psychiatric disorders or even death. It is currently believed that neuronal damage and inflammatory response due to cerebral ischemia/reperfusion injury induced by transient or repeated global cerebral ischemia during surgery are the key mechanisms for the development of postoperative cognitive dysfunction. Therefore, repairing postoperative neuronal damage and reducing neuroinflammatory responses may be an effective means of early intervention for postoperative cognitive dysfunction. Extracellular vesicles, a therapeutic tool with clear advantages in regenerative medicine, have been suggested as potential nanopathways to modulate postoperative cognitive dysfunction due to their pro-regenerative, pro-repair, and influence on immune responses. In this paper, we will summarize studies related to extracellular vesicles in the treatment of postoperative cognitive dysfunction and discuss the potential function of extracellular vesicles in nerve repair and inhibition of acute neurological inflammation, which will expand the therapeutic strategies for postoperative cognitive dysfunction and may represent the development of novel cell-free therapeutic pathways for modulating postoperative cognitive dysfunction.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1613378"},"PeriodicalIF":4.6,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256582/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636589","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":"Neuronal guidance behaviours: the primary cilium perspective.","authors":"Melody Atkins, Coralie Fassier, Xavier Nicol","doi":"10.3389/fcell.2025.1612555","DOIUrl":"10.3389/fcell.2025.1612555","url":null,"abstract":"<p><p>The establishment of functional neuronal circuits critically relies on the ability of developing neurons to accurately sense and integrate a variety of guidance signals from their surrounding environment. Such signals are indeed crucial during key steps of neuronal circuit wiring, including neuronal migration and axon guidance, to guide developing neurons or extending axons towards their target destination in the developing brain. The growth cone, located at the tip of developing neurons, is a key subcellular structure in this process, that concentrates many different guidance receptors and signalling molecules and specialises in the probing and integration of extracellular signals into various guidance behaviours. Interestingly, the small primary cilium, long considered as a vestigial organelle, has progressively emerged as a cellular antenna specialised in cell signalling, and has been reported, just like the growth cone, to harbour a variety of guidance receptors. How primary cilium-elicited signals are then transduced into specific cellular processes to guide developing neurons and axons remains however obscure. In this review, we will summarise our emerging understanding of the role of primary cilium-elicited signalling pathways on neuronal guidance processes, by focusing on neuronal migration and axon guidance. We will highlight the primary cilium molecular diversity, and how it shapes the primary cilium functional versatility, allowing the ciliary compartment to instruct various guidance behaviours through the regulation of different cellular processes. We will moreover discuss current and future avenues of research, to unravel the different molecular effectors activated downstream of specific ciliary signals, and clues to be gained from studies performed in non-neuronal cells. Rising challenges of the field will also be addressed, such as the technical challenge induced by the dual subcellular localisation (<i>i.e</i>., ciliary and extra-ciliary) of many ciliary guidance receptors, and the importance of the development of new genetic/chemo-genetic/optogenetic tools. Finally, we will highlight the insight such studies will bring for our understanding of the aetiology of different disorders, including ciliopathies, neurodevelopmental and neurodegenerative disorders, but also cancer cell migration/invasion, which are associated with defective primary cilium formation and function.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1612555"},"PeriodicalIF":4.6,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256549/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636600","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 in neurodegenerative diseases: potential mechanisms of exercise intervention.","authors":"Shaokai Tang, Jianhua Zhang, Jiawei Chen, Zeng Zhou, Qinqin Lin","doi":"10.3389/fcell.2025.1622544","DOIUrl":"10.3389/fcell.2025.1622544","url":null,"abstract":"<p><p>Neurodegenerative diseases represent a major global cause of mortality and disability. These disorders are characterized by complex pathogenesis and currently lack effective therapeutic strategies. Iron, a vital trace element for normal brain function, has been implicated in the pathogenesis of neurodegenerative diseases via the ferroptosis pathway. Emerging evidence indicates that exercise can suppress ferroptosis directly or indirectly by regulating iron metabolism, oxidative stress, and exerkine expression, thereby conferring neuroprotection. This review summarizes current insights into the role of ferroptosis in neurodegenerative diseases and explores the mechanisms by which exercise modulates the ferroptosis pathway, offering a scientific rationale for exercise-based interventions in brain health.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1622544"},"PeriodicalIF":4.6,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256474/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636585","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}