Frontiers in Cell and Developmental Biology最新文献

{"title":"Autophagy inhibition improves sensitivity to the multi-kinase inhibitor regorafenib in preclinical mouse colon tumoroids.","authors":"Giulia Agostini, Morgane Leprovots, Jérôme Jeandriens, Anne Lefort, Frédérick Libert, Francesco Sclafani, Ingrid Langer, Alain Hendlisz, Marie-Isabelle Garcia","doi":"10.3389/fcell.2025.1631116","DOIUrl":"10.3389/fcell.2025.1631116","url":null,"abstract":"<p><p>Colorectal cancer (CRC) remains the second leading cause of cancer-related deaths worldwide, with its incidence continuing to rise. Regorafenib, a multi-kinase inhibitor approved for palliative treatment, has been shown to extend survival in patients with metastatic CRC (mCRC) who have failed standard therapies. However, its clinical benefit is limited to a subset of patients, is typically short-lived, and is often accompanied by significant toxicity. The mechanisms by which CRC cells develop resistance to regorafenib remain incompletely understood. In this study, we investigated the mechanisms of regorafenib resistance using a preclinical mouse colon organoid model. Transcriptomic analysis of Apc wild-type and Apc-deficient organoids treated with regorafenib revealed upregulation of epithelial-to-mesenchymal transition (EMT), alterations in the secretome, and increased activation of phosphorylated Erk1/2. Notably, co-treatment with an autophagy inhibitor suppressed regorafenib-induced EMT and its associated secretory phenotype, leading to reduced cell proliferation and enhanced apoptosis in mouse organoids. The efficacy of this drug combination was further supported by cell viability assays in human CRC cell lines. In contrast, primary mouse colon fibroblasts exhibited greater resistance to both single-agent and combination regorafenib treatments. In summary, our findings using an organoid model suggest that autophagy inhibition may represent a promising strategy to overcome chemoresistance to regorafenib in mCRC patients.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1631116"},"PeriodicalIF":4.6,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12325355/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793812","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":"Saliva-derived exosomes regulate fibroblast metabolic reprogramming in skin wound healing.","authors":"Sijia Song, Rong Xiang, Siyu Chen, Jianbo Wu, Wenxia Chen, Xianyu Li","doi":"10.3389/fcell.2025.1606716","DOIUrl":"10.3389/fcell.2025.1606716","url":null,"abstract":"<p><strong>Background: </strong>Effective skin repair requires rapid wound closure accompanied by precise extracellular matrix (ECM) remodeling and balanced cellular metabolism. Saliva-derived exosomes (S-Exo) have emerged as promising therapeutic agents due to their rich bioactive components; however, their mechanisms in ECM remodeling and metabolic regulation remain unclear. This study aimed to elucidate how S-Exo modulate ECM turnover through metabolic reprogramming, particularly glycolysis, in human skin fibroblasts (HSFs), and identify critical exosomal molecules mediating these effects.</p><p><strong>Methods: </strong>S-Exo were isolated and characterized. A rat full-thickness skin defect model and <i>in vitro</i> assays with human skin fibroblasts and HaCaT keratinocytes were employed to evaluate S-Exo effects on wound closure, ECM remodeling, and cellular metabolism. Transcriptomic profiling of wound tissues, targeted metabolomic analysis of fibroblasts, and proteomic evaluation of S-Exo cargo were performed to explore underlying mechanisms. Metabolic interventions further confirmed the contribution of metabolic modulation to S-Exo-mediated wound healing.</p><p><strong>Results: </strong>S-Exo significantly accelerated wound healing by enhancing fibroblast viability, migration, and ECM remodeling, characterized by elevated secretion of matrix metalloproteinases (MMP1 and MMP3). Transcriptomic, metabolomic, and proteomic analyses revealed that S-Exo robustly activated key metabolic pathways, particularly glycolysis, reflected by increased expression of glycolytic genes (e.g., GLUT1, HK2, PFKM) and enhanced glycolytic flux in fibroblasts. Remarkably, S-Exo were found to carry nearly all enzymes involved in glycolysis, indicating an underlying enzyme-transfer mechanism for sustained metabolic modulation. Importantly, glycolytic activity positively correlated with MMP secretion, and inhibition of glycolysis significantly reduced MMP production, highlighting glycolysis as a crucial regulator of ECM remodeling.</p><p><strong>Conclusion: </strong>Saliva-derived exosomes promote wound healing by potentially modulating fibroblast metabolism via exosome-associated glycolytic enzymes, enhancing glycolytic flux, and thereby regulating ECM remodeling via increased MMP secretion. These findings provide novel insights into metabolism-targeted exosome therapies for wound healing.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1606716"},"PeriodicalIF":4.6,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12325227/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793914","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":"Recent advances in aptamer-based biosensing technology for isolation and detection of extracellular vesicles.","authors":"Osama Alnaser-Almusa, Mohammed Mahmoud, Mohammed Ilyas, Raghda Adwan, Farah Abul Rub, Noha Alnaser-Almusa, Fayrouz Mustafa, Sana Ahmed, Alaa Alzhrani, Tanveer Ahmad Mir, Mubarak Alabudahash, Raja Chinnappan, Ahmed Yaqinuddin","doi":"10.3389/fcell.2025.1555687","DOIUrl":"10.3389/fcell.2025.1555687","url":null,"abstract":"<p><p>Since their discovery in the 1970s, extracellular vesicles (EVs) have garnered significant scientific attention due to their involvement in diverse pathological processes, including tumorigenesis. Their unique properties have also piqued interest for various applications such as transporting biomolecules for drug delivery. Researchers have developed numerous isolation and detection methods for EVs, including ultracentrifugation, immunoaffinity capture, and antibody-based biosensors. However, these techniques often suffer from limitations in sensitivity, specificity, and efficiency, hindering their performance and reliability in research and clinical settings. Aptamers are short, single-stranded DNA or RNA molecules created to selectively bind to a specific target and offer a promising alternative to antibodies. These aptamers are identified by a process known as SELEX. By repeatedly selecting and amplifying aptamers with high binding affinity, SELEX can generate aptamers with exceptional specificity and sensitivity. Aptamers can then be incorporated into biosensors, known as aptasensors, for EV isolation, detection, and analysis. Aptasensors offer several advantages over antibody-based methods. They are often more stable, can be produced synthetically at lower cost, and can be easily modified for various applications. Additionally, aptamers can be selected against a wide range of targets, including proteins, nucleic acids, and small molecules, making them versatile tools for EV research. This review discusses various SELEX methods for aptamer detection, the clinical uses of aptamers, and the types of EV analysis methods.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1555687"},"PeriodicalIF":4.6,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326547/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793913","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":"MicroRNA: role in macrophage polarisation and colorectal cancer pathogenesis.","authors":"Haihong Lin, Jun Zhou, Ying He, Yifan Zhu, Puwen Chen, Hongwei Yan, Junyun Huang, Ersheng Gong, Xiaoling Wang","doi":"10.3389/fcell.2025.1619526","DOIUrl":"10.3389/fcell.2025.1619526","url":null,"abstract":"<p><p>Colorectal cancer (CRC) represents a highly common gastrointestinal malignancy ranking among the top three most frequently diagnosed cancers in the digestive system. The disease's high mortality rate makes treatment particularly difficult. As a result, thorough research into the cause and effective treatment of CRC is especially crucial. The macrophage's remarkable functional flexibility, as a cell with strong immunological effects, allows it to demonstrate both anti-tumor and tumor-inducing activities. MicroRNAs (miRNAs), functioning as short non-protein-coding RNAs, mediate post-transcriptional regulation through mRNA destabilization and translational suppression, and they play a unique function in macrophage formation, polarization processes, and anti-inflammatory activity. Elucidating the crosstalk between miRNA-mediated gene regulation and macrophage functional polarization in CRC pathogenesis constitutes a critical research priority. We first provide a brief overview of the epidemiological of CRC, systematically summarising the origin of macrophages, their physiological functions, and their potential pathogenic mechanisms in colorectal carcinogenesis. Subsequently, we elaborated in depth on the critical role of miRNAs in regulating macrophage polarisation status. Ultimately, this paper comprehensively explores the mechanistic involvement of miRNA-macrophage interactions in CRC progression.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1619526"},"PeriodicalIF":4.6,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12325328/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793911","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: Microbiota homeostasis and metabolic reprogramming in cancer development and digestive diseases.","authors":"Kai Li","doi":"10.3389/fcell.2025.1653798","DOIUrl":"https://doi.org/10.3389/fcell.2025.1653798","url":null,"abstract":"","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1653798"},"PeriodicalIF":4.6,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12322600/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788658","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":"Spatiotemporal regulation by downstream genes of <i>Prok2</i> in the olfactory system: from development to function.","authors":"Bo-Ra Kim, Min-Seok Rha, Hyung-Ju Cho, Joo-Heon Yoon, Chang-Hoon Kim","doi":"10.3389/fcell.2025.1550845","DOIUrl":"10.3389/fcell.2025.1550845","url":null,"abstract":"<p><strong>Introduction: </strong>Olfaction is important for the quality of life; however, in Kallmann syndrome (KS), defective development results in olfactory dysfunction. Notably, the mechanism underlying olfactory development, especially in the olfactory epithelium (OE), which detects olfactory signals, remains unclear. Mutations in PROK2, which encodes prokineticin-2, have been identified in approximately 9% of the KS patients with olfactory defects.</p><p><strong>Methods: </strong>We examined olfactory function and analyzed the causes of olfactory dysfunction based on spatiotemporal development and gene expression changes in <i>Prok2</i> knockout (KO) model mice with KS.</p><p><strong>Results: </strong>The ability of the OE to detect olfactory signals was diminished in adult <i>Prok2</i> KO mice. Maturation of olfactory sensory neurons (OSNs) in the OE and formation of glomeruli in the olfactory bulb (OB) in adult <i>Prok2</i> KO mice were disrupted, thus causing olfactory dysfunction. Furthermore, molecular analysis of <i>Prok2</i> KO mice during embryonic development revealed abnormal development of OB layers and diminished differentiation to mature OSNs in the OE at the later stage, which caused defects in the entire olfactory system. Remarkably, downstream signaling genes of <i>Prok2</i>, including intermediate filament genes and genes expressed in the putative OB, were found to mediate olfactory system organization.</p><p><strong>Discussion: </strong>Overall, these findings reveal the role of <i>Prok2</i> in olfactory system organization and elucidate how olfactory development defects translate to olfactory function.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1550845"},"PeriodicalIF":4.6,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12321839/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788660","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 effects of TGF-β receptor I inhibitors on myofibroblast differentiation and myotube formation.","authors":"Zhihao Wang, Edwin M Ongkosuwito, Johannes W Von den Hoff, Frank A D T G Wagener","doi":"10.3389/fcell.2025.1636884","DOIUrl":"10.3389/fcell.2025.1636884","url":null,"abstract":"<p><strong>Introduction: </strong>Fibrosis frequently occurs in muscle wounds, ultimately leading to suboptimal function. This study investigates the effects of TGF-βRI inhibitors AZ12799734, Galunisertib, and SM16, on myofibroblast differentiation and myotube formation.</p><p><strong>Methods: </strong>Human gingival fibroblasts were treated with TGF-β1 (0, 1, 5, and 10 ng/mL) to induce myofibroblasts. Then, fibroblasts were incubated with TGF-βRI inhibitors (0, 1, 5, 10, and 20 µM) together with 10 ng/mL TGF-β1. Myofibroblast marker expression was assessed using RT-PCR (day 3), while myofibroblast differentiation was analyzed by immunofluorescence staining for α-SMA (day 6). C2C12 myoblasts were also cultured with TGF-βRI inhibitors, and gene expression (day 3) and myotube formation (day 6) were analyzed.</p><p><strong>Results: </strong>TGF-β1 (10 ng/mL) increased the proportion of myofibroblasts from 9.3% ± 3.5% to 38.1% ± 4.4%, which was reduced by all TGF-βRI inhibitors even at 1 µM [for example, Galunisertib 23.5% ± 2.1% (p < 0.05)]. All inhibitors reduced ACTA2 and COL1A1 gene expression, while only AZ12799734 and SM16 inhibited Ki-67 expression. In C2C12 cultures, AZ12799734 and SM16 reduced the fusion index, whereas Galunisertib did not. Moreover, only Galunisertib increased myotube size from 0.09 ± 0.01 to 0.13 ± 0.01 mm²/nucleus (p < 0.05). Galunisertib inhibited MyoD gene expression (at 20 µM), but not MyoG nor MyHC.</p><p><strong>Discussion: </strong>Galunisertib may have potential for improving muscle wound healing following injury.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1636884"},"PeriodicalIF":4.6,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12321840/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788661","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":"Dysregulation of decidual NK cell proliferation by impaired decidual cells: a potential contributor to excessive trophoblast invasion in placenta accreta spectrum.","authors":"You-Zhen Liu, Hsin-Hung Lin, Meng-Shiue Wu, Jin-Chung Shih, Thai-Yen Ling","doi":"10.3389/fcell.2025.1618461","DOIUrl":"10.3389/fcell.2025.1618461","url":null,"abstract":"<p><p>Aberrant interactions among decidual stromal cells, decidual natural killer (dNK) cells, and trophoblasts are implicated in placenta accreta spectrum (PAS) pathogenesis, though the underlying mechanisms remain unclear. This study investigates the relationship between defective decidualization of endometrial stromal cells and dysregulated dNK cell proliferation, which may contribute to excessive trophoblast invasion and the development of PAS. We established an <i>in vitro</i> system that mimics the decidual microenvironment to investigate these interactions. Maternal decidua-derived mesenchymal stem cells (MD-MSCs) from healthy pregnancies and PAS patients (PA-MSCs) were isolated and induced to undergo decidualization using hormonal and chemical stimuli. Peripheral natural killer (pNK) cells were then co-cultured with these MSCs to generate dNK-like cells. Cellular interactions among MSCs, dNK-like cells, and trophoblasts were evaluated using an <i>in vitro</i> co-culture system. Decidualization defects in PA-MSCs were marked by reduced morphological changes and dysregulated expression of decidual markers, potentially associated with estrogen receptor (ER) overexpression. Furthermore, both PA-MSCs and normal MD-MSCs similarly regulated trophoblast invasion, suggesting an indirect impact of impaired decidual cells on trophoblast behavior. Interestingly, decidualized MD-MSCs (De-MD-MSCs) showed the potential to induce the conversion of pNK cells into dNK-like cells, which displayed reduced cytotoxicity on trophoblasts and elevated KIR2DL4 expression. These dNK-like cells exhibited increased proliferation when co-cultured with PA-MSCs, enhancing trophoblast invasion and spiral artery remodeling. Conditioned medium derived from PA-MSCs-induced dNK-like cells demonstrated a higher capacity to promote trophoblast invasion in a dose-dependent manner. The abnormal proliferation of dNK cells induced by impaired decidual cells may contribute to the pathogenesis of PAS, providing valuable insights into its mechanisms and potential therapeutic interventions.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1618461"},"PeriodicalIF":4.6,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320386/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144783947","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":"Dynamic crosstalk between HSCs and liver microenvironment: multicellular interactions in the regulation of liver fibrosis.","authors":"Luping Wang, Yi Huang, Jingrong Chen, Jialu Gao, Sihan Chen, Mingqi Zhao, Jiguo Lin, Shunqing Zhou, Yannan Shen, Yunyun Cheng","doi":"10.3389/fcell.2025.1635763","DOIUrl":"10.3389/fcell.2025.1635763","url":null,"abstract":"<p><p>Liver fibrosis is induced by persistent stimulation of various factors, resulting from complex multicellular interactions and multifactorial networks. Without intervention, it can progress to cirrhosis and even liver cancer. Current understanding suggests that liver fibrosis is reversible, making it crucial to explore effective therapeutic strategies for its alleviation. Although the activation and proliferation of hepatic stellate cells (HSCs) play a pivotal role in liver fibrosis, the importance of hepatocytes, cholangiocytes, liver sinusoidal endothelial cells (LSECs) and immune cells cannot be ignored, the interactions of these cells with HSCs are worth discussing. Therefore, based on the diversity of cell composition in the liver organ, this review summarizes the impact of the parenchymal and nonparenchymal hepatic cells on liver fibrosis, including hepatocytes, cholangiocytes, hepatic macrophages, T cells, NK cells, B cells and LSECs, as well as the fibroblast subpopulations. And further discussed the interactions of these cells with HSCs and illustrated intercellular signal transduction among these cells in contributing to liver fibrosis. Clarifying the roles and interactions of various cells in the development of liver fibrosis will be helpful to explore effective strategies for the treatment of liver fibrosis.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1635763"},"PeriodicalIF":4.6,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12319055/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144783946","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":"Research progress on the role of the NEIL family in cancer.","authors":"Yinghan Chen, Muyun Ma, Aixue Zou, Xinjia Wang, Weiwei Dong","doi":"10.3389/fcell.2025.1612329","DOIUrl":"10.3389/fcell.2025.1612329","url":null,"abstract":"<p><p>Cancer is the primary cause of death worldwide. Cancer occurrence and progression are closely associated with DNA damage repair. DNA glycosylase were the first enzymes to initiate base excision repair, and the Nei-like DNA glycosylase (NEIL) family has attracted increasing attention as an important component of DNA glycosylases. Here, we introduce the role of the NEIL family in the malignant biological behaviors of cancer, including cell proliferation, chemoradiotherapy resistance, invasion and migration, apoptosis, and stemness. Mechanisms affecting the expression of the NEIL protein family range from the transcriptional level and mRNA editing to the level of post-translational modification. Additionally, we emphasize the different functions of the NEIL family in various malignancies and present useful information that supports the hypothesis that the NEIL family could be a potential target in the treatment and diagnosis of various cancers.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1612329"},"PeriodicalIF":4.6,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144783949","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}