Frontiers in Cell and Developmental Biology最新文献

{"title":"ELOVL2 mediated stabilization of AR contributes to enzalutamide resistance in prostate cancer.","authors":"Jinpeng Cen, Jiading Guo, Xianzi Zeng, Xianlu Song, Shengdong Ge, Mingkun Chen, Qianyi Li, Yuzhong Yu, Daojun Lv, Shanchao Zhao","doi":"10.3389/fcell.2025.1598400","DOIUrl":"https://doi.org/10.3389/fcell.2025.1598400","url":null,"abstract":"<p><strong>Introduction: </strong>To investigate the molecular mechanisms underlying enzalutamide resistance in castration-resistant prostate cancer (CRPC) and explore potential therapeutic strategies to overcome resistance.</p><p><strong>Methods: </strong>We conducted comprehensive bioinformatic analysis using LNCaP/enzalutamide-resistant cells to identify key pathways associated with resistance. Functional validation was performed through targeted inhibition of the elongation of very-long chain fatty acid protein 2 (ELOVL2), followed by assays to assess cancer cell proliferation and enzalutamide sensitivity. Mechanistic studies were conducted to evaluate the impact of ELOVL2 on the ubiquitin-proteasome system and AR signaling pathways.</p><p><strong>Results: </strong>Bioinformatic analysis revealed that activation of fatty acid metabolism, particularly through upregulation of ELOVL2, plays a critical role in driving enzalutamide resistance in PCa. Functional studies demonstrated that targeted inhibition of ELOVL2 significantly suppressed cancer cell proliferation and restored enzalutamide sensitivity in resistant cells. Mechanistically, ELOVL2 facilitates enzalutamide resistance by impairing the ubiquitin-proteasome system, leading to the subsequent activation of AR signaling pathways.</p><p><strong>Discussion: </strong>Our findings demonstrate that ELOVL2 drives enzalutamide resistance in CRPC by stabilizing AR through inhibition of ubiquitin-proteasome-mediated degradation. Targeting ELOVL2 represents a promising therapeutic strategy to overcome resistance in CRPC, with potential to improve clinical outcomes for patients.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1598400"},"PeriodicalIF":4.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12183063/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144474521","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":"Hypoxia-induced metabolic reprogramming in mesenchymal stem cells: unlocking the regenerative potential of secreted factors.","authors":"Wendy V Jaraba-Álvarez, Ashanti C Uscanga-Palomeque, Vanesa Sanchez-Giraldo, Claudia Madrid, Hector Ortega-Arellano, Karolynn Halpert, Carolina Quintero-Gil","doi":"10.3389/fcell.2025.1609082","DOIUrl":"https://doi.org/10.3389/fcell.2025.1609082","url":null,"abstract":"<p><p>Mesenchymal stem cells (MSCs) are a cornerstone of regenerative medicine, primarily due to their ability to secrete bioactive factors that modulate inflammation, promote tissue repair, and support regeneration. Recent research highlights the importance of preserving the native cellular microenvironment to optimize MSC function and survival post-transplantation. Preconditioning strategies, such as hypoxia exposure, have emerged as powerful tools to enhance MSC therapeutic potential by mimicking physiological conditions in their natural niche. This perspective article explores the metabolic adaptations induced by hypoxia in MSCs, focusing on shifts in mitochondrial function, glycolysis, oxidative phosphorylation, and metabolic intermediates that enhance cellular survival and bioactivity. We also discuss how these metabolic changes influence the composition and function of MSC-derived secreted factors, particularly exosomes and other extracellular vesicles, in modulating tissue repair. Furthermore, we provide an overview of preclinical and clinical studies that have evaluated hypoxia-preconditioned MSCs and their byproducts, assessing their efficacy in various therapeutic contexts. Special attention is given to the role of hypoxia-induced mitochondrial adaptations in improving MSC function and the emerging potential of metabolic inhibitors or respiration modulators as strategies to further refine MSC-based therapies. By integrating metabolic insights with clinical evidence, we aim to offer a comprehensive perspective on optimizing MSC culture conditions to enhance their regenerative properties, acknowledging that this remains a theoretical standpoint, as conventional culture methods are generally not conducted under hypoxic conditions. This approach holds promise for the development of more effective therapeutic strategies that leverage metabolic modulation to improve MSC-based interventions for a range of diseases.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1609082"},"PeriodicalIF":4.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12183037/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144474523","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 recurrent miscarriage: a critical review of pathophysiology and emerging therapeutic targets.","authors":"Mohammad Masoud Khodaei, Zahra Noori, Fateme Zare, Ahmad Meshkin","doi":"10.3389/fcell.2025.1559300","DOIUrl":"https://doi.org/10.3389/fcell.2025.1559300","url":null,"abstract":"<p><p>Ferroptosis is characterized as a specialized type of regulated cellular death that relies on iron and lipid peroxidation, which has recently been highlighted as playing a crucial role in the etiology of recurrent miscarriage (RM). Ferroptosis in RM is driven by dysregulated iron metabolism and increased oxidative stress, resulting from impaired antioxidant defense, which leads to lipid peroxidation and consequent cell death in trophoblasts. The cellular changes compromise placental development and impair trophoblast invasion and maternal-fetal tolerance. Therapeutic interventions targeting ferroptosis are promising for the mitigation of its effects and improvement of pregnancy outcomes. Strategies include Glutathione Peroxidase 4 (GPX4) activity enhancement, glutathione replenishment, ferroptosis inhibitors, and iron metabolism modulation. Further, new strategies targeting non-coding RNAs, and epigenetic regulators emphasize ferroptosis as a viable therapeutic target. This review emphasizes the importance of ferroptosis in the pathophysiology of RM and highlights its potential for guiding innovative treatments.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1559300"},"PeriodicalIF":4.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12183038/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144474522","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":"Cilia and transcription: a mini review.","authors":"Jason M Brown","doi":"10.3389/fcell.2025.1582796","DOIUrl":"https://doi.org/10.3389/fcell.2025.1582796","url":null,"abstract":"<p><p>Cilia assembly is accompanied by rapid and highly coordinated transcription of hundreds of genes. Cilia gene regulation has been studied extensively in both metazoans and unicellular model organisms. The forkhead and RFX family transcription factors regulating cilia genes in animals were first identified 25 years ago and considerable molecular details of the regulatory processes have been described since then. While many of the most important early studies of cilia gene regulation were done in unicellular organisms, additional molecular players need to be discovered for a more complete understanding in these organisms. In this concise review, written primarily for students new to the field, I present a brief history of research on cilia gene regulation, highlight some key metazoan discoveries from the last decade, and discuss gaps in our understanding of cilia gene regulation in unicellular model organisms with a focus on <i>Chlamydomonas reinhardtii</i>.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1582796"},"PeriodicalIF":4.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12183034/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144474520","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":"Vesicular trafficking and cell-cell communication in neurodevelopment and neurodegeneration.","authors":"Salma Amin, Elena Taverna","doi":"10.3389/fcell.2025.1600034","DOIUrl":"https://doi.org/10.3389/fcell.2025.1600034","url":null,"abstract":"<p><p>Regulation of vesicle biology and trafficking plays a critical role in cell viability. Vesicular trafficking is a process that entails vesicle biogenesis, transport, and sorting of materials such as proteins, enzymes, hormones, and neurotransmitters to different cellular compartments. This phenomenon is especially important in cells of the central nervous system, including neural progenitors, neurons, and glial cell populations, because of their highly polarized architecture. In line with that, disruption in vesicular trafficking during cortical development affects progenitor proliferation and differentiation and leads to brain malformations. On the other hand, neuronal cells require long-range vesicular trafficking to reach distant locations, such as the distal part of the axons, and synaptic vesicles are essential for cell-cell communication. Neurons have high energy demands. Therefore, any malfunction in vesicular trafficking is a trigger to spiraling into neurodegeneration. Here, we give a comprehensive review of the role of intracellular and extracellular vesicles in cortical development and neurodegeneration, and we discuss how trafficking between organelles in specific cell types contributes to brain pathologies. Finally, we highlight the emerging evidence linking disruption in vesicular trafficking to neurological disorders such as Alzheimer's disease, Parkinson's disease, and autism.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1600034"},"PeriodicalIF":4.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12183288/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144474525","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":"Skin lamellar bodies: a unique set of lysosome-related organelles.","authors":"Sarmistha Mahanty","doi":"10.3389/fcell.2025.1597696","DOIUrl":"https://doi.org/10.3389/fcell.2025.1597696","url":null,"abstract":"<p><p>Skin lamellar bodies (LBs) are crucial for forming and renewing the protective skin barrier, which regulates the body's internal environment and integrity. LB dysfunction is associated with severe disease conditions such as atopic dermatitis, Netherton syndrome and Harlequin ichthyosis, among others. Despite its importance in human physiology, the intracellular origin and biogenesis mechanism of LBs remain largely unknown. LBs are lysosome-related organelles (LRO), a group of cell type-specific organelles having unique structures, cargo content, and function. Classical LROs such as melanosomes, lung lamellar bodies and Weibel-Palade bodies share overlapped molecular machinery/mechanisms and are co-affected in genetic disorders like Hermansky-Pudlak syndrome (HPS) or Chédiak-Higashi syndrome (CHS). In contrast, LBs contain a diverse array of protein and lipid cargo that are notably different from those found in other LROs, and LBs are not reported to be affected in HPS/CHS. LBs form in an advanced differentiation state of keratinocytes while cells are experiencing high ions and low nutrients in their exterior, the plasma membrane (PM) undergoing modifications, and intracellular organelles starting to disappear. This article discusses atypical conditions of LB biogenesis in comparison to classical LROs, which may potentially guide future research on LB biogenesis.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1597696"},"PeriodicalIF":4.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12183049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144474524","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":"17β-estradiol maintains extracellular matrix homeostasis of nucleus pulposus cells by activating p70 S6K1 signaling pathway.","authors":"Tao Liu, Zhaohui Li, Wei Zhang, Xuzhao Guo, Guobin Liu, Dalong Yang, Sidong Yang","doi":"10.3389/fcell.2025.1564458","DOIUrl":"10.3389/fcell.2025.1564458","url":null,"abstract":"<p><strong>Background: </strong>Estrogen can inhibit the apoptosis of nucleus pulposus cells (NPCs) through the PI3K/AKT/mTOR signaling pathway. However, the downstream of mTOR signaling pathway remains elusive. This study investigates the effect of 17β-estradiol (E2) on intervertebral disc degeneration (IVDD) through the p70 S6K1 signaling pathway, downstream of mTOR.</p><p><strong>Methods: </strong>The IVDD model of rats was established by needle puncture and bilateral ovariectomy. Fifteen Sprague-Dawley rats were randomly assigned to the following three groups: (A) Sham surgery group (Sham); (B) Bilateral ovariectomy, 21G needle puncture and carrier injection (OVX + veh); (C) Bilateral ovariectomy, 21G needle puncture, E2 supplementation (OVX + E2). The degree of IVDD was evaluated by X-ray, magnetic resonance imaging (MRI), hematoxylin and eosin (H&E), and Safranin O-Fast Green staining. The expression levels of target protein p70S6K1 and its phosphorylated products were detected by immunohistochemistry (IHC). Finally, Western blot analysis and immunofluorescence staining were used to investigate the effect of E2 on the p70 S6K1 signaling pathway <i>in vitro</i>.</p><p><strong>Results: </strong>Histological staining and radiological results showed that E2 supplementation altered signaling, suggesting that it may have a protective effect against IVDD. IHC showed that compared with the Sham and OVX + E2 groups, the level of p70 S6K1 in the OVX + veh group was significantly increased while the expression of phosphorylated products (p-S6) was significantly decreased, suggesting that E2 could inhibit IVDD by activating p70 S6K1 signaling pathway, the downstream of mTOR. Furthermore, cellular immunofluorescence and Western blot showed that E2 can maintain extracellular matrix (ECM) balance and inhibits apoptosis of nucleus pulposus cells (NPCs) by activating the p70 S6K1 signaling pathway.</p><p><strong>Conclusion: </strong>In summary, 17β-estradiol mitigates IVDD progression by maintaining ECM homeostasis and inhibiting NPCs apoptosis through activation of the p70 S6K1 signaling pathway downstream of mTOR.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1564458"},"PeriodicalIF":4.6,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12179197/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368748","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":"Hedgehog signaling controls astral microtubules and mitotic spindle orientation in neural progenitors and iPSCs.","authors":"Fengming Liu, Anna Medyukhina, Kris M Olesen, Abbas Shirinifard, Hongjian Jin, Lei Li, Marina Mapelli, Khaled Khairy, Young-Goo Han","doi":"10.3389/fcell.2025.1582924","DOIUrl":"10.3389/fcell.2025.1582924","url":null,"abstract":"<p><p>Mitotic spindle orientation is crucial for cell fate determination and tissue organization. Although the intracellular machinery governing spindle orientation is well characterized, whether and how secreted factors, such as morphogens, regulate this process remains poorly understood. This study investigated the role of Hedgehog (HH) signaling in modulating mitotic spindle orientation in neural progenitor cells and in induced pluripotent stem cells (iPSCs). Time-lapse microscopy of cerebral organoids and iPSCs revealed that HH signaling increases the angle of the mitotic spindle relative to the apical surface, prolongs mitosis, and enhances spindle rotation. Mechanistically, HH signaling reduces both the number and the length of astral microtubules, key regulators of spindle orientation. This reduction correlates with increased spindle angle in iPSCs. Furthermore, we show that canonical HH signaling, involving GLI-dependent transcriptional regulation, contributes to these effects. RNA sequencing and gene set enrichment analysis (GSEA) revealed that HH signaling upregulates genes associated with microtubule depolymerization, suggesting a transcriptional mechanism by which HH signaling influences astral microtubule dynamics and, consequently, mitotic spindle orientation. These findings highlight a novel link between a morphogen, transcriptional regulation, and the control of mitotic spindle orientation, with implications for development and tissue homeostasis.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1582924"},"PeriodicalIF":4.6,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12179144/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368749","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":"MSLI-Net: retinal disease detection network based on multi-segment localization and multi-scale interaction.","authors":"Zhenjia Qi, Jin Hong, Jilan Cheng, Guoli Long, Hanyu Wang, Siyue Li, Shuangliang Cao","doi":"10.3389/fcell.2025.1608325","DOIUrl":"10.3389/fcell.2025.1608325","url":null,"abstract":"<p><strong>Background: </strong>The retina plays a critical role in visual perception, yet lesions affecting it can lead to severe and irreversible visual impairment. Consequently, early diagnosis and precise identification of these retinal lesions are essential for slowing disease progression. Optical coherence tomography (OCT) stands out as a pivotal imaging modality in ophthalmology due to its exceptional performance, while the inherent complexity of retinal structures and significant noise interference present substantial challenges for both manual interpretation and AI-assisted diagnosis.</p><p><strong>Methods: </strong>We propose MSLI-Net, a novel framework built upon the ResNet50 backbone, which enhances the global receptive field via a multi-scale dilation fusion module (MDF) to better capture long-range dependencies. Additionally, a multi-segmented lesion localization module (LLM) is integrated within each branch of a modified feature pyramid network (FPN) to effectively extract critical features while suppressing background noise through parallel branch refinement, and a wavelet subband spatial attention module (WSSA) is designed to significantly improve the model's overall performance in noise suppression by collaboratively processing and exchanging information between the low- and high-frequency subbands extracted through wavelet decomposition.</p><p><strong>Results: </strong>Experimental evaluation on the OCT-C8 dataset demonstrates that MSLI-Net achieves 96.72% accuracy in retinopathy classification, underscoring its strong discriminative performance and promising potential for clinical application.</p><p><strong>Conclusion: </strong>This model provides new research ideas for the early diagnosis of retinal diseases and helps drive the development of future high-precision medical imaging-assisted diagnostic systems.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1608325"},"PeriodicalIF":4.6,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12179138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368750","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":"Proteasome caspase-like activity regulates stress granules and proteasome condensates.","authors":"Shirel Steinberger, Julia Adler, Nadav Myers, Yosef Shaul","doi":"10.3389/fcell.2025.1570499","DOIUrl":"10.3389/fcell.2025.1570499","url":null,"abstract":"<p><p>The 20S proteasome maintains cellular protein homeostasis, particularly during stress responses. In a previous study, we identified numerous 20S proteasome substrates through mass spectrometry analysis of peptides generated from cellular extracts degraded by purified 20S proteasome. Many substrates were found to be components of liquid-phase separation, such as stress granules (SGs). Here, we demonstrate the degradation products arise from the caspase-like (CL) proteasomal activity. To investigate the functional implications of CL activity, we generated cell lines devoid of CL function by introducing the PSMB6 T35A mutation. These mutant cells exhibited slower growth rates, heightened sensitivity to stress, and activation of the unfolded protein response (UPR), as indicated by elevated levels of spliced XBP1 (sXBP1) and stress markers. Cells were subjected to arsenite and osmotic stress to assess their responses. Our findings reveal that CL activity is crucial for efficient SG assembly but does not significantly affect SG clearance. Interestingly, in these mutant cells, proteasomes were more cytoplasmic under normal conditions but formed nuclear condensates/granules (PGs) upon NaCl osmotic stress. However, the PGs were unstable and rapidly dispersed. These findings underscore the important role of the proteasome's CL activity in managing stress-induced dynamics of liquid-liquid phase, highlighting its importance in cellular adaptation to proteotoxic and genotoxic stress conditions.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1570499"},"PeriodicalIF":4.6,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12176758/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332768","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}