Frontiers in Cell and Developmental Biology最新文献

{"title":"3D-ASC-Exos as a novel drug carrier for glioma treatment.","authors":"Xintong Han, Xin Li, Xinrui Yan, Yu Zhang, Chang Liu, Wei Liu, Rui Han, Yaxin Li, Jianming Li, Naichao Diao, Boyin Jia, Rui Du","doi":"10.3389/fcell.2025.1677555","DOIUrl":"10.3389/fcell.2025.1677555","url":null,"abstract":"<p><strong>Introduction: </strong>It is known that extracts from deer antler stem cells have an inhibitory effect on glioma growth. Therefore, it is hypothesized that exosomes derived from deer antler stem cells (ASC-Exos) can be used as a new drug carrier for the treatment of glioma.</p><p><strong>Methods: </strong>To begin with, we established a 3D culture system to obtain more exosomes and characterized the 3D-ASC-Exos. Subsequently, we loaded TMZ into 3D-ASC-Exos. Evaluate the effects of 3D-ASC-Exos loaded with TMZ on glioma cell proliferation, migration, invasion, and apoptosis at the cellular level. Additionally, the safety and efficacy of 3D-ASC-Exos loaded with TMZ against glioma were evaluated using tumor-bearing mice.</p><p><strong>Results: </strong>Compared with the 2D-ASC-Exos obtained from the traditional 2D culture, the 3D-ASC-Exos obtained from our constructed 3D culture system were concentrated nearly 30 times in the culture medium volume, which was more convenient for subsequent puriffcation. The two forms of ASC-Exos had similar morphologies and surface markers, but 3D-ASC-Exos were enriched with more miRNAs related to tumor suppression. In vitro experiments demonstrated that 3D-ASC-exosomes loaded with temozolomide (TMZ) inhibited the proliferation, migration and invasion abilities of glioma cells and promoted the apoptosis of glioma cells. The vivo tumor-bearing mouse model demonstrated that 3D-ASC-Exos loaded with TMZ exerted tumor-suppressive effects by inhibiting tumor growth and promoting tumor apoptosis. Meanwhile, the treatment with 3D-ASC-Exos loaded with TMZ caused no damage to the various tissues and organs of mice compared with the TMZ group.</p><p><strong>Discussion: </strong>3D-ASC-Exos can be used as a novel drug carrier for glioma treatment. The development of 3D-ASC-Exos as a drug carrier not only provides a better strategy for tumor treatment, but also demonstrates the broad potential of exosomes in targeted tumor therapy.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1677555"},"PeriodicalIF":4.6,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12507771/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145279379","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":"Osteocytes: master orchestrators of skeletal homeostasis, remodeling, and osteoporosis pathogenesis.","authors":"Yan Wu, Donghao Gan, Zhikang Liu, Daodi Qiu, Guoqing Tan, Zhanwang Xu, Haipeng Xue","doi":"10.3389/fcell.2025.1670716","DOIUrl":"10.3389/fcell.2025.1670716","url":null,"abstract":"<p><p>The skeleton functions as an endocrine organ. Osteocytes maintenance of skeletal strength and energy balance by sensing mechanical stress and communicating with surrounding cells. They are currently considered key regulators of bone remodeling, mineral metabolism, and systemic homeostasis. Osteocytes originate from osteoblasts and are embedded in the lacunar-tubular network. They express proteins such as DMP1, sclerostin, and FGF23, and influence Wnt signaling, the RANKL/OPG axis, and phosphate metabolism. We review the latest studies in the field of osteocyte biology, focusing on their mechanotransduction through Piezo1 and integrins, regulation of osteoclastogenesis and osteogenesis, and their interactions with the bone marrow microenvironment, including immune and vascular cells. In osteoporosis, osteocyte dysfunction is manifested by apoptosis, ferroptosis, and pyroptosis. These changes, together with altered secretion, lead to uncoupled remodeling, disruption of the lacuno-canalicular network and metabolic imbalances that are intertwined with inflammation and bone marrow fat deposition. Osteocytes play an important role in fracture healing and adaptive remodeling under mechanical stimulation, promoting angiogenesis and stem cell recruitment. A growing number of emerging approaches, including stem cell therapy, CRISPR editing, and AI-driven multi-omics for precision medicine, are accelerating osteocyte-related research and the development of therapeutic strategies. These studies reveal the clinical potential of osteocyte-targeted therapies to prevent osteoporosis, improve bone strength, and enhance regeneration. By integrating molecular, cellular, and systems knowledge, we highlight osteocytes as a key therapeutic target to combat bone diseases and promote bone regeneration.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1670716"},"PeriodicalIF":4.6,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12508660/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145279477","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":"Genetic modulation of mitochondrial NAD+ regeneration does not prevent dopaminergic neuron dysfunction caused by mitochondrial complex I impairment.","authors":"Karis B D'Alessandro, Enrico Zampese, Jenna L E Blum, Britta Kuusik, Alec Palmiotti, Shawn M Davidson, Colleen R Reczek, D James Surmeier, Navdeep S Chandel","doi":"10.3389/fcell.2025.1650462","DOIUrl":"10.3389/fcell.2025.1650462","url":null,"abstract":"<p><p>Dysfunction of mitochondrial complex I (MCI) has been implicated in the degeneration of dopaminergic neurons in Parkinson's disease. Here, we report the effect of expressing MitoLbNOX, a mitochondrial-targeted version of the bacterial enzyme LbNOX, which increases regeneration of NAD+ in the mitochondria to maintain the NAD+/NADH ratio, in dopaminergic neurons with impaired MCI (MCI-Park mice). MitoLbNOX expression did not ameliorate the cellular or behavioral deficits observed in MCI-Park mice, suggesting that alteration of the mitochondrial NAD+/NADH ratio alone is not sufficient to compensate for loss of MCI function in dopaminergic neurons.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1650462"},"PeriodicalIF":4.6,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12507863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145279357","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":"Systematic characterization of cross-source miRNA biomarkers in prostate cancer with computational-experimental integrated analysis.","authors":"Huimin Lu, Wenjin Li, Zhongxin Huang, Libo Chen, Mingyong Li, Weiming Deng","doi":"10.3389/fcell.2025.1605297","DOIUrl":"10.3389/fcell.2025.1605297","url":null,"abstract":"<p><strong>Purpose: </strong>Prostate cancer (PCa) is occult and remains largely incurable once it metastasizes. Our research aims to identify the key miRNAs and construct miRNA-mRNA networks for PCa.</p><p><strong>Methods: </strong>The microarray dataset GSE112264, consisting of 1,591 male serum samples, and tissue miRNA data from TCGA, including 497 prostate cancer and 52 normal samples, were included in the analysis. Differentially expressed miRNAs (DE-miRNAs) were detected, and miRTarBase was used to predict the common target genes. Then, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed for the target genes. The protein-protein interaction (PPI) network, which revealed the top 10 hub genes, was constructed using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and Cytoscape. The expression of the potential hub genes was examined using the UALCAN database. Finally, GSE112264, TCGA datasets, and clinical samples were used to verify the consistency of miRNA expressions in serum and tissue.</p><p><strong>Results: </strong>A total of 948 target genes of the two overlapped downregulated miRNAs (miR-146a-3p and miR-136-3p) were predicted. Functional enrichment analysis indicated that significant DE-miRNAs were related to PCa-related pathways, such as protein binding, the mammalian target of rapamycin (mTOR) signaling pathway, and porphyrin and chlorophyll metabolisms. Four hub genes were identified from the PPI network, namely, NSF, HIST2H2BE, IGF2R, and CADM1, and verified to be aberrantly expressed in the UALCAN database. Experiment results indicated that only miR-136-3p was markedly reduced in both serum and tissue.</p><p><strong>Conclusion: </strong>In this study, we established the miRNA-mRNA network, offering potential PCa targets.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1605297"},"PeriodicalIF":4.6,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12507830/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145279468","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":"Primary cilia in the mature brain: emerging roles in Alzheimer's disease pathogenesis.","authors":"Alexis Shiying Huang, Amy Sze Man Li, Catherine Hong Huan Hor","doi":"10.3389/fcell.2025.1650884","DOIUrl":"10.3389/fcell.2025.1650884","url":null,"abstract":"<p><p>Primary cilia are microtubule-based structures that resemble antennae and function as sensory organelles. Dysfunction of primary cilia has been linked to various age-related conditions. Alzheimer's disease, which affects more than 38.5 million individuals worldwide, is a prominent neurodegenerative disorder, with aging being its most significant risk factor. In this review, we provide an overview of current findings on the role of primary cilia in the mature brain and the mechanisms by which alteration of primary cilia may influence the progression of Alzheimer's disease. Growing evidence reveals that primary cilia in the mature brain play dynamic roles in cell type, region, and age-dependent manners. In Alzheimer's disease, anomalies in primary cilia functions and morphology are closely associated with key pathologies. However, the exact mechanisms remain unclear. Future studies on neuronal and glial cilia dynamics during aging and neurodegeneration are essential to explore their potential as therapeutic targets.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1650884"},"PeriodicalIF":4.6,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12504367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145257697","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":"Mesenchymal stem cell-conditioned medium accelerates type 2 diabetic wound healing by targeting TNF and chemokine signaling.","authors":"Long Huang, Zhongbao Lin, Haiyun Liu, Xiankun Lin, Naishun Liao, Xiaodan Wu","doi":"10.3389/fcell.2025.1659444","DOIUrl":"10.3389/fcell.2025.1659444","url":null,"abstract":"<p><strong>Introduction: </strong>Given the crucial role of paracrine signaling in the therapeutic function of adipose tissue-derived mesenchymal stem cells (ADSCs) for skin wound repair, this study aimed to evaluate the efficacy of ADSC-conditioned medium (ACM) in enhancing type 2 diabetic (T2D) wound healing.</p><p><strong>Methods: </strong>The effect of ACM on the viability and angiogenesis of human umbilical vein endothelial cells (HUVECs) was first evaluated using the CCK-8 assay and q-PCR analysis, respectively. Next, a T2D rat model was established through the combination of a high-fat diet and streptozotocin (STZ). Following the establishment of full-thickness skin defects in T2D rats, ACM or serum-free cultured medium was daily injected around the wound edges for 7 days. Afterward, the skin wound healing rate was analyzed, and the skin tissues were assessed by histopathological examination. The mRNA levels of TNF-α, IL-1β, IL-6, COX-2, IL-12, and IFN-γ were evaluated by q-PCR analysis. Additionally, transcriptome sequencing and immunohistochemistry were performed to reveal the potential mechanisms of ACM in T2D skin wound healing.</p><p><strong>Results: </strong>ACM significantly enhanced HUVEC proliferation and angiogenesis while upregulating the expression of EGF, bFGF, VEGF, and KDR. In T2D rats, ACM accelerated wound closure and suppressed pro-inflammatory mediators (TNF-α, IL-1β, IL-6, COX-2, IL-12, and IFN-γ). Notably, transcriptome analysis revealed ACM-mediated downregulation of TNF and chemokine signaling pathways.</p><p><strong>Discussion: </strong>ACM promotes diabetic wound healing through dual mechanisms: (1) stimulating vascularization by inducing growth factor expression and (2) modulating the inflammatory microenvironment by inhibiting TNF/chemokine cascades. These findings position ACM as a promising cell-free therapy for impaired wound healing in diabetes.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1659444"},"PeriodicalIF":4.6,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12504491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145257756","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":"Left-right symmetry breaking: learning from the chicken.","authors":"Tobias Karl Pieper, Nikoloz Tsikolia","doi":"10.3389/fcell.2025.1672263","DOIUrl":"10.3389/fcell.2025.1672263","url":null,"abstract":"<p><p>Morphological left-right asymmetry of visceral organs in most cases reveals a typical arrangement. This implies directed symmetry breaking which is suggested to be based on the existence of structural chirality. At early developmental stages many vertebrate model organisms display so-called leftward flow of extracellular fluid which is based on the unidirectional rotation of chiral cilia. Cytoskeletal chirality has been shown to contribute to the left-right asymmetry of invertebrates including <i>Caenorhabditis elegans</i> and <i>Drosophila melanogaster</i>. The mechanisms of left-right symmetry breaking in vertebrates without ciliary flow remain mysterious. Here, we present our perspective on left-right patterning and symmetry breaking in the chick within a broader context.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1672263"},"PeriodicalIF":4.6,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12504268/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145257669","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":"Enlargement of the muscle stem cell pool in linc-MYH-deficient mice does not prevent sarcopenia during aging.","authors":"Qing Yin, Christelle Labib, Thomas Boettger, Thomas Braun","doi":"10.3389/fcell.2025.1667437","DOIUrl":"10.3389/fcell.2025.1667437","url":null,"abstract":"<p><p>Loss of skeletal muscle mass and muscle strength during aging (sarcopenia) and reduced skeletal muscle regeneration are often attributed to the age-dependent decline of muscle stem cells (MuSCs). However, it has not been analyzed whether enlargement of the MuSC pool in old animals can attenuate sarcopenia or restore regenerative potential. Here, we directly tested this idea by taking advantage of linc-MYH-mutant mice, which show a substantially increased number of MuSCs in young mice. We found that 24-month-old geriatric linc-MYH knockout mice still maintain a consistently enlarged MuSC pool compared to age-matched controls. MuSCs in geriatric linc-MYH knockout mice were located beneath the basal lamina and remained mostly in a quiescent state. Importantly, enlargement of the MuSC pool did not prevent sarcopenia, or improve muscle function and regeneration. Instead, the larger MuSC pool in geriatric linc-MYH^-/- mice resulted in the formation of smaller muscles during regeneration with thicker fibers, characterized by an increased myonuclei content per fiber. Furthermore, we observed shifts of the muscle fiber-type composition in linc-MYH^-/- mice during aging, including a reduction of type IIb fibers in the tibialis anterior muscle and a reduction of type IIa fibers in the soleus, combined with an increase of type I fibers.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1667437"},"PeriodicalIF":4.6,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12504259/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145257644","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":"From macrophage polarization to clinical translation: immunomodulatory hydrogels for infection-associated bone regeneration.","authors":"Rui Zhang, Suk Fei Tan, Ye Wang, Junxue Wu, Chao Zhang","doi":"10.3389/fcell.2025.1684357","DOIUrl":"10.3389/fcell.2025.1684357","url":null,"abstract":"<p><p>Bone infections such as osteomyelitis and fracture-related infections are a significant clinical challenge, characterized by complex interactions between pathogenic microorganisms, disrupted immune responses, and impaired regenerative processes. A pathological hallmark of these conditions is the persistent pro-inflammatory macrophage (M1) polarization, which prevents the essential transition to anti-inflammatory M2 macrophages required for successful bone healing. This review examines the emerging paradigm of immunomodulatory hydrogels as a multifaceted therapeutic strategy that addresses both infection control and bone regeneration through targeted modulation of macrophage polarization. We systematically analyze the fundamental role of macrophage phenotypic switching in osteoimmune responses, demonstrating how infection disrupts the normal M1-to-M2 transition and perpetuates a chronic inflammatory state that impairs osteogenesis while promoting bone resorption. The review details innovative hydrogel design strategies that incorporate antimicrobial agents, immunomodulatory factors, and bioactive components to create materials capable of eliminating pathogens while simultaneously steering macrophages toward a pro-regenerative phenotype. Key approaches include integration of sequential drug-release systems, reactive oxygen species (ROS)-scavenging mechanisms, photothermal activation, and cell delivery platforms within biodegradable hydrogel matrices. Recent advances in multifunctional hydrogel systems have demonstrated superior performance compared to conventional treatments-including enhanced bacterial clearance, accelerated bone healing, and reduced infection recurrence rates in preclinical models. The pathway from laboratory findings to clinical application is critically evaluated, addressing challenges in biocompatibility, manufacturing consistency, regulatory approval, and clinical trial design. This comprehensive analysis reveals that immunomodulatory hydrogels represent a promising convergence of infection control and regenerative medicine, offering new therapeutic avenues for treating complex bone defects where traditional approaches have proven insufficient.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1684357"},"PeriodicalIF":4.6,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12504304/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145257594","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":"Fueling the fire-a pan-cancer analysis of MYC-regulated lipid metabolism.","authors":"Tilottama Chatterjee, Ethan Beffert, Daniel Liefwalker","doi":"10.3389/fcell.2025.1669544","DOIUrl":"10.3389/fcell.2025.1669544","url":null,"abstract":"<p><p>The oncogene MYC and its product c-Myc are responsible for a multitude of changes in cancerous cells that trigger cell growth, proliferation and metastasis. The efforts to understand the multifaceted role of MYC in malignancies have highlighted metabolic reprogramming as a prominent function of this transcription factor, with effects across glycolysis, protein and lipid metabolism, mitochondrial respiration and energy storage. In particular, the role of MYC in lipid metabolism has been the focus of several studies in the past two decades, elucidating how the balance of lipid production and breakdown aids in tumor proliferation. Here, we provide a comprehensive summary of how modulation of MYC alters fatty acid synthesis and degradation, the metabolism of compound lipids, and the consequences for other metabolic pathways. The observed effects are highly cell type-specific, highlighting the MYC network's ability to harness the existing cellular signaling pathways and specific tumor microenvironment to promote tumor growth and metastasis.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1669544"},"PeriodicalIF":4.6,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12504247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145257651","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}