Frontiers in Cell and Developmental Biology最新文献

{"title":"Interplay between MAPK signaling pathway and autophagy in skin aging: mechanistic insights and therapeutic implications.","authors":"Xu Liu, Bo Chen, Xuefeng Liu, Xiaoqing Zhang, Jingdong Wu","doi":"10.3389/fcell.2025.1625357","DOIUrl":"10.3389/fcell.2025.1625357","url":null,"abstract":"<p><p>Skin aging manifests as structural degradation, functional decline, and heightened disease susceptibility. Central to this process is the overactivation of the mitogen-activated protein kinase (MAPK) signaling pathway triggered by reactive oxygen species (ROS). Autophagy, a lysosomal degradation mechanism essential for maintaining cellular homeostasis, demonstrates context-dependent duality in skin aging by mediating cytoprotective effects and stress-induced dysfunction. Emerging evidence highlights that the interplay between MAPK signaling and autophagy critically modulates skin aging progression. Despite its therapeutic potential, the lack of effective targeting strategies severely hinders clinical translation. Therefore, this review synthesizes current evidence on MAPK-autophagy interplay across key cutaneous cell populations, namely, keratinocytes, fibroblasts, and melanocytes (including melanoma), revealing cell-type-specific regulatory networks that influence skin aging. Subsequently, we explore the therapeutic potential of natural bioactive compounds targeting this interplay to accelerate the translation of evidence into the progression of strategies for combating skin aging.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1625357"},"PeriodicalIF":4.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12245914/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625851","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":"Comparative analysis of small molecule and growth factor-derived human induced pluripotent stem cell-derived hepatocyte-like cells.","authors":"Faizal Z Asumda, Shadia Alzoubi, Kiyasha Padarath, Kimya Jones, Ravindra Kolhe, Ashis Kumar Mondal, Ahmet Alptekin, Wenbo Zhi, Tae Jin Lee, Robert C Huebert, Nathan P Staff, Lewis R Roberts, Lindsey A Kirkeby","doi":"10.3389/fcell.2025.1594340","DOIUrl":"10.3389/fcell.2025.1594340","url":null,"abstract":"<p><p>The growth factor and small molecule protocol are the two primary approaches for generating human induced pluripotent stem cell-derived hepatocyte-like cells (iPSC-HLCs). We compared the efficacy of the growth factor and small molecule protocols across fifteen different human iPSC lines. Morphological assessment, relative quantification of gene expression, protein expression and proteomic studies were carried out. HLCs derived from the growth factor protocol displayed mature hepatocyte morphological features including a raised, polygonal shape with well-defined refractile borders, granular cytoplasm with lipid droplets and/or vacuoles with multiple spherical nuclei or a large centrally located nucleus; significantly elevated hepatocyte gene and protein expression including AFP, HNF4A, ALBUMIN, and proteomic and metabolic features that are more aligned with a mature phenotype. HLCs derived from the small molecule protocol showed a dedifferentiated, proliferative phenotype that is more akin to liver tumor-derived cell lines. These experimental results suggest that HLCs derived from growth factors are better suited for studies of metabolism, biotransformation, and viral infection.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1594340"},"PeriodicalIF":4.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12240953/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607954","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":"Azithromycin mitigates human rhinovirus impact on barrier integrity and function in non-diseased airway epithelium.","authors":"Kevin Looi, Erika N Sutanto, Thomas Iosifidis, Luke J Berry, Anthony Kicic, Stephen M Stick","doi":"10.3389/fcell.2025.1532656","DOIUrl":"10.3389/fcell.2025.1532656","url":null,"abstract":"<p><strong>Introduction: </strong>Azithromycin improves symptomology in various chronic airway diseases exacerbated by viral infections. However, the mechanisms underlying the apparent antiviral effects of azithromycin remain unclear.</p><p><strong>Methods: </strong>Airway epithelial cells from healthy children were cultured, expanded and differentiated into air-liquid interface cultures. Submerged and differentiated primary cultures were treated with 10 µM of AZM for 24 h and subsequently infected with human rhinovirus (HRV)-1b for 24 h. Virus receptor expression, replication, progeny release and inflammatory cytokines (IL-1β, -6, -8 and IP-10) were then measured. Barrier integrity was determined via qPCR, in-cell western (ICW), immunofluorescence confocal microscopy, confocal microscopy, transepithelial electrical resistance (R_T) measurement and an apparent permeability (P _<i>app</i> ) assay.</p><p><strong>Results: </strong>Treatment with AZM for 24 h at the concentrations of 0.1, 1 and 10 µM did not have any significant impact on either cellular viability or cytotoxicity in un-infected cells. No significant effect on viral receptor, cytokine expression was observed in non-infected cells treated with 10 µM AZM. Similarly, there was no significant change in both occludin and ZO-1 expression in non-infected cells. However, <i>claudin-1</i> gene expression was significantly reduced but corresponding protein expression was significantly increased following 10 µM AZM. Although R_T was significantly lower, this was not corroborated by any significant change in epithelial permeability after 10 µM AZM treatment. Subsequent to HRV-1b infection, 10 µM AZM treatment significantly reduced cytotoxicity induced by infection. Viral receptor expression were not affected with AZM pre-treatment but a significant decrease in viral replication was observed. Except for IP-10, expression of IL-1β, -6, and -8 was significantly reduced. Gene and protein expression of key epithelial junctions were significantly higher in treated, infected cells, which were concomitant with epithelial barrier function.</p><p><strong>Discussions: </strong>This study identified that AZM can protect against HRV-1b-induced epithelial damage. Our data, demonstrating the antiviral, anti-inflammatory, and barrier-protective effects <i>in vitro</i> are strongly indicative of pleiotropic mechanisms of AZM for mitigating viral infection and its consequences. These effects are likely to contribute to the benefits observed in clinical trials of AZM in a number of chronic respiratory diseases.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1532656"},"PeriodicalIF":4.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12241080/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607953","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":"Oocyte and dietary supplements: a mini review.","authors":"Hao Chen, Shuoqi Wang, Meiying Song, Dongxia Yang, Hongmei Li","doi":"10.3389/fcell.2025.1619758","DOIUrl":"10.3389/fcell.2025.1619758","url":null,"abstract":"<p><p>Rising rates of infertility have stimulated interest in dietary supplements to improve oocyte quality through mitochondrial function, antioxidant activity, and epigenetically regulated metabolic pathways. Mitochondria provides adenosine triphosphate for oocyte maturation, with Coenzyme Q10 (CoQ10) demonstrating efficacy in animal models by alleviating oxidative damage and enhancing blastocyst formation. In aged mice, CoQ10 restored mitochondrial activity and reduced chromosomal abnormalities, while preliminary human studies noted improved embryo quality in poor responders, though randomized controlled trials (RCTs) remain inconclusive. Antioxidants like melatonin counter reactive oxygen species (ROS)-induced spindle defects and mitochondrial dysfunction, showing benefits in murine oocyte maturation and blastocyst development. Resveratrol enhanced bovine oocyte quality through metabolic modulation. Human trials on antioxidants show reduced granulosa cell stress but lack robust evidence. Epigenetically, folate supports DNA methylation critical for embryonic gene expression, with deficiencies linked to hyperhomocysteinemia and developmental defects in animal models. Human observational studies associate folate-rich diets with lower aneuploidy and better assisted reproductive technology outcomes, while omega-3 fatty acids aid chromatin remodeling via histone deacetylase regulation. Despite compelling preclinical data, human trials face inconsistencies due to variable designs and confounders. Standardized RCTs are urgently needed to translate mechanistic insights into clinical guidelines, addressing the disconnect between animal studies and human reproductive outcomes.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1619758"},"PeriodicalIF":4.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12241077/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607957","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":"FOXK2 regulates fatty acid metabolism and promotes cervical cancer progression by activating the mTOR/DRP1 signaling axis.","authors":"Dan Liao, Saitian Zeng, Cuifen Li, Yuhong Yao, Min Guo, Yejia Cui, Haohai Huang","doi":"10.3389/fcell.2025.1615454","DOIUrl":"10.3389/fcell.2025.1615454","url":null,"abstract":"<p><strong>Background: </strong>Cervical cancer is a prevalent malignancy among women, and its pathogenesis is highly complex. Lipid metabolism plays a crucial role in providing sufficient metabolites and energy for the rapid proliferation and progression of tumors, significantly influencing the advancement of cervical cancer. However, the specific lipid metabolism mechanisms remain to be thoroughly investigated. This study aims to elucidate the lipid metabolism mechanisms by which FOXK2 promotes the progression of cervical cancer.</p><p><strong>Methods: </strong>FOXK2 overexpression and knockdown cell lines were constructed, The cell activity and invasion were evaluated using CCK8, Edu, transwell, and flow cytometry. The oxygen consumption rate (OCR) values were detected by the XFe96 analyzer. The expression of fatty acid oxidation (FAO) related genes was analyzed by WB and qRT-PCR. The binding of FOXK2 to mTOR and mTOR to DRP1 was detected by co-immunoprecipitation (CoIP). Ultimately FOXK2-knockdown cells were applied to construct the Xenograft tumors in nude mice, and the relevant experiments were verified <i>in vivo</i>.</p><p><strong>Results: </strong><i>In vitro</i> experiments, our findings demonstrated that FOXK2 enhances the proliferation and invasive capabilities of cervical cancer cells. FOXK2 expression was found to upregulate the expression of CPT1A, a key enzyme involved in FAO while downregulating the expression of critical lipogenic enzymes ACC1 and FASN. FOXK2 was shown to increase the phosphorylation levels of mTOR and interact with both mTOR and DRP1. Mechanistically, FOXK2 promotes lipid metabolic reprogramming in cervical cancer by interacting with the mTOR/DRP1 signaling axis. Furthermore, the role of FOXK2 in regulating lipid metabolism reprogramming in cervical cancer and its effects on the mTOR/DRP1 axis were validated in xenograft tumor models.</p><p><strong>Conclusion: </strong>FOXK2 interacts with and phosphorylates mTOR, which facilitates the expression of DRP1 and activates the mTOR/DRP1 signaling axis. This activation regulates lipid metabolic reprogramming and promotes the progression of cervical cancer.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1615454"},"PeriodicalIF":4.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12240978/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607955","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":"Light-induced epigenetic modifications in the hypothalamus during avian embryonic development enhance phenotypic plasticity.","authors":"Joanna Bartman, Tali Rosenberg, Hadar Parnas, Ronit Yosofov, Natalie Avital-Cohen, Ron Weiss, Gal Harmatz, Israel Rozenboim, Asaf Marco","doi":"10.3389/fcell.2025.1573705","DOIUrl":"10.3389/fcell.2025.1573705","url":null,"abstract":"<p><strong>Introduction: </strong>Early brain development is highly sensitive to environmental cues, which can exert lasting phenotypic effects. Targeted external interventions during this critical period can shape developmental trajectories and influence an animal's phenotype. Aligned with this concept, fetal responses to light-induced stimuli-varying in wavelength, frequency, and duration-are thought to facilitate adaptive reactions that enhance phenotypic plasticity and equip organisms to meet environmental challenges.</p><p><strong>Methods: </strong>In this study, broiler eggs were exposed to green monochromatic illumination (GMI) either continuously throughout incubation (Green) or during the final 3 days only (G3D) and compared to dark and white light controls.</p><p><strong>Results: </strong>Genome-wide analyses revealed significant transcriptional changes in the hypothalamus of the G3D group, identifying over 500 differentially expressed genes related to growth, metabolism, appetite, and immunity. Epigenetically, GMI exposure increased phosphorylated CREB1 (pCREB1) binding levels and chromatin accessibility at specific gene promoters, underscoring the role of light-induced developmental programming. Notably, these effects were exclusive to the G3D group, highlighting the last 3 days of incubation as a critical window for intervention. In G3D, cFOS immunostaining revealed heightened hypothalamic responsiveness to a post-hatch green light pulse, indicating that in-ovo GMI primed the brain's circuitry for future stimuli. Mechanistically, our findings suggest that GMI-induced hypothalamic adaptations are mediated, at least partially, through retinal green photoreceptors. Pre-exposure to blue light, which disrupts green photoreceptor activity, reduced retinal green opsin levels and nullified the epigenetic changes typically observed in the G3D group. Last, G3D chicks exhibited enhanced growth and improved food conversion ratios (FCR), particularly during early post-hatch development. Consistent with our transcriptomic and epigenetic data, the BG6D group showed no significant changes in body weight or FCR.</p><p><strong>Discussion: </strong>Collectively, these findings highlight how specific wavelengths and precise timing of light exposure during embryogenesis can shape post-hatch phenotypes through transcriptional and epigenetic mechanisms.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1573705"},"PeriodicalIF":4.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12241980/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607956","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 multifaceted roles of BAF60 subunits in muscle: regulation of differentiation, reprogramming, and metabolic homeostasis.","authors":"Yaoxia Liu, Zhen Fan, Yang Zhai, Haotian Huang, Ruifeng Shi, Tao Wang","doi":"10.3389/fcell.2025.1594423","DOIUrl":"10.3389/fcell.2025.1594423","url":null,"abstract":"<p><p>Muscle development and metabolic homeostasis are critical aspects of human health. As a key component of the SWI/SNF chromatin remodeling complex, the BAF60 subunit plays a widespread and crucial role in the differentiation, reprogramming, and metabolic regulation of skeletal, cardiac, and smooth muscle. Recent studies reveal that BAF60c promotes skeletal muscle differentiation and regeneration by interacting with MyoD, while also driving cardiac-specific gene expression and cooperating with transcription factors such as NKX2.5 and GATA Binding Protein 4 (GATA4) during heart development and remodeling. In smooth muscle, BAF60c interacts with serum response factor to maintain contractility and homeostasis by reducing inflammation and apoptosis. In contrast, BAF60a promotes inflammatory responses and extracellular matrix degradation, contributing to vascular diseases such as abdominal aortic aneurysm and atherosclerosis. Importantly, different BAF60 isoforms exhibit antagonistic, synergistic, or mutually exclusive effects in different muscle types, highlighting their complexity. This review provides a comprehensive overview of BAF60 isoforms' regulatory roles, with an emphasis on their potential as therapeutic targets for muscle-related metabolic and vascular diseases.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1594423"},"PeriodicalIF":4.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12240974/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607958","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":"Correction: 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.2025.1646699","DOIUrl":"https://doi.org/10.3389/fcell.2025.1646699","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fcell.2025.1598400.].</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1646699"},"PeriodicalIF":4.6,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12238949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599943","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 of ferroptosis in acute kidney injury.","authors":"Lin Zhang, Feng Luo, Nan Yuan, Jiaming Yin, Bing Shen, Yalin Chai, Lijie Sun, Xuan Wang, Le Yin, Congjuan Luo","doi":"10.3389/fcell.2025.1614156","DOIUrl":"10.3389/fcell.2025.1614156","url":null,"abstract":"<p><p>Acute kidney injury (AKI) is a life-threatening condition characterized by a rapid decline in kidney function caused by various underlying factors. Despite advancements in medical science, effective treatments for AKI remain limited, highlighting the necessity for novel therapeutic strategies. Ferroptosis, an iron-dependent regulated cell death characterized by lipid peroxidation, has been recently linked to AKI development. Studies indicate that ferroptosis plays a role in multiple AKI types, such as those caused by ischemia-reperfusion, sepsis, nephrotoxic agents, and rhabdomyolysis. In these conditions, ferroptosis markers are elevated in renal tubular epithelial cells, and inhibiting ferroptosis has been shown to reduce kidney injury. However, the precise regulatory mechanisms of ferroptosis in AKI remain unclear. This review summarizes current understanding of ferroptosis, including its definition, molecular regulation, involvement in various AKI types, and potential therapeutic targets. By elucidating these aspects, we hope to provide a foundation for future research and the development of effective interventions for AKI.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1614156"},"PeriodicalIF":4.6,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12237994/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599877","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":"LRO biogenesis and function: what can we learn from mast cells?","authors":"Juan Eduardo Montero-Hernández, Kerui Zhang, Ulrich Blank, Gaël Ménasché","doi":"10.3389/fcell.2025.1613677","DOIUrl":"10.3389/fcell.2025.1613677","url":null,"abstract":"<p><p>Lysosome-related organelles (LROs) are specialized compartments with cell type-specific roles. In mast cells (MCs), which are tissue-localized hematopoietic effector cells, LROs refer to secretory lysosomes also known as secretory granules (SGs) containing numerous pre-formed inflammatory mediators including proteases, proteoglycans, lysosomal enzymes, histamine and serotonin. Their release during MC activation is responsible for allergic, inflammatory manifestations, the fight against parasitic agents or the neutralization of toxins. Here, we provide an overview of knowledge describing the mechanisms underlying the biogenesis, secretion and biological functions of LROs in MCs. Decoding molecular mechanisms involved in LRO biogenesis and biology of MCs will benefit i) to other immune or non-immune cell types containing LROs and ii) can be exploited to design novel therapeutic approaches for the treatment of allergic and chronic inflammatory diseases caused by MC activation.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1613677"},"PeriodicalIF":4.6,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12237990/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599876","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}