The FASEB Journal最新文献

{"title":"Microglial repopulation alleviates surgery-induced neuroinflammation and cognitive impairment in a ZEB1-dependent manner","authors":"Xinyue Zhang,&nbsp;Xiaotong Cui,&nbsp;Naihui Sun,&nbsp;Xinyi Wu,&nbsp;Xue Pan,&nbsp;Renyi Wang,&nbsp;Zitong Chen,&nbsp;Yilong Li,&nbsp;Yue Hu,&nbsp;Fang Liu,&nbsp;Xuezhao Cao","doi":"10.1096/fj.202402492R","DOIUrl":"https://doi.org/10.1096/fj.202402492R","url":null,"abstract":"<p>Microglia play a crucial role in postoperative cognitive dysfunction (POCD). This study investigated the effects of microglial depletion and subsequent repopulation on POCD and its underlying mechanisms. An aged mouse model of POCD was induced by partial hepatectomy, and the colony-stimulating factor 1 receptor (CSF1R) inhibitor PLX5622 was administered to facilitate microglial depletion and repopulation. Neutrophil involvement was assessed with anti-Ly6G antibodies, while ZEB1 was manipulated through shRNA knockdown and lentiviral overexpression in the BV2 microglial cell line. A TGF-β1 neutralizing antibody was employed to elucidate the relationship between ZEB1 and its downstream pathways. The results indicated that microglial depletion alone did not reverse cognitive impairments. However, microglial repopulation significantly reduced neutrophil infiltration and improved cognitive function post-surgery. This improvement correlated with ZEB1 upregulation in microglia, which decreased CXCL1 production by astrocytes via TGF-β1 signaling, thereby reducing neutrophil migration to the hippocampus. These findings suggest that microglial repopulation, dependent on ZEB1 and TGF-β1 signaling, effectively alleviates neuroinflammation, reduces neutrophil infiltration, and enhances cognitive function, highlighting microglia as a promising target for the prevention and treatment of POCD.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 5","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143564645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SPP1 macrophages across diseases: A call for reclassification?","authors":"Alessio Reggio,&nbsp;Claudia Fuoco,&nbsp;Rebecca Deodati,&nbsp;Alessandro Palma","doi":"10.1096/fj.202403227R","DOIUrl":"https://doi.org/10.1096/fj.202403227R","url":null,"abstract":"<p>SPP1+ macrophages, characterized by elevated expression of the osteopontin gene (secreted phosphoprotein 1, SPP1), have emerged as key players in various pathological contexts, including aging, chronic inflammatory diseases, and cancer. While frequently classified as a subclass of tumor-associated macrophages in oncological settings, their presence in noncancer conditions, such as aging-related disorders and muscular diseases, suggests a broader role beyond tumors. These macrophages share conserved traits, including fibrosis promotion, extracellular matrix remodeling, and immune modulation, often linked to poor clinical outcomes. This perspective explores the multifaceted roles of SPP1+ macrophages across diseases and advocates for their reclassification as a distinct macrophage subtype associated with chronic or prolonged inflammation. Recognizing their cross-disease relevance could reshape macrophage biology and inform targeted therapeutic strategies.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 5","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1096/fj.202403227R","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143554837","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":"A satellite cell-dependent epigenetic fingerprint in skeletal muscle identity genes after lifelong physical activity","authors":"Kevin A. Murach,&nbsp;Davis A. Englund,&nbsp;Toby L. Chambers,&nbsp;Cory M. Dungan,&nbsp;Hunter L. Porter,&nbsp;Jonathan D. Wren,&nbsp;Willard M. Freeman,&nbsp;Esther E. Dupont-Versteegden,&nbsp;Yuan Wen","doi":"10.1096/fj.202500177R","DOIUrl":"https://doi.org/10.1096/fj.202500177R","url":null,"abstract":"<p>Satellite cells comprise a small proportion of mononuclear cells in adult skeletal muscle. Despite their relative rarity, satellite cells have critical functions in muscle adaptation, particularly during prolonged exercise training. The mechanisms by which satellite cells mediate skeletal muscle responsiveness to physical activity throughout the lifespan are still being defined, but epigenetic regulation may play a role. To explore this possibility, we analyzed global DNA methylation patterns in muscle tissue from female mice that engaged in lifelong voluntary unweighted wheel running with or without satellite cells. Satellite cells were ablated in adulthood using the tamoxifen-inducible Pax7-DTA model. Compared to sedentary mice, wheel running for 13 months caused muscle DNA methylation differences in the promoter regions of numerous muscle fiber-enriched genes—<i>Cacgn1</i>, <i>Dnm2</i>, <i>Mlip</i>, <i>Myl1</i>, <i>Myom2</i>, <i>Mstn</i>, <i>Sgca</i>, <i>Sgcg</i>, <i>Tnnc1</i>, <i>Tnni2</i>, <i>Tpm1</i>, and <i>Ttn</i>—only when satellite cells were present. These genes relate to muscle fiber identity, cytoarchitecture, and size as well as overall muscle function. Epigenetic alterations to such genes are consistent with previously observed histological and in vivo impairments to running adaptation after satellite cell depletion in these same mice. <i>Musk</i> promoter region methylation was affected only in the absence of satellite cells with lifelong running relative to sedentary; this dovetails with work showing that satellite cells influence skeletal muscle innervation. Defining the epigenetic effects of satellite cells on identity genes in muscle fibers after lifelong physical activity provides new directions for how these rare stem cells can promote muscle adaptation and function throughout the lifespan.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 5","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1096/fj.202500177R","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143554836","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":"A promising fusion: Traditional Chinese medicine and probiotics in the quest to overcome osteoporosis","authors":"Kangcheng Fan,&nbsp;Xin Hua,&nbsp;Shuwan Wang,&nbsp;Thomas Efferth,&nbsp;Shengnan Tan,&nbsp;Zhuo Wang","doi":"10.1096/fj.202403209R","DOIUrl":"https://doi.org/10.1096/fj.202403209R","url":null,"abstract":"<p>Botanical drugs and probiotic supplements present safer alternative options for the prevention and treatment of osteoporosis (OP). However, pathological disorders of the gut microbiota and the specific properties of probiotics and traditional Chinese medicine (TCM) significantly limit their therapeutic efficacy. Given the favorable synergistic and complementary effects between probiotics and herbal medicines, a creative combination of these approaches may address the issue of their current limited efficacy. A comprehensive analysis is necessary to provide a detailed review of their potential for combination, the mechanisms behind their synergy, scientific applications, and future developments. There exists a complex relationship between gut microbiota and OP, and the underlying regulatory mechanisms are multidimensional, involving the production of pro-inflammatory metabolites, immune system disruption, and the impairment of the intestinal mucosal barrier. Furthermore, we analyzed the complex mechanisms and potential connections between probiotics, TCM, and their combined applications. We highlighted the principle of complementary gain and the substantial therapeutic potential of their organic combination, which facilitates the release of active substances in TCM, increases the bioavailability of TCM, enhances probiotic delivery efficiency, and exerts synergistic effects. The combined use of probiotics and TCM offers a safe and effective strategy for managing OP and presents an innovative and promising direction for the future development of modern phytomedicine.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 5","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1096/fj.202403209R","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143554838","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":"Refining the impact of early intermittent hyperlipidemia on atherosclerosis: Unveiling the role of neutrophil reprogramming, sex differences, gut microbiota, and maternal hypercholesterolemia","authors":"Hector A. Cabrera-Fuentes,&nbsp;William A. Boisvert","doi":"10.1096/fj.202403281R","DOIUrl":"https://doi.org/10.1096/fj.202403281R","url":null,"abstract":"<p>Atherosclerotic cardiovascular diseases (ASCVDs) remain a leading cause of mortality, with early cholesterol control being pivotal in mitigating long-term risk. Recent findings suggest that intermittent hyperlipidemia, characterized by oscillatory cholesterol exposure, uniquely accelerates atherosclerosis compared to continuous high-fat diets. This review synthesizes emerging evidence on early intermittent hyperlipidemia's impact on atherogenesis, emphasizing macrophage dysfunction, autophagy impairment, and efferocytosis deficits. We also discuss critical gaps, including sex-specific differences, gut-microbiota interactions, and the influence of maternal hypercholesterolemia. Notably, recent insights into IL-1β-dependent neutrophil reprogramming under oscillatory diets reveal novel inflammatory mechanisms driving plaque destabilization. Addressing these gaps will advance our understanding of early atherogenesis and guide the development of innovative prevention strategies and therapeutic interventions.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 5","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143554854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Compression force regulates cementoblast mineralization via S1PR1/mitophagy axis","authors":"Han Wang,&nbsp;Jingwen Cai,&nbsp;Linxin Chen,&nbsp;Sihang Chen,&nbsp;Xinhan Yang,&nbsp;Zhonghan Chen,&nbsp;Linyu Xu","doi":"10.1096/fj.202403234RR","DOIUrl":"https://doi.org/10.1096/fj.202403234RR","url":null,"abstract":"<p>Orthodontically induced inflammatory root resorption (OIIRR) poses a significant clinical challenge, as excessive orthodontic force shortens tooth longevity by impairing cementoblast-mediated cementum mineralization and promoting root resorption. Cementoblasts, essential for mineralized cementum formation and resistance to resorption, exhibit altered mechanosensitivity and mechanotransduction under orthodontic force, yet the role of mitophagy in this process remains poorly understood. In this study, we investigated how the S1PR1/mitophagy axis modulates cementoblast mineralization and OIIRR progression. The in vivo orthodontic loading model revealed that heavy compression force triggered OIIRR and impaired cementoblast mineralization along with suppression of mitophagy in cementoblasts by downregulating PINK1 and PARKIN expression. The in vitro experiments further confirmed that heavy compression force increased reactive oxygen species (ROS) levels, disrupted mitochondrial membrane potential (MMP), and inhibited mitophagy in OCCM30 cells, thereby impairing their mineralization capacity. Mechanistically, S1PR1 upregulation activated mitophagy, which in turn restored cementoblast mineralization under heavy compression force. Moreover, pharmacological activation of S1PR1 with SEW2871 alleviated OIIRR in vivo. These findings highlight the pivotal role of the S1PR1/mitophagy axis in maintaining cementoblast function and mineralization under orthodontic force, offering novel insights into the molecular mechanisms underlying OIIRR and suggesting potential therapeutic strategies to prevent OIIRR during orthodontic treatment.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 5","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143535769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NAT10 regulates zygotic genome activation and the morula-to-blastocyst transition","authors":"Zhi Cui,&nbsp;Cong Fu,&nbsp;Di Ai,&nbsp;Haibo Zhu,&nbsp;Fang Wang,&nbsp;Xinglan An,&nbsp;Ziyi Li,&nbsp;Sheng Zhang","doi":"10.1096/fj.202402751R","DOIUrl":"https://doi.org/10.1096/fj.202402751R","url":null,"abstract":"<p>As the first acetylated nucleoside to be discovered, N-acetyltransferase 10 (NAT10)-catalyzed RNA N4-acetylcytidine (ac⁴C) modification is involved in the occurrence of various diseases. However, the roles of RNA ac⁴C in preimplantation embryo development still need more detailed studies. Here, we analyzed the role of RNA ac⁴C in preimplanted embryonic development in mice through <i>Nat10</i> siRNA microinjection and growing oocyte stage-specific <i>Nat10</i> knockout (Zp3-<i>Nat10</i>^lox/lox). We found that NAT10 was indispensable for both the morula-to-blastocyst transition and zygotic genome activation (ZGA). <i>Nat10</i> knockdown by <i>Nat10</i> siRNA microinjection caused most embryos to arrest at the morula stage, and the expression levels of NANOG and CDX2 were significantly decreased. Moreover, the mRNA stability of <i>Nanog</i> was also significantly decreased in morulae after <i>Nat10</i> knockdown. Zp3-<i>Nat10</i>^lox/lox female mice were completely sterile, and the embryos from Zp3-<i>Nat10</i>^lox/lox females were arrested at the 2-cell stage. Both the degradation of maternal mRNA and ZGA were deficient in 2-cell embryos from Zp3-<i>Nat10</i>^lox/lox females. In conclusion, our findings demonstrate that NAT10 is crucial for both ZGA and the morula-to-blastocyst transition processes during mouse preimplantation embryonic development.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 5","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143535770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex-specific characterization of aortic function and inflammation in a new diet-induced mouse model of metabolic syndrome","authors":"Vivian Tran,&nbsp;Holly Brettle,&nbsp;Henry Diep,&nbsp;Hericka Bruna Figueiredo Galvao,&nbsp;Kerry V. Fanson,&nbsp;Christopher G. Sobey,&nbsp;Grant R. Drummond,&nbsp;Antony Vinh,&nbsp;Maria Jelinic","doi":"10.1096/fj.202401871R","DOIUrl":"https://doi.org/10.1096/fj.202401871R","url":null,"abstract":"<p>Perivascular adipose tissue (PVAT) expansion promotes inflammation and vascular dysfunction in metabolic syndrome (MetS), but the sexual dimorphisms of PVAT are poorly understood. Using a new mouse model of diet-induced MetS, we characterized the aorta and determined the influence of PVAT on vascular function in males and females. Six-week-old C57BL/6 mice were fed either a high-fat diet (43% kcal in food) with high sugar and salt in their drinking water (10% high fructose corn syrup and 0.9% NaCl; HFSS), or a normal chow diet (NCD) for 10 weeks. The aorta was characterized at endpoint using pin myography, flow cytometry, bulk RNA-sequencing, GSEA analysis, and histology. Compared to NCD-fed mice, HFSS-fed mice displayed higher weight gain, fasting blood glucose, systolic blood pressure, aortic fibrosis, and perivascular adipocyte cross-sectional area, regardless of sex (<i>p</i> &lt; .05). Circulating adiponectin levels were also higher in HFSS-fed males compared to NCD males. PVAT enhanced U46619-mediated contraction in HFSS males only. HFSS increased the expression of immune regulation genes in female PVAT and ion transport genes in male PVAT but had no effect on total numbers of immune cells in the aorta in either sex. Despite having similar effects on metabolic parameters in males and females, HFSS caused contrasting effects on vascular function with and without PVAT. These data highlight the sexual dimorphisms of PVAT in regulating the vasculature in healthy and diseased states.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 5","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1096/fj.202401871R","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143535810","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":"Angiogenic factor AGGF1 is a general splicing factor regulating angiogenesis and vascular development by alternative splicing of SRSF6","authors":"Wenchao Lv,&nbsp;Jingwen Zhang,&nbsp;Dayin Lyu,&nbsp;Rui Zhang,&nbsp;Chengqi Xu,&nbsp;Kang Ning,&nbsp;Mian Li,&nbsp;Yan Zhao,&nbsp;Jinxiang Han,&nbsp;Qing K. Wang","doi":"10.1096/fj.202403156R","DOIUrl":"https://doi.org/10.1096/fj.202403156R","url":null,"abstract":"<p>AGGF1 encodes an angiogenic factor that causes vascular disease Klippel–Trenaunay syndrome when mutated. AGGF1 also acts at the top of the genetic regulatory hierarchy for mesodermal differentiation of hemangioblasts, multipotent stem cells for differentiation of blood cells and vascular cells. Alternative splicing (AS) is a post-transcriptional process that generates multiple mature mRNAs from a single primary transcript (pre-mRNA), producing protein diversity. Deregulation of AS leads to many human diseases. The physiological role and mechanism of AGGF1 in AS are not clear. Full-length transcriptome sequencing of human pulmonary artery endothelial cells (HPAECs) with AGGF1 silencing revealed 63 121 genes, including 1144 new unannotated genes, and showed that AGGF1 is a general splicing factor regulating AS of 436 genes, including <i>SRSF6</i> regulating AS of many target genes. AGGF1 promoted the skipping of exon 3 that produces the full-length SRSF6 protein, an evolutionarily conserved AS event. Overexpression of full-length SRSF6 reversed the reduced cell proliferation, migration, and capillary tube formation of HPAECs with AGGF1 silencing. Knockdown of SRSF6 and overexpression of the shorter, alternatively spliced isoform of SRSF6 both inhibited HPAEC proliferation, migration, and capillary tube formation, whereas opposite results were obtained for overexpression of full-length SRSF6. Knockdown of <i>srsf6</i> impaired development of ISVs in zebrafish, whereas overexpression of <i>srsf6</i> enhanced vascular development and partially rescued impaired ISV development in zebrafish embryos with <i>aggf1</i> knockdown. Overall, our findings reveal that AGGF1 is a general splicing factor, and that AGGF1-mediated exon 3 skipping of <i>SRSF6</i> pre-mRNA is important for endothelial cell functions, angiogenesis, and vascular development.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 5","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143535913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Normal embryo development needs MEIG1-mediated sperm formation","authors":"Yi Sheng,&nbsp;Yi Tian Yap,&nbsp;Wei Li,&nbsp;Opeyemi Dhikhirullahi,&nbsp;Changmin Niu,&nbsp;Mashiat Rabbani,&nbsp;Stephen A. Krawetz,&nbsp;Saher Sue Hammoud,&nbsp;Kyle E. Orwig,&nbsp;Zhibing Zhang","doi":"10.1096/fj.202500109R","DOIUrl":"https://doi.org/10.1096/fj.202500109R","url":null,"abstract":"<p>Normal embryo development is a complex process that requires normal sperm to fertilize normal oocytes. Abnormal embryogenesis can be caused by either abnormal oocytes or abnormal sperm. However, the impact of sperm-associated factors is often underappreciated. Association between defects in sperm chromatin and poor embryo development has been consistently reported. In sperm cells, most histones are replaced by protamines to remodel sperm cell chromatin. However, the mechanism of nuclear protein replacement is largely unknown. Meiosis expressed gene 1 (MEIG1) plays a unique role in male fertility. The protein is recruited to the manchette at a late stage of spermatogenesis. The manchette is a unique structure only present in male germ cells, and one of the proposed functions is replacing histones with protamines. In this study, ICSI was conducted using sperm heads from the Meig1 KO mice. Significantly reduced fertilization was observed, and few embryos developed to blastocysts, which were associated with severe sperm DNA damage. Thus, we discovered an unexpected role for MEIG1 extending beyond spermatogenesis to include a role in embryogenesis, likely through remodeling sperm chromatin.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 5","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143535767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}