International Journal of Biological Sciences最新文献

{"title":"The novel role of LOC344887 in the enhancement of hepatocellular carcinoma progression via modulation of SHP1-regulated STAT3/HMGA2 signaling axis.","authors":"Yang-Hsiang Lin, Hsiang-Cheng Chi, Meng-Han Wu, Chia-Jung Liao, Cheng-Yi Chen, Po-Shuan Huang, Wei-Chieh Huang, Yi-Wen Wang, Tzu-Kang Lin, Ming-Wei Lai, Chau-Ting Yeh, Kwang-Huei Lin","doi":"10.7150/ijbs.99683","DOIUrl":"10.7150/ijbs.99683","url":null,"abstract":"<p><p>Pseudogene-derived long non-coding RNAs (lncRNAs) have become crucial regulators in cancer progression. Extensive research highlights the pivotal role of signal transducer and activator of transcription 3 (STAT3) in promoting hepatocellular carcinoma (HCC) progression. As a result, targeting aberrant STAT3 activation presents a promising therapeutic strategy for HCC. Our study aims to identify the key pseudogene-derived lncRNA involved in modulating STAT3 activation and driving HCC progression. Our study is the first to identify a significant upregulation of LOC344887, a pseudogene-derived lncRNA, in HCC tissues. Elevated LOC344887 levels correlated with poor overall survival (OS) and recurrence-free survival (RFS), highlighting its potential as a biomarker for HCC. The rapid amplification of cDNA ends (RACE) and RT-PCR experiments revealed the expression of a novel LOC344887 transcript, named LOC344887-v2, alongside the annotated RefSeq transcript NR_151491 (LOC344887-v1) in both HCC tissues and hepatoma cell lines. Functional assays demonstrated that LOC344887 enhances cellular migration and invasion, with its variant LOC344887-v2 exhibiting a more pronounced effect. Further, LOC344887 mechanistically regulates STAT3 phosphorylation at tyrosine 705, which is crucial for maintaining STAT3 activation in HCC. Our findings unravel that LOC344887 not only physically interacts with p-STAT3 but also prevents its dephosphorylation by src homology region 2 domain-containing phosphatase 1 (SHP-1), thereby sustaining oncogenic signaling. In addition, we identified HMGA2 as a target of the LOC344887/SHP-1/STAT3 axis, with higher HMGA2 expression correlating with poorer prognosis in HCC patients. The ability of LOC344887 to regulate HMGA2 through direct binding of STAT3 to its promoter underlines its role in HCC progression. Collectively, these findings elucidate a novel oncogenic role of LOC344887 in HCC and suggest that targeting this lncRNA and its associated pathways may provide novel therapeutic strategies for improving patient outcomes in HCC.</p>","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"20 15","pages":"6281-6296"},"PeriodicalIF":8.2,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813105","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":"Erratum: Cyclovirobuxine inhibits the progression of clear cell renal cell carcinoma by suppressing the IGFBP3-AKT/STAT3/MAPK-Snail signalling pathway: Erratum.","authors":"Yadong Liu, Huiyan Lv, Xingyi Li, Jiannan Liu, Song Chen, Yaodong Chen, Yinshan Jin, Ruihua An, Shiliang Yu, Zhigang Wang","doi":"10.7150/ijbs.87837","DOIUrl":"https://doi.org/10.7150/ijbs.87837","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.7150/ijbs.62114.].</p>","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"20 15","pages":"6279-6280"},"PeriodicalIF":8.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812765","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":"Extracellular Vesicles from Human Induced Pluripotent Stem Cells Exhibit a Unique MicroRNA and CircRNA Signature.","authors":"Mario Barilani, Valeria Peli, Paolo Manzini, Clelia Pistoni, Francesco Rusconi, Eva Maria Pinatel, Francesca Pischiutta, Dorian Tace, Maria Chiara Iachini, Noemi Elia, Francesca Tribuzio, Federica Banfi, Alessandro Sessa, Alessandro Cherubini, Vincenza Dolo, Valentina Bollati, Luisa Fiandra, Elena Longhi, Elisa R Zanier, Lorenza Lazzari","doi":"10.7150/ijbs.100113","DOIUrl":"10.7150/ijbs.100113","url":null,"abstract":"<p><p>Extracellular vesicles (EV) have emerged as promising cell-free therapeutics in regenerative medicine. However, translating primary cell line-derived EV to clinical applications requires large-scale manufacturing and several challenges, such as replicative senescence, donor heterogeneity, and genetic instability. To address these limitations, we used a reprogramming approach to generate human induced pluripotent stem cells (hiPSC) from the young source of cord blood mesenchymal stem/stromal cells (CBMSC). Capitalizing on their inexhaustible supply potential, hiPSC offer an attractive EV reservoir. Our approach encompassed an exhaustive characterization of hiPSC-EV, aligning with the rigorous MISEV2023 guidelines. Analyses demonstrated physical features compatible with small EV (sEV) and established their identity and purity. Moreover, the sEV-shuttled non-coding (nc) RNA landscape, focusing on the microRNA and circular RNA cargo, completed the molecular signature. The kinetics of the hiPSC-sEV release and cell internalization assays unveiled robust EV production and consistent uptake by human neurons. Furthermore, hiPSC-sEV demonstrated <i>ex vivo</i> cell tissue-protective properties. Finally, via bioinformatics, the potential involvement of the ncRNA cargo in the hiPSC-sEV biological effects was explored. This study significantly advances the understanding of pluripotent stem cell-derived EV. We propose cord blood MSC-derived hiPSC as a promising source for potentially therapeutic sEV.</p>","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"20 15","pages":"6255-6278"},"PeriodicalIF":8.2,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812779","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 Quiet Giant: Identification, Effectors, Molecular Mechanism, Physiological and Pathological Function in mRNA 5-methylcytosine Modification.","authors":"Ruyue Wang, Lifeng Ding, Yudong Lin, Wenqin Luo, Zhehao Xu, Weilin Li, Yi Lu, Ziwei Zhu, Zeyi Lu, Fan Li, Xudong Mao, Liqun Xia, Gonghui Li","doi":"10.7150/ijbs.101337","DOIUrl":"10.7150/ijbs.101337","url":null,"abstract":"<p><p>5-Methylcytosine (m5C) is a prevalent nucleotide alteration observed in transfer RNA (tRNA) and ribosomal RNA (rRNA), and it is also widely distributed in the transcriptome, serving as one of the internal modifications of messenger RNA (mRNA) in higher eukaryotes. Increasing evidence has substantiated the presence of m5C in mRNA. As research on m5C progresses, there is an initial comprehension of its molecular mechanisms and biological significance in mRNA. This work aims to provide a comprehensive summary of the most recent advancements in the identification and screening, distribution, molecular functions, and biological effects of m5C in mRNA. We outline the current status of research and provide prospects for potential future applications.</p>","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"20 15","pages":"6241-6254"},"PeriodicalIF":8.2,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628344/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813108","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":"BRD7 enhances the radiosensitivity of nasopharyngeal carcinoma cells by negatively regulating USP5/METTL3 axis-mediated homologous recombination repair.","authors":"Mengna Li, Jianxia Wei, Changning Xue, Shipeng Chen, Xiangting Zhou, Lemei Zheng, Yumei Duan, Hongyu Deng, Songqing Fan, Wei Xiong, Faqing Tang, Ming Zhou","doi":"10.7150/ijbs.100833","DOIUrl":"10.7150/ijbs.100833","url":null,"abstract":"<p><p>An important reason for the poor prognosis of nasopharyngeal carcinoma (NPC) patients is radioresistance. Our previous studies demonstrated that BRD7 is expressed at low levels in NPC and functions as a tumor suppressor to inhibit NPC progression and metastasis. However, the role and mechanism of BRD7 in the development of radioresistance in NPC cells remain unclear. In this study, we first found that BRD7 was lowly expressed in radioresistant NPC tissues and cells compared to radiosensitive tissues and cells and that overexpression of BRD7 promoted the induction of DNA double-strand breaks and increased radiosensitivity in NPC cells. Mechanistically, BRD7 competitively inhibits the binding of the deubiquitinating enzyme USP5 to METTL3, thereby reducing the protein stability of METTL3 through the ubiquitin-proteasome pathway. Furthermore, METTL3 was confirmed to suppress the induction of DSBs and promote the development of NPC radioresistance by regulating BRCA1- and RAD51-mediated homologous recombination repair. Moreover, high BRD7 expression and low METTL3 expression are positively correlated with radiosensitivity and good prognosis in NPC patients. Taken together, our findings reveal that BRD7 promotes the radiosensitization of NPC cells by negatively regulating USP5/METTL3 axis activity and indicate that targeting the BRD7/METTL3 axis might be a novel therapeutic strategy for NPC radiosensitization.</p>","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"20 15","pages":"6130-6145"},"PeriodicalIF":8.2,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628346/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812794","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":"High-Throughput Screening of an FDA-Approved Compound Library Reveals a Novel GAS6 Receptor Agonist for Therapeutic Intervention in Septic Myocardial and microvascular Injury via Modulation of Danger-Associated Molecular Patterns.","authors":"Haowen Zhuang, Chun Li, Lingjun Wang, Bei Zhou, Zhijiang Guo, Yusheng Huang, Bo Deng, Yulin Ouyang, Junxiong Qiu, Xing Chang, Wei Wang, Junyan Wang","doi":"10.7150/ijbs.104427","DOIUrl":"10.7150/ijbs.104427","url":null,"abstract":"<p><p>PGAM5 and VDAC1 have both been reported to regulate mitophagy. However, the mechanisms by which they regulate sepsis-induced inflammatory microvascular injury remain unverified. In previous studies, we established the role of this regulatory axis in various phenotypic processes, including mitophagy, mitochondrial biogenesis, the mitochondrial unfolded protein response, and mitochondrial dynamics, while further confirming the interactive regulatory proteins within this axis. However, the validation and elucidation of these regulatory phenotypes have primarily focused on ischemic heart diseases such as ischemic myocardial injury and heart failure. Sepsis-related myocardial injury is currently recognized as a significant cardiac impairment, and although there are cardioprotective and nutritional agents available for supportive therapy, fundamental research validating the upstream targets and mechanisms of microvascular injury is still lacking. Based on our previous research, we further explored the role of mitophagy dysfunction mediated by VDAC1 and its upstream regulatory protein PGAM5 in sepsis-induced coronary microvascular injury. We also confirmed the material basis and metabolic pathway regulation targeting the PGAM5- VDAC1 interactive mechanism with relevant drugs. Our findings suggest that PGAM5-mediated mitophagy dysfunction may be a crucial factor leading to sepsis-induced microvascular injury, primarily interacting with VDAC1-mediated mitochondrial membrane dysfunction. Animal experiments revealed that cardiac-specific knockout of PGAM5 could reverse LPS-induced coronary microvascular injury and inflammatory damage, restoring cardiac ejection function and mitophagy functionality. <i>In vitro</i> studies also confirmed that the PGAM5-VDAC1 interaction can normalize mitophagy, restoring the normal morphology and structure of mitochondria while maintaining normal mitochondrial energy metabolism levels and respiratory chain function. Further pharmacological research indicated that the active ingredients of traditional Chinese medicine-Puerarin (TCM, a GAS6 Receptor Agonist) can target the PGAM5- VDAC1 axis to regulate mitophagy and inhibit LPS-induced necrotic apoptosis in cardiomyocytes, potentially reversing mitochondrial pathway-related cardiac injury. TCM may emerge as a prospective therapeutic agent targeting the PGAM5- VDAC1 axis.</p>","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"20 15","pages":"6222-6240"},"PeriodicalIF":8.2,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628332/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812986","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":"Smad4 Deficiency in S100A4⁺ Macrophages Enhances Colitis-associated Tumorigenesis by Promoting Macrophage Lipid Metabolism Augmented M2 Polarization.","authors":"Ting Liu, Xinyuan Zhang, Xuanxuan Yan, Leirong Cheng, Xinlong Yan, Fanxin Zeng, Xue Li, Zhinan Chen, Jianchun Gu, Jinhua Zhang","doi":"10.7150/ijbs.98529","DOIUrl":"10.7150/ijbs.98529","url":null,"abstract":"<p><p>S100A4 is primarily expressed in intestinal macrophages, and promotes colonic inflammation and colitis-associated colon tumorigenesis. Smad4 is also expressed in the colon; however, it inhibits colitis-associated cancer (CAC) development. The specific role of Smad4 in S100A4⁺ cells in CAC remains unknown. In this study, an azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced CAC model was established in mice with S100A4⁺ cell-specific Smad4 deletion (S100A4 ^Smad4-/-). Smad4 deficiency in S100A4⁺ cells exacerbated DSS-induced colitis and promoted colorectal tumorigenesis. In addition, S100A4⁺ cell-specific Smad4 ablation promoted the M2 polarization of macrophages in CAC. Mechanistically, Smad4 depletion in macrophages enhanced lipid metabolism by activating the FA binding protein 2 (Fabp2)/STAT6 pathway. Furthermore, Smad4 deficiency in macrophages promoted MC38 tumor growth in myeloid-specific Smad4 deficient (Lyz ^Smad4-/-) mice, whereas blocking Fabp2 expression reversed the tumor growth. Additionally, high Smad4 expression was associated with prolonged survival in patients with colorectal cancer. Thus, Smad4 in S100A4⁺ macrophages plays a tumor-inhibiting role in CAC development and supports its use as a prognostic marker in CRC patients.</p>","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"20 15","pages":"6114-6129"},"PeriodicalIF":8.2,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628331/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813097","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 Crosstalk between Autophagy and Nrf2 Signaling in Cancer: from Biology to Clinical Applications.","authors":"Chan Shan, Yuan Wang, Yin Wang","doi":"10.7150/ijbs.103187","DOIUrl":"10.7150/ijbs.103187","url":null,"abstract":"<p><p>Autophagy is a catabolic process that has been conserved throughout evolution, serving to degrade and recycle cellular components and damaged organelles. Autophagy is activated under various stress conditions, such as nutrient deprivation, viral infections, and genotoxic stress, and operates in conjunction with other stress response pathways to mitigate oxidative damage and maintain cellular homeostasis. One such pathway is the Nrf2-Keap1-ARE signaling axis, which functions as an intrinsic antioxidant defense mechanism and has been implicated in cancer chemoprevention, tumor progression, and drug resistance. Recent research has identified a link between impaired autophagy, mediated by the autophagy receptor protein p62, and the activation of the Nrf2 pathway. Specifically, p62 facilitates Keap1 degradation through selective autophagy, leading to the translocation of Nrf2 into the nucleus, where it transcriptionally activates downstream antioxidant enzyme expression, thus safeguarding cells from oxidative stress. Furthermore, Nrf2 regulates p62 transcription, so a positive feedback loop involving p62, Keap1, and Nrf2 is established, which amplifies the protective effects on cells. This paper aims to provide a comprehensive review of the roles of Nrf2 and autophagy in cancer progression, the regulatory interactions between the Nrf2 pathway and autophagy, and the potential applications of the Nrf2-autophagy signaling axis in cancer therapy.</p>","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"20 15","pages":"6181-6206"},"PeriodicalIF":8.2,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628323/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNA-495 Modulates Neuronal Layer Fate Determination by Targeting <i>Tcf4</i>.","authors":"Yunli Pang, Xiangbin Ruan, Wei Liu, Lin Hou, Bin Yin, Pengcheng Shu, Xiaozhong Peng","doi":"10.7150/ijbs.94739","DOIUrl":"10.7150/ijbs.94739","url":null,"abstract":"<p><p>During cortical development, the differentiation potential of neural progenitor cells (NPCs) is one of the most critical steps in normal cortical formation and function. Defects in this process can lead to many brain disorders. MicroRNA dysregulation in the dorsolateral prefrontal cortex is associated with risk for a variety of developmental and psychiatric conditions. However, the molecular mechanisms underlying this process remain largely unknown. In this study, we found that microRNA-495-3p (miR-495) is expressed in NPCs of the developing mouse cerebral cortex. Furthermore, aberrant expression of miR-495 promotes the formation of superficial neurons. Our results suggest that miR-495 can target transcription factor 4 (TCF4), a gene linked to the neurodevelopmental disorder Pitt-Hopkins syndrome (PTHS), to ensure normal differentiation of NPCs in the developing cerebral cortex. Furthermore, TCF4 loss-of-function and gain-of-function experiments show opposite effects on miR-495 regulation of neural progenitor differentiation potential. Together, these results demonstrated that miR-495 regulates cortical development through TCF4 for the first time.</p>","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"20 15","pages":"6207-6221"},"PeriodicalIF":8.2,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628341/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813017","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":"Multi-Omics Approaches to Discover Biomarkers of Thyroid Eye Disease: A Systematic Review.","authors":"Haiyang Zhang, Yuyu Zhou, Baiguang Yu, Yuyang Deng, Yang Wang, Sijie Fang, Xuefei Song, Xianqun Fan, Huifang Zhou","doi":"10.7150/ijbs.103977","DOIUrl":"10.7150/ijbs.103977","url":null,"abstract":"<p><p>Thyroid eye disease (TED) is an organ-specific autoimmune disorder that significantly impacts patients' visual function, appearance, and well-being. Despite existing clinical evaluation methods, there remains a need for objective biomarkers to facilitate clinical management and pathogenesis investigation. Rapid advances in multi-omics technologies have enabled the discovery and development of more informative biomarkers for clinical use. This systematic review synthesizes the current landscape of multi-omics approaches in TED research, highlighting the potential of genomics, transcriptomics, proteomics, metabolomics, and microbiomics to uncover novel biomarkers. Our review encompasses 69 studies involving 1,363 TED patients and 1,504 controls, revealing a wealth of biomarker candidates across various biological matrices. The identified biomarkers reflect alterations in gene expression, protein profiles, metabolic pathways, and microbial compositions, underscoring the systemic nature of TED. Notably, the integration of multi-omics data has been pivotal in enhancing our understanding of TED's molecular mechanisms and identifying diagnostic and prognostic markers with clinical potential.</p>","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"20 15","pages":"6038-6055"},"PeriodicalIF":8.2,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813023","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}