Molecular and Cellular Biochemistry最新文献

{"title":"Identification of pathogenic variants in the ABCG2 gene in patients with severe familial hyperuricemia and gout.","authors":"Yu Toyoda, Katerina Pavelcova, Jana Masinova, Lenka Hasikova, Jakub Zavada, Petra Hanova, Martin Klein, Jiri Vavra, Tappei Takada, Blanka Stiburkova","doi":"10.1007/s11010-025-05252-9","DOIUrl":"https://doi.org/10.1007/s11010-025-05252-9","url":null,"abstract":"<p><p>We report the identification of two pathogenic variants in the ABCG2 gene, encoding a urate exporter, in two probands (male and female) with severe familial gouty phenotypes and hyperuricemia. Clinico-genetic analyses identified p.I63YfsTer54 (rs565722112) and p.G74D (rs199976573) as potentially causal mutations; functional analyses demonstrated that these two variants are deficient in plasma membrane localization and functionally null. Our data show that dysfunctional variants in the ABCG2 gene are strong risk factors for hyperuricemia and gout in both males and females.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625426","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":"Single-cell RNA sequencing generates an atlas of normal tibia cartilage under mechanical loading conditions.","authors":"Junjie Wang, Zewen Sun, Chenghao Yu, Haibo Zhao, Mingyue Yan, Shenjie Sun, Xu Han, Tianrui Wang, Yingze Zhang, Jianjun Li, Tengbo Yu","doi":"10.1007/s11010-025-05234-x","DOIUrl":"https://doi.org/10.1007/s11010-025-05234-x","url":null,"abstract":"<p><p>Chondrocytes in articular cartilage can secrete extracellular matrix to maintain cartilage homeostasis. It is well known that articular cartilage chondrocytes are sensitive to mechanical loading and that mechanical stimuli can be translated to biological processes. This study provides deep insight into the impact of mechanical loading on chondrocytes via single-cell RNA sequencing (scRNA-seq). Five cartilage tissue samples from the high-loading region of medial cartilage from the upper tibia (the TL group) and six cartilage tissue samples from the low-loading region of lateral cartilage from the upper tibia (the TN group) were obtained from six donors and subjected to scRNA-seq. TL and TN cartilage tissues from another donor were subjected to immunohistochemical staining. In total, 132,685 cells were analyzed and assigned to 11 cell types. The functions, developmental relationships and interactions of these cell types were determined, and gene transcription data were also evaluated. In addition, differentially expressed genes between the TL and TN groups and their functions were identified. The hub genes for the TL group were identified as GAPDH, FN1, VEGFA, LDHA, SOD1, CTGF, DCN, SERPINE1, ENO1 and CAV1, whereas the hub genes for the TN group included ACTB, CD44, MMP2, COL1A1, COL1A2, SPP1, CTGF, MYC, CCL2, and IGF1. The different enrichment terms indicated that physiological mechanical loading may induce reactive oxygen species accumulation and thus cause ferroptosis in chondrocytes.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616009","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":"Human-induced pluripotent stem cell-derived exosomes promote skin wound healing through activating FGF2-mediated p38 pathway.","authors":"Rongrong Zhang, Huilan Wu, Yongmiao Peng, Ke Sheng, Feifei Chen, Guanghui Zhu, Xiaoling Guo","doi":"10.1007/s11010-025-05244-9","DOIUrl":"https://doi.org/10.1007/s11010-025-05244-9","url":null,"abstract":"<p><p>The acute and large area skin healing has been an intractable problem for both clinician and patient. Exosomes derived from human-induced pluripotent stem cells (hiPSC-Exos) have been a novel promising cell-free treatment on skin damage repair. In this study, in vivo skin trauma model of full-layer skin damage on mouse back and in vitro skin-like trauma model of human keratinocytes (HaCaT) scratches were established to investigate the effects of hiPSC-Exos on the acute wound healing, and its potential regulation mechanism would be tried to explore. Our in vivo results showed that hiPSC-Exos labeled with PKH26 could be well taken up by cells in the wound area, and could effectively accelerate acute skin wound healing by inhibiting the mRNA expressions of inflammation factors and chemokines such as Il-1β, Ccl2, Cxcl5, Ccl7 as well as promoting PCNA positive cell ratio. The in vitro data showed that hiPCS-Exos could markedly increase the numbers of EdU positive keratinocytes and expedite keratinocyte migration, which could be reversed by fibroblast growth factor receptor 3 (FGFR3) antagonist AZD4547 and p38 inhibitor SB203580. In addition, fibroblast growth factor 2 (FGF-2) was existent in hiPSC-Exos, and hiPSC-Exos could upregulate the p-p38/p38 level, which could be significantly reversed by AZD4547, but not affect the p-ERK/ERK and p-JNK/JNK levels in wound model tissues and cells. In conclusion, hiPSC-Exos may have the potential to promote wound healing by inhibiting cell inflammation as well as promoting cell proliferation and migration based on inherent FGF-2 targeting to FGFR3 to activate p38 pathway, which may serve as a promising candidate for skin healing.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143597399","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":"SKA3 promotes lung adenocarcinoma progression via the EGFR/E2F1/SKA3/integrin β1 signaling loop.","authors":"Xiufen Zheng, Zedong Sun, Shi Wang, Qibing Liu, Biqing Zhu, Zhijian Ren, Dingwei Fan, Chunping Zhang, Xinyin Fu, Yan Jin, Jing Luo, Jie Wang, Binhui Ren","doi":"10.1007/s11010-025-05242-x","DOIUrl":"10.1007/s11010-025-05242-x","url":null,"abstract":"<p><p>Spindle and kinetochore-associated complex subunit 3 (SKA3) contributes to tumor growth and metastasis, but its specific roles have not been clearly elucidated. In this study, we found that SKA3 contributed to lung adenocarcinoma (LUAD) progression by interacting with integrin β1. The expression characteristics of SKA3 in LUAD patients were analyzed by The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets and validated in 33 paired LUAD tissues by immunohistochemistry. Our data confirmed that SKA3 was a crucial regulator of LUAD progression and was associated with worse patient survival. In vitro and in vivo studies showed that SKA3 increased cell migration and invasion. Mechanistically, it was demonstrated that SKA3 could bind to integrin β1 and promote its activation, which further promoted the activation of EGFR. As a positive feedback loop, the activation of EGFR in turn promoted the expression of SKA3 via E2F1-mediated transcriptional regulation. Inhibition of EGFR with AZD9291 blocked SKA3 signaling induced by E2F1. These results indicated that SKA3 was crucial for the activation of EGFR and its downstream signaling pathway. Our findings uncovered the oncogenic role of SKA3 in LUAD progression and elucidated a novel EGFR/E2F1/SKA3/integrin β1 signaling loop, providing a potential SKA3-directed therapeutic strategy for LUAD patients.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143582325","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":"Exploring the potential link between human papillomavirus infection and coronary artery disease: a review of shared pathways and mechanisms.","authors":"Dwaipayan Saha, Preyangsee Dutta, Kimberly R Rebello, Abhishek Shankar, Abhijit Chakraborty","doi":"10.1007/s11010-025-05236-9","DOIUrl":"https://doi.org/10.1007/s11010-025-05236-9","url":null,"abstract":"<p><p>The increasing prevalence of early onset coronary artery disease (CAD) in individuals under 50 presents a significant public health challenge, with substantial impacts on quality of life and escalating healthcare costs. Human papillomavirus (HPV), a pervasive sexually transmitted infection, has emerged as a potential contributor to atherosclerotic lesion development. This article explores the complex inflammatory pathways HPV infection activates that could contribute to atherogenesis. HPV may contribute to CAD by influencing components of metabolic syndrome. Investigating these interactions could provide new insights into disease mechanisms. The virus's capacity to cause cellular immortalization, leading to uncontrolled growth and proliferation, may also play a role in the advancement of atherosclerotic lesions in CAD patients. HPV may represent a novel risk factor for CAD, warranting further research into preventive strategies, including vaccination. This understanding opens new opportunities for effective research and intervention to address this significant public health issue. The significant association between HPV and CAD emphasizes the need for further investigation to develop preventive measures and treatment strategies, especially important for reducing the increasing incidence of CAD in younger populations.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567614","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":"Macrophage polarization-related gene SOAT1 is involved in inflammatory response and functional recovery after spinal cord injury.","authors":"Peng Peng, Huitao Wang, Zhen Pang, Hui Zhang, Sihan Hu, Xingyi Ma, Fangjing Yang, Yanqun Qiu, Fei Wang, Wendong Xu","doi":"10.1007/s11010-025-05246-7","DOIUrl":"https://doi.org/10.1007/s11010-025-05246-7","url":null,"abstract":"<p><p>Macrophages polarization play crucial roles in regulating inflammation and functional recovery after spinal cord injury (SCI). This study aimed to investigate the key macrophage polarization-related genes (MPRGs) for the treatment of SCI. Our research involved identifying differentially expressed genes (DEGs), using immune infiltration analysis, weighted gene co-expression network analysis (WGCNA) and machine learning to screening out key MPRGs in the GSE5296. The discriminative potential of MPRGs were validated using expression analysis and receiver operating characteristic (ROC) curves in the GSE45376, while the distribution of hub MPRGs in different cell subtypes were visualized in the single-cell dataset GSE189070. The relationship between the MPRGs and immune infiltration was investigated through correlation analysis. Finally, we detected the effect of blocking sterol O-acyltransferase 1 (SOAT1) on macrophage polarization and functional recovery of SCI. A total of 52 MPRGs were identified. Elevated immune infiltration levels and activation of macrophage-associated biological pathways were noted after SCI. Machine learning determined SOAT1, LGALS3, HAVCR2, IRF8 and PTPRC as the hub MPRGs. External validation confirmed their expression, robust predictive value and distribution patterns. Immune infiltration analysis highlighted the strong correlation between SOAT1 and macrophages. Further, inhibiting of SOAT1 could enhance M2 macrophage polarization, improve inflammatory environment and promote functional recovery of SCI. Our study enhances the understanding of macrophage polarization-related genes in the inflammatory responses of SCI. Targeting SOAT1 emerges as a promising therapeutic strategy for SCI repair.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573138","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":"MiR-3202-DTL signaling axis impedes NSCLC malignancy via regulating the ubiquitination-proteasome degradation of p21.","authors":"Hongjuan Guo, Qianbin Tang, Yujie Zhao, Jianghao Cheng, JunJie Wang, Dan Liu, Ruyu Yan, Dongjin Lv, Bingxiao Lu, Mingsong Wu, Hongtao Yu, Hao Leng, Bo Liu, Minxia Liu, Kecheng Zhou","doi":"10.1007/s11010-025-05239-6","DOIUrl":"https://doi.org/10.1007/s11010-025-05239-6","url":null,"abstract":"<p><p>Non-small cell lung cancer (NSCLC) is a highly prevalent and aggressive malignancy, where early diagnosis and therapeutic intervention are pivotal for enhancing patient prognosis. Nonetheless, the lack of reliable biomarkers remains a substantial hurdle in clinical practice. In this study, we identified dysregulated microRNAs (miRNAs) in NSCLC, revealing a significant downregulation of miR-3202 and an upregulation of miR-3182. We demonstrate that both miR-3202 and miR-3182 play critical roles in modulating NSCLC cell proliferation and motility. Notably, we identify DTL as a direct target of miR-3202, with sustained expression of DTL reversing the effects of miR-3202 on cell growth and migration. Mechanistically, we show that miR-3202 regulates the ubiquitination and proteasomal degradation of p21 through DTL. These findings provide novel insights into the miRNA landscape in NSCLC and underscore the functional significance of the miR-3202-DTL-p21 axis. Our results position miR-3202 as a potential biomarker for NSCLC, thereby offering a foundation for the development of targeted diagnostic and therapeutic strategies.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143557356","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":"Chloride channels and mast cell function: pioneering new frontiers in IBD therapy.","authors":"Ahmed M Aljameeli, Bader Alsuwayt, Deepak Bharati, Vaishnavi Gohri, Popat Mohite, Sudarshan Singh, Vijay Chidrawar","doi":"10.1007/s11010-025-05243-w","DOIUrl":"https://doi.org/10.1007/s11010-025-05243-w","url":null,"abstract":"<p><p>Emerging evidence indicates that chloride channels (ClCs) significantly affect the pathogenesis of inflammatory bowel disease (IBD) through their regulatory roles in mast cell function and epithelial integrity. IBD, encompassing conditions such as Crohn's disease and ulcerative colitis, involves chronic inflammation of the gastrointestinal tract, where channels influence immune responses, fluid balance, and cellular signalling pathways essential for maintaining mucosal homeostasis. This review examines the specific roles of ClC in mast cells, focussing on the regulation of mast cell activation, degranulation, cytokine release, and immune cell recruitment in inflamed tissues. Key channels, including Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) and ClC-2, are discussed in detail because of their involvement in maintaining intestinal epithelial barrier function, a critical factor disrupted in IBD. For example, CFTR facilitates chloride ion transport across epithelial cells, which is essential for mucosal hydration and maintenance of the intestinal barrier. Reduced CFTR function can compromise this barrier, permitting microbial antigens to penetrate the underlying tissues and triggering excessive immune responses. ClC-2, another chloride channel expressed in mast cells and epithelial cells, supports tight junction integrity, contributes to barrier function, and reduces intestinal permeability. Dysregulation of these channels is linked to altered mast cell activity and excessive release of pro-inflammatory mediators, exacerbating IBD symptoms, such as diarrhoea, abdominal pain, and tissue damage. Here, we review recent pharmacological strategies targeting ClC, including CFTR potentiators and ClC-2 activators, which show the potential to mitigate inflammatory responses. Additionally, experimental approaches for selective modulation of chloride channels in mast cells have been explored. Although targeting ClC offers promising therapeutic avenues, challenges remain in achieving specificity and minimizing side effects. This review highlights the therapeutic potential of Cl channel modulation in mast cells as a novel approach for IBD treatment, aiming to reduce inflammation and restore intestinal homeostasis in affected patients.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143557354","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":"High glucose facilitates hepatocellular carcinoma cell proliferation and invasion via WTAP-mediated HK2 mRNA stability.","authors":"Yongshen Niu, Siying Jia, Xuelian Xiao, Kangsheng Tu, Qingguang Liu","doi":"10.1007/s11010-025-05235-w","DOIUrl":"https://doi.org/10.1007/s11010-025-05235-w","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is one of the most common cancers, and diabetes is a risk factor for hepatocarcinogenesis. N6-methyladenosine (m6A) methyltransferase WT1-associated protein (WTAP) is highly expressed in HCC and contributes to tumor progression. However, its role in high glucose-driven HCC progression remains unclear. The m6A quantitative assay was used to detect the m6A modification level. The levels of mRNAs and proteins were detected by qPCR, Western blot, and immunohistochemistry. CCK-8, colony formation, EdU, and transwell assays were used to detect HCC cell proliferation, invasion, and migration. Immunoprecipitation and CHX assays were used to reveal the regulatory effect of high glucose on WTAP. An RNA degradation experiment was used to explore WTAP's regulation of HK2 mRNA. To demonstrate the effect of high glucose on HCC growth in vivo, a diabetic mouse model was constructed, and HCC cells were subcutaneously injected. High glucose prominently increased the global level of m6A in HCC cells. Interestingly, high glucose upregulated WTAP protein rather than mRNA expression. We found that WTAP expression was significantly upregulated in HCC tissues, especially in tumor tissues of diabetic patients. WTAP knockdown markedly attenuated high glucose-induced abilities of HCC cell proliferation, colony formation, migration, and invasion. Meanwhile, WTAP overexpression significantly enhanced the malignant behaviors of HCC cells under low glucose conditions. High glucose reduced the ubiquitination of WTAP, thereby inhibiting its proteasomal and lysosomal degradation. Phosphorylated ERK (p-ERK) was required for high glucose-mediated WTAP stability. WTAP knockdown prominently abrogated high glucose-induced global m6A levels and HK2 expression in HCC cells. WTAP positively regulated HK2 expression by increasing mRNA stability. HK2 overexpression remarkably reversed the suppressive effects of WTAP knockdown on HCC cells. HK2 knockdown prominently abolished the promoting role of WTAP in HCC cells. Importantly, the growth of HCC cells in diabetic mice was significantly faster than that in control mice, which was prominently attenuated by WTAP knockdown. Our study demonstrated that high glucose decreased WTAP degradation and maintained its protein level by activating ERK phosphorylation. WTAP promoted HCC cell proliferation, colony formation, migration, and invasion by stabilizing HK2 mRNA.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542630","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":"Molecular characterization underlying IFN-α2 treatment in polycythemia vera: a transcriptomic overview.","authors":"Fang-Fang Liu, Ke Li","doi":"10.1007/s11010-025-05238-7","DOIUrl":"https://doi.org/10.1007/s11010-025-05238-7","url":null,"abstract":"<p><p>Polycythemia vera (PV) is the most common chronic myeloproliferative neoplasm (MPN) in adults. Pegylated interferon-α2 (IFN-α2) is an effective and safe drug for the treatment of PV. However, the mechanisms of its action in PV are still not fully understood. Using the WGCNA and Limma algorithm, we found a subset of IFN-α2 sensitive genes and four gene co-expression modules. Meanwhile, we also found 820 genes were differentially expressed in PV compared with healthy controls. By integrating the above results, several differentially expressed genes (DEGs) that were up- or down-regulated in PV but showed opposite alterations in the IFN-α2-treated group were found. These genes were mainly related to three types of biological processes (metal ion homeostasis, metabolic/catabolic process, and Jak-STAT signaling pathway), the dysfunctions of which were prevalent in PV. Moreover, we applied another threshold-free analysis method to compare global gene expression between IFN-α2 treated PV, PV, and control groups. Results showed the transcriptome changes of PV versus controls were negatively correlated with that of IFN-α2 treated versus untreated PV, indicating IFN-α2 treatment could partially reverse the dysregulated gene expression profile due to PV pathology. In summary, interferon may alleviate the progression of PV through multiple pathways. The findings may be of assistance in understanding the molecular basis underlying this treatment.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542634","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}