BioFactors最新文献

{"title":"Lipid Codes and Lipid-Binding Proteins as Central Regulators of Autophagy","authors":"Abhishek Kumar,&nbsp;Debasish Kumar Ghosh","doi":"10.1002/biof.70124","DOIUrl":"https://doi.org/10.1002/biof.70124","url":null,"abstract":"<div>\u0000 \u0000 <p>Autophagy is increasingly understood as a lipid-governed membrane program rather than a solely protein-driven degradative pathway. This review combines molecular and mechanistic evidence showing how lipid molecules, metabolic enzymes, and membrane physical properties coordinate autophagy from induction to lysosomal degradation. We highlight phosphoinositide microdomains and their cognate kinases and phosphatases as spatial cues that nucleate phagophores, control maturation, and regulate lysosome reformation. We also discuss alternative phosphoinositide sources, sphingolipid and ceramide signaling, phosphatidic acid and diacylglycerol metabolism, fatty-acyl composition, and acyl-CoA signaling as determinants of membrane curvature, tension, leaflet asymmetry, and phase behavior in autophagy. Key protein effectors and their lipid binding motifs and domains are integrated into a model in which lipid chemistry and mechanics gate enzymatic activities. We present integrated lipid-protein-biophysics approaches to highlight outstanding questions and uncover predictive principles.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148238173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mesenchymal Stem Cell-Derived Exosomal miR-29a-3p Improves Hypertrophic Scar by Inhibiting the Proliferation and Migration of Schwann Cells via the PDGFRB/PAK1 Axis","authors":"Chengyu Zang,&nbsp;Ran Zhao,&nbsp;Zhang Feng,&nbsp;Linfeng Zhang,&nbsp;Chunyan Liu,&nbsp;Siyuan Yin,&nbsp;Ru Song,&nbsp;Zhenjie Wu,&nbsp;Linqi Su,&nbsp;Yibing Wang","doi":"10.1002/biof.70120","DOIUrl":"10.1002/biof.70120","url":null,"abstract":"<div>\u0000 \u0000 <p>Mesenchymal stem cell-derived exosomes (MSC-exo) can alleviate hypertrophic scar (HS) formation, whereas Schwann cells (SCs) promote HS formation. This study aimed to investigate whether MSC-exos attenuate HS by modulating SCs and to elucidate the underlying mechanisms. HS and normal skin tissues were obtained from patients. MSCs, SCs, and fibroblasts were isolated from BALB/c mice. SCs and HS mouse models were treated with MSC-exos. SCs under various treatments were co-cultured with fibroblasts. mRNA and protein levels were assessed by qRT-PCR, western blot, immunofluorescence, and immunohistochemical staining. Cell migration, proliferation, and apoptosis were evaluated by wound healing assay, CCK-8 assay, and TUNEL assay, respectively. HS tissue morphology was examined by Hematoxylin–eosin and Masson staining. The targeting of miR-29a-3p towards PDGFRB was validated using a dual-luciferase reporter assay. In patient HS tissues, downregulated miR-29a-3p was negatively correlated with upregulated PDGFRB. MSC-exo-delivered miR-29a-3p suppressed SCs proliferation and migration, promoted SCs apoptosis, and reduced SCs-secreted NGF, thereby inhibiting fibroblast migration and myofibroblast transformation. These effects were reversed by miR-29a-3p knockdown in MSCs. Furthermore, miR-29a-3p targeted and inhibited PDGFRB expression in SCs. Silencing PDGFRB abolished the promoting effects of miR-29a-3p inhibition on SCs, which was rescued by the PAK1 activator FTY720. MSC-exo-delivered miR-29a-3p ameliorates HS by inhibiting SCs proliferation, migration and NGF secretion via the PDGFRB/PAK1 axis to suppress myofibroblast transformation. Beyond the traditional focus on fibroblasts, this reveals an exosome-SCs-fibroblast network, providing a novel theoretical basis for HS treatment.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148142596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Multiple Roles and Targeting Strategies of LonP1 in the Occurrence and Development of Cancer","authors":"Qun Zeng,&nbsp;Shitian Huang,&nbsp;Tingting Jiang","doi":"10.1002/biof.70121","DOIUrl":"10.1002/biof.70121","url":null,"abstract":"<div>\u0000 \u0000 <p>LonP1, a mitochondrial AAA+ protease, serves as a pivotal integrator of mitochondrial quality control (MQC) and metabolic reprogramming in cancer progression. Alternative splicing generates three functionally distinct isoforms: full-length ISO1 maintains mitochondrial homeostasis by degrading oxidized proteins and stabilizing mitochondrial transcription factor A (TFAM) for mtDNA integrity; truncated ISO2 (Δ42–105 AA) drives glycolytic reprogramming and epithelial-mesenchymal transition (EMT) by upregulating Snail/vimentin; and cytoplasmic ISO3 (Δ1–196 AA) lacks protease activity and is tumor-irrelevant. Tumor microenvironment (TME) cues (hypoxia, <i>H. pylori</i> infection, PFOA exposure, glutamine depletion) regulate LonP1 via Akt phosphorylation/Sirt3 deacetylation, coordinating MQC and metabolic adaptation to support cancer cell survival and metastasis. Functional data confirm its pro-tumor role: LonP1 upregulation enhances cervical cancer mitophagy and gastric cancer glycolysis, while knockdown induces mitochondrial dysfunction and apoptosis. This review summarizes current advances by (1) systematically integrating the isoform-specific functions of LonP1; (2) constructing a “LonP1-MQC-metabolism” regulatory network based on published evidence; and (3) proposing isoform-specific targeted strategies for precision oncology. These insights position LonP1 as a promising candidate for precision oncology, offering a cohesive understanding of mitochondrial regulation in cancer.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148136484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “SUMO-Specific Proteases: SENPs in Oxidative Stress-Related Signaling and Diseases”","authors":"","doi":"10.1002/biof.70059","DOIUrl":"10.1002/biof.70059","url":null,"abstract":"<p>Jiao, Y. Zhang, X. Yang, Z “SUMO-specific proteases: SENPs in oxidative stress-related signaling and diseases”, BioFactors. 2024; 50: 910-921.</p><p>The listed affiliation Division of Oncology, Department of Clinical and Medical Sciences, Lund University for the author Yang Z was incorrect. Lund University has stated the research in the article was not associated in any way with the university. The affiliation has been removed and replaced with South China Agricultural University.</p><p>We apologize for this error.</p>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/biof.70059","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148136324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AND-1 Enhances Erastin-Induced Ferroptosis in Ovarian Cancer Cells by Down-Regulating SLC7A11 and NRF2","authors":"Jingjing Li,&nbsp;Lingyan Li,&nbsp;Xinye Xia,&nbsp;Muhammad Khan,&nbsp;Yaqi Zhang,&nbsp;Yingwei Zhang,&nbsp;Xiao Wu,&nbsp;Tonghui Ma,&nbsp;Yongming Li","doi":"10.1002/biof.70117","DOIUrl":"10.1002/biof.70117","url":null,"abstract":"<div>\u0000 \u0000 <p>Ferroptosis is a highly synchronized form of non-apoptotic intracellular iron-dependent cell death which is regulated by multiple cellular metabolic pathways. Extensive studies suggest that ferroptosis could efficiently set the therapy resistant cancer cells on the road to ruin, thus providing new opportunities for cancer therapy. And-1 is an acidic nucleoplasmic DNA binding protein which plays a vital role in DNA replication and repair. Here in this study, we report a novel function of And-1 in regulating erastin-induced ferroptosis in ovarian cancer cells. And-1 overexpression (OE) enhanced erastin-induced ferroptosis by modulating the level of ferroptosis biomarkers such as MDA, GSH, Fe²⁺ and lipid peroxidation; while knockdown (KD) of And-1 produces opposite results. Moreover And-1(OE) suppressed the expression of NRF2, SLC7A11, and FTH1 and promoted the expression of TFR1 and ATF3 while And-1 (KD) produces opposite results. Further mechanistic study revealed that And-1 inhibits the expression of SLC7A11 by increasing ATF3 expression. Moreover, using pharmacological inhibitors, we have shown that erastin induces ferroptosis through multiple mechanisms. Taken together, our data suggest that And-1 enhanced erastin-induced ferroptosis in OC cells by inhibiting system <i>x</i>_c⁻ expression through ATF3 and suppressing NRF2 expression.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148136336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-Omics Analysis and Mechanistic Validation Reveal RPS8 as a Novel Prognostic Biomarker and Therapeutic Target for Hepatocellular Carcinoma","authors":"Lichen Zhu,&nbsp;Hongjiao Liu,&nbsp;Jin Qian,&nbsp;Sile Wan,&nbsp;Fukai Wen,&nbsp;Qingyu Li,&nbsp;Zhaoyang Lu,&nbsp;Jiaming Liu","doi":"10.1002/biof.70116","DOIUrl":"10.1002/biof.70116","url":null,"abstract":"<div>\u0000 \u0000 <p>Despite its aggressiveness and unfavorable prognosis, the key molecular drivers of Hepatocellular carcinoma (HCC) are still not fully defined. The role of ribosomal protein S8 (RPS8) in HCC development and its regulatory mechanisms received little attention. We investigated the role of RPS8 in HCC progression by delineating its biological functions, clinical relevance, and mechanistic underpinnings. We conducted comprehensive multi-omics analysis using public datasets (TCGA, GEO) to evaluate RPS8 expression and its prognostic value in HCC. Single-cell RNA-seq was utilized to map the distribution of RPS8 expression within the tumor microenvironment. The biological functions of RPS8 were validated through a series of in vitro assays (e.g., colony formation, Transwell, wound healing) and in vivo subcutaneous xenograft models using RPS8 knockdown and overexpression systems. Whole-transcriptome sequencing was performed to identify the downstream pathways regulated by RPS8. RPS8 was elevated in HCC at both the transcriptional and protein levels, and its overexpression independently signaled poor prognosis. In functional assays, RPS8 increased HCC cell proliferation, migration, and invasion in vitro and stimulated tumor growth in vivo. This pro-tumorigenic activity was associated with the induction of epithelial-mesenchymal transition (EMT) and angiogenesis. Mechanistically, we revealed that RPS8 exerts these effects by activating the endoplasmic reticulum (ER) stress pathway. Furthermore, high RPS8 expression was associated with a remodeled tumor immune microenvironment, characterized by increased CD8+ T cell infiltration. Findings identify RPS8 as a critical oncogene that promotes HCC progression via activation of ER stress. RPS8 can be leveraged as a prognostic biomarker and as a potential focus of therapy in HCC.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148052309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lignans Alleviate Depression by Modulating the Gut–Brain Axis: Effect and Mechanism Based on Multi-Omics Analyses","authors":"Liang Liu,&nbsp;Kun-Ru Tan,&nbsp;Xing-Hua Zhang,&nbsp;Bao-Juan Yuan,&nbsp;Yuan-Bo Li,&nbsp;Zhi-Yuan Jiang,&nbsp;Shao-Xin Li,&nbsp;Yu-Hui Wang,&nbsp;Hong-Da Tian,&nbsp;Hui-di Liu,&nbsp;Li-Ping Wang,&nbsp;Xia Li,&nbsp;Yang Li,&nbsp;Xiao-Chen Zhang,&nbsp;Randal N. Johnston,&nbsp;Gui-Rong Liu,&nbsp;Xiu-Xian Yang,&nbsp;Shu-Lin Liu","doi":"10.1002/biof.70122","DOIUrl":"10.1002/biof.70122","url":null,"abstract":"<div>\u0000 \u0000 <p>Major depressive disorder (MDD) is a highly disabling psychiatric illness characterized by persistent low mood and psychomotor retardation, often leading to cognitive impairment or even suicidality. As the pathogenesis remains poorly understood, the currently available treatment regimens are mostly symptomatic therapies with little satisfactory curative effect. The emerging paradigm of gut–brain axis has highlighted gut dysbiosis as a key etiological factor to elicit neuro-inflammation and jeopardize the central nervous system homeostasis. In this study, we evaluated the ameliorating effects of flaxseed lignans on the gut microbiome to regain the gut micro-environmental functionality and alleviate MDD. The lignans significantly mitigated the severity of disease and markedly altered the gut microbiota structure in the participants. In the MDD mouse model, the lignans reversed the experimental depression-like behaviors, repaired neural and gut damage and restored barrier integrity. Of great significance, the lignans elevated the levels of 5-hydroxytryptamine (5-HT), brain-derived neurotrophic factor (BDNF) and γ-aminobutyric acid (GABA), and markedly attenuated microglial and systemic inflammation. Mechanistically, the lignans inhibited the IL-17/AP-1/NF-κB axis through direct interaction with the Fos protein. In the BV-2 cells, the lignan enterolactone reduced levels of nitric oxide and pro-inflammatory cytokines, further validating the anti-inflammatory mechanism of the lignans. Together, these findings demonstrate that lignans exert potent antidepressant effects by modulating the gut–brain axis and resolving neuro-inflammation, providing useful information for the development of novel therapeutic strategies for MDD prevention and treatment.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148052215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Naringenin and Hesperetin Alleviate Hepatic Aging Through Coordinated Modulation of Persulfidation, Senescence, and Nrf2/Sirt1 Signaling in Old Rats","authors":"Milica Vukojević,&nbsp;Vladimir Ajdžanović,&nbsp;Ana Stančić,&nbsp;Vesna Otašević,&nbsp;Branko Filipović,&nbsp;Jasmina Živanović,&nbsp;Marko Miler","doi":"10.1002/biof.70119","DOIUrl":"10.1002/biof.70119","url":null,"abstract":"<div>\u0000 \u0000 <p>Naringenin (NAR) and hesperetin (HES) are citrus flavanones that have been shown to exert various geroprotective effects. However, key regulators of these processes remain unexplored. To address this gap, we investigated the mechanisms through which NAR and HES modulate hepatic redox control, persulfidation, and senescence-associated pathways in 24-month-old male Wistar rats. Animals were treated orally with NAR or HES (15 mg/kg b.w.) for 4 weeks, while control groups remained physiologically intact or received vehicle. Liver tissue was analyzed using a dimedone-based switch method to evaluate overall protein persulfidation (P-SSH), Western blot, qPCR, and histological analysis, including quantification of IHC staining and IF labeling. Our results showed that both citrus flavanones increased total P-SSH levels while exerting distinct regulatory effects on the H₂S metabolic network. Only HES upregulated gene expression of H₂S-producing enzymes (cystathionine beta-synthase CBS, cystathionine gamma-lyase CSE, and mercaptopyruvate sulfurtransferase MST) and catabolic enzymes (sulfide:quinone oxidoreductase SQR and thiosulfate sulfurtransferase TST), together with CBS protein, whereas NAR decreased CSE protein expression. Both NAR and HES treatment activated the Nrf2 signaling pathway, as evidenced by increased nuclear translocation of Nrf2 in the treated groups. Concurrently, NAR and HES increased Sirt1 expression, which was accompanied by decreases in p16 and β-galactosidase expression, indicating attenuation of hepatic senescence. Together, these findings highlight a synergistic interplay among persulfidation, H₂S metabolism, and Nrf2/Sirt1 signaling as a key mechanism by which citrus flavanones support hepatic resilience during aging.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148052312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SEMI-1, A Novel Neuronal Selenium-Binding Protein 1 Homolog Without Methanethiol Oxidase Activity, Modulates Stress Resistance, Lifespan, and Thermotaxis in C. elegans","authors":"Weiye Gong,&nbsp;Karl Köhnlein,&nbsp;Josephine Priebs,&nbsp;Lara Biegel,&nbsp;Nadine Urban,&nbsp;Verena Alexia Ohse,&nbsp;David Guerrero-Gómez,&nbsp;Priscila Yumi Tanaka Shibao,&nbsp;Janine Kirstein,&nbsp;Anna Patricia Kipp,&nbsp;Holger Steinbrenner,&nbsp;Antonio Miranda-Vizuete,&nbsp;Martin Srayko,&nbsp;Lars-Oliver Klotz","doi":"10.1002/biof.70118","DOIUrl":"10.1002/biof.70118","url":null,"abstract":"<p>Human selenium-binding protein 1 (SELENBP1) catalyzes the oxidation of the gaseous methionine degradation product, methanethiol. We previously identified a <i>Caenorhabditis elegans</i> ortholog, SEMO-1, that has the same methanethiol oxidase (MTO) activity. Here, we report the identification and functional characterization of another <i>C. elegans</i> ortholog of human SELENBP1, SEMI-1. In contrast to SELENBP1 and SEMO-1, SEMI-1 (SELENBP1-homolog, MTO inactive) lacks MTO activity. Notably, <i>semi-1</i> expression is confined to thermosensory AFD (amphid finger-like endings D) and oxygen-sensing BAG (bag-like dendritic ending) neurons, as demonstrated using a SEMI-1::GFP reporter. Depletion of SEMI-1 results in increased lifespan, improved physiological parameters (motility, progeny), and reduced accumulation of age pigments during aging. SEMI-1-deficient nematodes are more resistant to the redox cycler paraquat than wild-type worms. On the other hand, they show enhanced susceptibility to selenite exposure, indicating a role for SEMI-1 in conferring selective stress resistance. We also show that SEMI-1 deficiency is associated with impaired thermotaxis in <i>C. elegans,</i> which is consistent with the role of AFD neurons in thermosensation. In conclusion, SEMI-1 is a neuronal SELENBP1 ortholog in <i>C. elegans</i> that lacks MTO activity and impairs oxidative stress resistance and shortens lifespan. As a trade-off, it contributes to <i>C. elegans</i> selenite resistance and thermotaxis. The observed phenotypes of SEMI-1 deficiency suggest the existence of MTO-independent effects of other SELENBP1 homologs.</p>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/biof.70118","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148013328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148092796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}