Biochimica et biophysica acta. Molecular cell research最新文献

{"title":"Hypoxia enhances IL-8 signaling through inhibiting miR-128-3p expression in glioblastomas","authors":"Kuo-Hao Ho ,&nbsp;Shao-Yuan Hsu ,&nbsp;Peng-Hsu Chen ,&nbsp;Chia-Hsiung Cheng ,&nbsp;Ann-Jeng Liu ,&nbsp;Ming-Hsien Chien ,&nbsp;Ku-Chung Chen","doi":"10.1016/j.bbamcr.2024.119885","DOIUrl":"10.1016/j.bbamcr.2024.119885","url":null,"abstract":"<div><div>Glioblastoma multiforme (GBM) is an aggressive type of brain tumor known for its hypoxic microenvironment. Understanding the dysregulated mechanisms in hypoxic GBM is crucial for its effective treatment. Through data mining of The Cancer Genome Atlas (TCGA) with hypoxia enrichment scores and in vitro experiments, miR-128-3p was negatively correlated with hypoxia signaling and the epithelial-mesenchymal transition (EMT). Additionally, lower miR-128-3p levels existed in hypoxic GBM, leading to desensitizing temozolomide (TMZ)'s efficacy, a first-line therapeutic drug for GBM. Overexpressing miR-128-3p enhanced both the in vitro and in vivo sensitivity of hypoxic gliomas to TMZ treatment. Mechanistically, HIF-1α suppressed miR-128-3p expression in hypoxic GBM. Through establishing miR-128-3p-mediated transcriptomic profiles and data mining, interleukin (IL)-8 was selected. IL-8 respectively showed positive and negative correlations with hypoxia and miR-128-3p, and was associated with poor TMZ therapeutic results in GBM. Elevated miR-128-3p, which targets both the 3′-untranslated region (UTR) and 5′UTR of IL-8, resulted in suppression of IL-8 expression. Moreover, IL-8 was validated to be involved in HIF-1α/miR-128-3p-regulated TMZ sensitivity and the EMT in hypoxic GBM cells. Collectively, the HIF-1α/miR-128-3p/IL-8 signaling pathway plays a critical role in promoting the progression of hypoxic GBM. Targeting this signaling pathway holds promise as a potential therapeutic strategy.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 2","pages":"Article 119885"},"PeriodicalIF":4.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142779305","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":"Functional analysis of yak alveolar type II epithelial cells at high and low altitudes based on single-cell sequencing","authors":"Jingyi Li ,&nbsp;Nating Huang ,&nbsp;Xun Zhang ,&nbsp;Huizhen Wang ,&nbsp;Jiarui Chen ,&nbsp;Qing Wei","doi":"10.1016/j.bbamcr.2024.119889","DOIUrl":"10.1016/j.bbamcr.2024.119889","url":null,"abstract":"<div><div>The adaptation of lung cells to high-altitude environments represents a notable gap in our understanding of how animals cope with hypoxic conditions. Alveolar epithelial cells type II (AEC II) are crucial for lung development and repair. However, their, specific role in the adaptation of yaks to high-altitude environments remains unclear. In this study, we aimed to address this gap by investigating the differential responses of AEC II in yaks at high and low altitudes (4000 m and 2600 m, respectively). We used the 10 × scRNA-seq technology to construct a comprehensive cell atlas of yak lung tissue, and identified 15 distinct cell classes. AEC II in high-altitude yaks revealed increased immunomodulatory, adhesive, and metabolic activities, which are crucial for maintaining lung tissue stability and energy supply under hypoxic conditions. Furthermore, alveolar epithelial progenitor cells within AEC II can differentiate into both Alveolar epithelial cell type I (AEC I) and AEC II. <em>SHIP1</em> and other factors are promoters of AEC I transdifferentiation, whereas <em>SFTPC</em> and others promote AEC II transdifferentiation. This study provides new insights into the evolutionary adaptation of lung cells in plateau animals by elucidating the molecular mechanisms underlying AEC II adaptation to high-altitude environments.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 2","pages":"Article 119889"},"PeriodicalIF":4.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142833691","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":"Unraveling the role of the P2X7 receptor in cancer radioresistance: Molecular insights and therapeutic implications","authors":"Seyedeh Nasibeh Mousavikia ,&nbsp;Maryam M. Matin ,&nbsp;Mohammad Taghi Bahreyni Tossi ,&nbsp;Hosein Azimian","doi":"10.1016/j.bbamcr.2025.119910","DOIUrl":"10.1016/j.bbamcr.2025.119910","url":null,"abstract":"<div><div>The P2X7 receptor, a key player in purinergic signaling, is a crucial factor in modulating the response of cancer cells to radiotherapy. The aim of this study was to elucidate the molecular mechanisms by which P2X7 receptor activation contributes to radioresistance in different cancer types. P2X7 receptor signaling influences cellular processes such as DNA damage repair and inflammatory responses, thereby improving tumor survival after radiation exposure. Activation of the P2X7 receptor leads to changes in the tumor microenvironment and promotes an adaptive response that enables cancer cells to resist therapeutic interventions. Therefore, targeting the P2X7 receptor could represent a new therapeutic strategy against cancer. By linking molecular insights with therapeutic implications, this research highlights the P2X7 receptor as a promising target for overcoming radioresistance in cancer therapy and paves the way for novel combination approaches that could significantly improve patient outcomes.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 3","pages":"Article 119910"},"PeriodicalIF":4.6,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143073591","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":"SLC26A9 promotes the initiation and progression of breast cancer by activating the PI3K/AKT signaling pathway","authors":"Zhiyuan Ma ,&nbsp;Hu Wang ,&nbsp;Zhengxing Zhou ,&nbsp;Chengli Lu ,&nbsp;Minglin Zhang ,&nbsp;Renmin Mu ,&nbsp;Chengmin Zhang ,&nbsp;Zhiqiang Yi ,&nbsp;Zilin Deng ,&nbsp;Yingying Zhao ,&nbsp;Jiaxing Zhu ,&nbsp;Guorong Wen ,&nbsp;Hai Jin ,&nbsp;Jiaxing An ,&nbsp;Biguang Tuo ,&nbsp;Peng Yuan ,&nbsp;Xuemei Liu ,&nbsp;Taolang Li","doi":"10.1016/j.bbamcr.2025.119912","DOIUrl":"10.1016/j.bbamcr.2025.119912","url":null,"abstract":"<div><div>SLC26A9 is a member of the Slc26a family of multifunctional anion transporters that function as Cl⁻ channels in the stomach. We reported for the first time that SLC26A9 is involved in gastric tumorigenesis. However, the role of SLC26A9 in breast cancer has not yet been investigated. We first demonstrated that the upregulation of SLC26A9 is associated with the clinicopathological progression and poor prognosis of patients with breast cancer and is positively correlated with HER2 amplification. SLC26A9 alters the proliferation, migration, and invasion potential of breast cancer cells by regulating the PI3K/AKT signaling pathway. SLC26A9 acts as an oncogene in the development of breast cancer. These findings provide valuable insights for the development of future diagnostic and therapeutic strategies for BC.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 3","pages":"Article 119912"},"PeriodicalIF":4.6,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063512","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":"Inhibition of hydrogen peroxide-induced senescence markers by yeast-derived vacuoles in human lung fibroblasts","authors":"Su-Min Lee ,&nbsp;Eunsu Seo ,&nbsp;Yang-Hoon Kim ,&nbsp;Jiho Min","doi":"10.1016/j.bbamcr.2025.119907","DOIUrl":"10.1016/j.bbamcr.2025.119907","url":null,"abstract":"<div><div>Senescence significantly contributes to aging in various tissues, influenced by factors such as lysosomal alkalinization, which disrupts autophagic flux and accumulates toxic substances. This disruption leads to oxidative stress, increased lysosomal permeability, cellular senescence, and apoptosis. Similar to mammalian lysosomes, <em>S. cerevisiae</em>-derived vacuoles degrade macromolecules using hydrolytic enzymes and mitigate these aging effects. Our study assessed the anti-aging potential of yeast vacuoles in human lung fibroblasts treated with hydrogen peroxide (H₂O₂). Pretreatment with vacuoles at concentrations of 1, 5, and 10 μg/ml decreased SA-β-gal-positive cell counts, reduced mRNA levels of senescence markers (p21 and p53), and senescence-associated secretory phenotype (SASP) factors (IL-6 and TNF-α) compared to controls treated with H₂O₂ alone. Additionally, these vacuoles significantly diminished intracellular reactive oxygen species (ROS) levels, indicating their potential as effective lung anti-senescence agents. This study suggests that yeast vacuoles could be used as a preventive measure against changes associated with lung aging.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 3","pages":"Article 119907"},"PeriodicalIF":4.6,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063509","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":"H2S inhibition of xanthine dehydrogenase to xanthine oxidase conversion reduces uric acid levels and improves myoblast functions","authors":"Joshua MacNeil ,&nbsp;Yuehong Wang ,&nbsp;Guangdong Yang","doi":"10.1016/j.bbamcr.2025.119909","DOIUrl":"10.1016/j.bbamcr.2025.119909","url":null,"abstract":"<div><div>Hydrogen sulfide (H₂S) is an important gasotransmitter that regulates a wide range of pathophysiological processes. Higher uric acid levels are associated with an increased risk of metabolic diseases. The causal mechanism linking H₂S signalling and uric acid metabolism in skeletal muscles has not yet been elucidated. This study aimed to explore the intertwined metabolisms of H₂S and uric acid as well as their integrated roles in controlling myoblast cell functions. It was first found that purine overload increased uric acid levels, promoted oxidative stress, mitochondrial damage, and apoptosis in cultured mouse myoblasts, which could be reversed by the exogenously application of H₂S at physiologically relevant concentration. In addition, H₂S significantly inhibited the expressions of inflammatory genes (encoding IL2, IL4, and TNFα) but had no effect on oxidative stress, mitochondrial damage and cell death induced by excessive uric acid. Mechanistically, H₂S inhibited xanthine oxidoreductase (XOR) activity by blocking the conversion of xanthine dehydrogenase (XDH) to xanthine oxidase (XO), thus reducing uric acid levels and improving myoblast functions. In addition, purine and uric acid attenuated the expression of cystathionine gamma-lyase (CSE, an H₂S-generating enzyme) and suppressed endogenous H₂S production. Blood uric acid levels and skeletal muscle XOR activity were significantly higher in CSE knockout mice than in wild-type mice. This study revealed a mutual interaction between H₂S signalling and uric acid metabolism in the regulation myoblast functions. Thus, the CSE/H₂S system may be a target for the prevention of hyperuricemia-related metabolic syndromes.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 3","pages":"Article 119909"},"PeriodicalIF":4.6,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063462","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":"MARCH5 ameliorates aortic valve calcification via RACGAP1-DRP1 associated mitochondrial quality control","authors":"Jialiang Zhang ,&nbsp;Yaoyu Zhang ,&nbsp;Wenhua Lei ,&nbsp;Jing Zhou ,&nbsp;Yanjiani Xu ,&nbsp;Zhou Hao ,&nbsp;Yanbiao Liao ,&nbsp;Fangyang Huang ,&nbsp;Mao Chen","doi":"10.1016/j.bbamcr.2025.119911","DOIUrl":"10.1016/j.bbamcr.2025.119911","url":null,"abstract":"<div><h3>Background</h3><div>Mitochondrial E3 ubiquitin ligase (MARCH5) as an important regulator in maintaining mitochondrial function. Our aims were to investigate the role and mechanism of MARCH5 in aortic valve calcification.</div></div><div><h3>Methods</h3><div>Human aortic valves, both calcified and non-calcified, were analyzed for MARCH5 expression using western blotting. Mitochondrial fragmentation was evaluated using transmission electron microscope. Osteogenic differentiation of human aortic valvular interstitial cells (HVICs) was induced with osteoblastic medium (OM), confirmed by western blotting and Alizarin red staining. Mitochondrial morphology and oxidative phosphorylation were assessed using MitoTracker and Seahorse, respectively. MARCH5-knockdown and ApoE-knockout mice fed high-fat diet were used to study aortic valve calcification.</div></div><div><h3>Results</h3><div>The mitochondrial quality control was impaired in calcified valves, and the level of MARCH5 protein was also decreased in calcified valves. Inhibition of MARCH5 impaired mitochondrial quality control, increased mitochondrial stress and accelerates osteogenic transformation in OM treated HVICs. While, overexpression MARCH5 has the opposite effects. Co-immunoprecipitation, mass spectrometry and molecular docking found MARCH5 interacted Rac GTPase-activating protein 1 (RACGAP1) and promoted its ubiquitination, leading to impaired mitochondrial quality control. Inhibiting RACGAP1 reversed osteogenic transformation induced by MARCH5 silencing in OM treated HVICs. Silencing dynamin-related protein 1 (DRP1) under RACGAP1 inhibition had no additional benefit. In vivo, deficiency of MARCH5 promoted aortic valve calcification, while inhibition RACGAP1 reversed aortic valve calcification in MARCH5 deficiency mice.</div></div><div><h3>Conclusion</h3><div>Downregulation of MARCH5 promotes RACGAP1 ubiquitination, activating DRP1 and impairing mitochondrial quality control, which contributes to aortic valve calcification. This identifies a potential therapeutic target for aortic valve calcification.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 3","pages":"Article 119911"},"PeriodicalIF":4.6,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063510","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":"Serum starvation induces cytosolic DNA trafficking via exosome and autophagy-lysosome pathway in microglia","authors":"Liyan Zhou,&nbsp;Zilong Wu,&nbsp;Xiaoqing Yi,&nbsp;Dongxue Xie,&nbsp;Jufen Wang,&nbsp;Wenhe Wu","doi":"10.1016/j.bbamcr.2025.119905","DOIUrl":"10.1016/j.bbamcr.2025.119905","url":null,"abstract":"<div><div>The imbalance of microglial homeostasis is highly associated with age-related neurological diseases, where cytosolic endogenous DNA is also likely to be found. As the main medium for storing biological information, endogenous DNA could be localized to cellular compartments normally free of DNA when cells are stimulated. However, the intracellular trafficking of endogenous DNA remains unidentified. In this study, we demonstrated that nuclear DNA (nDNA) and mitochondrial DNA (mtDNA), as the components of endogenous DNA, undergo different intracellular trafficking under conditions of microglial homeostasis imbalance induced by serum starvation. Upon detecting various components of endogenous DNA in the cytoplasmic and extracellular microglia, we found that cytosolic nDNA primarily exists in a free form and undergoes degradation through the autophagy-lysosome pathway. In contrast, cytosolic mtDNA predominantly exists in a membrane-wrapped form and is trafficked through both exosome and autophagy-lysosome pathways, with the exosome pathway serving as the primary one. When the autophagy-lysosome pathway was inhibited, there was an increase in exosomes. More importantly, the inhibition of the autophagy-lysosome pathway resulted in enhanced trafficking of mtDNA through the exosome pathway. These findings unveiled the crosstalk between these two pathways in the trafficking of microglial cytosolic DNA and thus provide new insights into intervening in age-related neurological diseases.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 3","pages":"Article 119905"},"PeriodicalIF":4.6,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063511","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":"The key vulnerabilities and therapeutic opportunities in the USP7-p53/MDM2 axis in cancer","authors":"Gouranga Saha ,&nbsp;Mrinal K. Ghosh","doi":"10.1016/j.bbamcr.2025.119908","DOIUrl":"10.1016/j.bbamcr.2025.119908","url":null,"abstract":"<div><div>The MDM2/MDMX-p53 circuitry is essential for controlling the development, apoptosis, immune response, angiogenesis, senescence, cell cycle progression, and proliferation of cancer cells. Research has demonstrated that USP7 exerts strong control over p53, MDM2, and MDMX stability, with multiple mediator proteins influencing the USP7-p53-MDM2/MDMX axis to modify p53 expression level and function. In cases where p53 is of the wild type (Wt-p53) in tumors, inhibiting USP7 promotes the degradation of MDM2/MDMX, leading to the activation of p53 signaling. This, in turn, results in cell cycle arrest and apoptosis. Hence, targeting USP7 presents a promising avenue for cancer therapy. Targeting USP7 in tumors that harbor mutant p53 (Mut-p53) is unlikely and remains largely unexplored due to the existence of numerous USP7 targets that function independently of p53. Considering that Mut-p53 exhibits resistance to degradation by MDM2 and other E3 ligases and also shares the same signaling pathways as Wt-p53, it is reasonable to suggest that USP7 may play a role in stabilizing Mut-p53. However, there is still much to be done in this area. If the hypothesis is correct, USP7 may be a potent target in cancers containing both Wt-p53 and Mut-p53.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 3","pages":"Article 119908"},"PeriodicalIF":4.6,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063513","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":"GPSM1 interacts and cooperates with MMP19 to promote proliferation and EMT in colorectal cancer cells","authors":"Lu Wang ,&nbsp;Na Li ,&nbsp;Yang Chen,&nbsp;Yehua Qiao,&nbsp;Yaolin Song,&nbsp;Xiangyan Zhang,&nbsp;Han Zhao,&nbsp;Wenwen Ran,&nbsp;Guangqi Li,&nbsp;Xiaoming Xing","doi":"10.1016/j.bbamcr.2025.119903","DOIUrl":"10.1016/j.bbamcr.2025.119903","url":null,"abstract":"<div><div>Among patients with colorectal cancer (CRC), metastasis accounts for the majority of deaths, and epithelial–mesenchymal transition (EMT) is important in the metastatic process. However, the mechanism underlying the correlation between the two in CRC is unknown. Here, we verified that a receptor-independent protein, G-protein signaling modulator 1 (GPSM1), was increased in CRC and had a significant positive correlation with matrix metalloproteinase 19 (MMP19). GPSM1 and MMP19 knockdown or overexpression decreased and increased proliferation, migration and invasion of CRC cells, respectively. In addition, overexpression or knockdown of GPSM1 and MMP19 upregulated and inhibited EMT, respectively. Interfering with MMP19 reversed EMT activation via GPSM1 overexpression. Apoptosis was induced by GPSM1 and MMP19 knockdown and activated the caspase3/Bcl-2/Bax signaling pathway. In conclusion, these results support the role of GPSM1 and MMP19 in CRC progression.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 3","pages":"Article 119903"},"PeriodicalIF":4.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143036156","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}