Free Radical Biology and Medicine最新文献

{"title":"Cold atmospheric plasma restores skewed macrophage polarization in triple negative breast cancers via enhancing KAT6A acetylation","authors":"Kaiyuan Zhu ,&nbsp;Qing lv ,&nbsp;Xiaoxia Lu ,&nbsp;Yuchen Wang ,&nbsp;Xiaofeng Dai","doi":"10.1016/j.freeradbiomed.2024.11.028","DOIUrl":"10.1016/j.freeradbiomed.2024.11.028","url":null,"abstract":"<div><div>Breast cancer is the most common cancer diagnosed and the second leading cause of death of cancer among women in the world, due to inappropriate diagnosis and choice of therapeutic approach. The molecular profiles of breast cancers may switch among subtypes during treatments, leading to a phenotype such as triple negative breast cancers (TNBCs) that is more difficult to treat. Cold atmospheric plasma (CAP) has been demonstrated by many studies on its efficacy in arresting the malignancies of multiple cancer types including TNBCs that lack surface receptor expression and are thus the most difficult to treat among breast cancers. By analyzing the genetic testing reports of a breast cancer clinical case misdiagnosed with BRCA1 mutation, we characterized the importance of KAT6A in driving disease progression of this patient. Through exploring genes differentially regulated under physical interactions between KAT6A and SMAD3, we proposed the KAT6A/SMAD3/IL6/CD163 molecular axis capable of driving macrophage M2 polarization in the immune microenvironment of breast cancers. Through examining the expression landscapes of KAT6A at both transcriptional and translational levels, we proposed a possible role of KAT6A acetylation in reducing its ability in acetylating SMAD3 and subsequent oncogenic roles. Through analyzing the whole transcriptome and acetylome of TNBC cells in response to CAP treatment, we predicted the efficacy of CAP in resolving TNBCs via increasing KAT6A acetylation, which were validated both <em>in vitro</em> and <em>in vivo</em>. Our study, for the first time, presented the role of CAP in re-polarizing macrophages from the M2 to M1 state in the microenvironment of breast cancers via elevating KAT6A acetylation, and warranted careful interpretation of patients’ genetic testing reports by clinicians for the sake of minimizing mortalities due to inappropriate choice of therapeutic modalities.</div></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":"226 ","pages":""},"PeriodicalIF":7.1,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142699651","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":"Oxygen control in cell culture – Your cells may not be experiencing what you think!","authors":"Zachary J. Rogers ,&nbsp;Darragh Flood ,&nbsp;Cormac T. Taylor","doi":"10.1016/j.freeradbiomed.2024.11.036","DOIUrl":"10.1016/j.freeradbiomed.2024.11.036","url":null,"abstract":"<div><div>Oxygen (O₂)-controlled cell culture has been pivotal in studying mammalian mechanisms of O₂ sensing, regulation, and utilization. We posit, however, that O₂-controlled cell culture is paradoxically not controlling O₂. There is overwhelming evidence that the pericellular O₂ is lower than the surrounding gas phase due to cellular O₂ consumption. Standard hypoxic cell culture is at high risk of inducing pericellular anoxia. We discuss the implications of poor O₂ control for cellular O₂ regulation mechanisms, bioenergetics, and redox signaling. We also highlight the evidence of frequent under-oxygenation in standard (<em>i.e.</em>, normoxic) cell culture. This issue has been largely overlooked because strategies to control pericellular O₂ have been lacking. Here, we propose a framework to control pericellular O₂ based on our recent investigation into the nature of the gas/pericellular O₂ gradient. Implementing this framework into standard practice will unlock quantitative O₂ control <em>in vitro</em>, improving our ability to understand the role of O₂ in biology.</div></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":"226 ","pages":"Pages 279-287"},"PeriodicalIF":7.1,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692645","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":"Dynamics of intracellular and intercellular redox communication","authors":"Helmut Sies","doi":"10.1016/j.freeradbiomed.2024.11.002","DOIUrl":"10.1016/j.freeradbiomed.2024.11.002","url":null,"abstract":"<div><div>Cell and organ metabolism is organized through various signaling mechanisms, including redox, Ca²⁺, kinase and electrochemical pathways. Redox signaling operates at multiple levels, from interactions between individual molecules in their microenvironment to communication among subcellular organelles, single cells, organs, and the entire organism. Redox communication is a dynamic and ongoing spatiotemporal process. This article focuses on hydrogen peroxide (H₂O₂), a key second messenger that targets redox-active protein cysteine thiolates. H₂O₂ gradients across cell membranes are controlled by peroxiporins, specialized aquaporins. Redox-active endosomes, known as redoxosomes, form at the plasma membrane. Cell-to-cell redox communication involves direct contacts, such as per gap junctions that connect cells for transfer of molecules via connexons. Moreover, signaling occurs through the release of redox-active molecules and enzymes into the surrounding space, as well as through various types of extracellular vesicles (EVs) that transport these signals to nearby or distant target cells.</div></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":"225 ","pages":"Pages 933-939"},"PeriodicalIF":7.1,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567758","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":"Clerodane diterpene 3-deoxycaryoptinol (Clerodin) selectively induces apoptosis in human monocytic leukemia (THP-1) cells and upregulates apoptotic protein caspase-3","authors":"Bharathkumar Nagaraj ,&nbsp;Arvind Sivasubramanian ,&nbsp;Shazia Anjum Musthafa ,&nbsp;Sadiq Muhammad ,&nbsp;Aswathy Karanath Anilkumar ,&nbsp;Ganesh Munuswamy-Ramanujam ,&nbsp;Chinnaperumal Kamaraj ,&nbsp;Sivaraman Dhanasekaran ,&nbsp;Vetriselvan Subramaniyan","doi":"10.1016/j.freeradbiomed.2024.10.275","DOIUrl":"10.1016/j.freeradbiomed.2024.10.275","url":null,"abstract":"<div><div>3-deoxycaryoptinol (Clerodin) is a clerodane diterpene isolated from the leaves of <em>Clerodendrum infortunatum.</em> The present research investigates the anticancer therapeutic efficacy of clerodin in human monocytic leukemic (THP-1) cells for the first time. <em>In vitro</em> assay using THP-1 cells showed the cytotoxic ability of clerodin. Further, Annexin-V(FITC)/PI and intracellular ROS (DCFDA) assays carried out using flow cytometry, and confocal laser scanning microscopy confirmed the apoptotic potential of clerodin. Moreover, the Western blot was used to detect mitochondrial apoptosis of THP-1 cells. RT-PCR, ELISA, and Western blot analysis clearly indicated that clerodin significantly increased the expression of pro-apoptotic marker caspase-3 in THP-1 cells. clerodin also selectively targeted the G2/M phase of THP-1 cells, a key feature for anticancer molecules. Importantly, the clerodin did not exhibit cytotoxicity against human peripheral blood cells. These properties of clerodin make it a potential chemotherapeutic agent that can selectively induce apoptosis in leukemia-like cancer cells.</div></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":"225 ","pages":"Pages 925-932"},"PeriodicalIF":7.1,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142406314","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":"Itaconic acid ameliorates necrotizing enterocolitis through the TFEB-mediated autophagy-lysosomal pathway","authors":"Baozhu Chen ,&nbsp;Yufeng Liu ,&nbsp;Shunchang Luo ,&nbsp;Jialiang Zhou ,&nbsp;Yijia Wang ,&nbsp;Qiuming He ,&nbsp;Guiying Zhuang ,&nbsp;Hu Hao ,&nbsp;Fei Ma ,&nbsp;Xin Xiao ,&nbsp;Sitao Li","doi":"10.1016/j.freeradbiomed.2024.11.035","DOIUrl":"10.1016/j.freeradbiomed.2024.11.035","url":null,"abstract":"<div><div>Excessive autophagy has been implicated in the pathogenesis of necrotizing enterocolitis (NEC), yet the molecular underpinnings of the autophagy-lysosomal pathway (ALP) in NEC are not well characterized. This study aimed to elucidate alterations within the ALP in NEC by employing RNA sequencing on intestinal tissues obtained from affected infants. Concurrently, we established animal and cellular models of NEC to assess the therapeutic efficacy of itaconic acid (ITA). Our results indicate that the ALP is significantly disrupted in NEC. Notably, ITA was found to modulate the ALP, enhancing autophagic flux and lysosomal function, which consequently alleviated NEC symptoms. Further analysis revealed that ITA's beneficial effects are mediated through the promotion of TFEB nuclear translocation, thereby augmenting the ALP. These findings suggest that targeting the ALP with ITA to modulate TFEB activity may represent a viable therapeutic approach for NEC.</div></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":"226 ","pages":"Pages 251-265"},"PeriodicalIF":7.1,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686455","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":"Discovery of Gallic Acid-Based Mitochondriotropic Antioxidant Attenuates LPS-Induced Neuroinflammation.","authors":"Shubham Garg, Aniket Jana, Sanju Gupta, Mohammad Umar Arshi, Prabir Kumar Gharai, Juhee Khan, Rajsekhar Roy, Surajit Ghosh","doi":"10.1016/j.freeradbiomed.2024.11.020","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2024.11.020","url":null,"abstract":"<p><p>Mitochondria are complex organelle that plays a pivotal role in energy metabolism, regulation of stress responses, and also serve as a major hub for biosynthetic processes. In addition to their well-established function in cellular energetics, it also serves as the primary site for the origin of intracellular reactive oxygen species (ROS), which function as signaling molecules and can lead to oxidative stress when generated in excess. Moreover, mitochondrial dysfunction is one of the leading cause of neuroinflammation. In this regard, we have rationally designed a triazine derived mitochondriotropic antioxidants (Mito-TBA), based on gallic acid and triphenylphosphonium (TPP) cation to specifically target mitochondria to mitigate neuroinflammation. In vitro Mito-TBA-3 inhibits mitoautophagy, offers neuroprotection by inhibiting the LPS induced TLR-4 activation and activating the Nrf-2/ ARE pathway in PC-12 derived neurons. In vivo Mito-TBA-3 rescue memory deficit, reversed depression like behavior, inhibited neuroinflammation, and decreased proinflammatory cytokines in LPS induced neuroinflammation rat model. Overall, based on biophysical, in vitro and in vivo analysis, Mito-TBA-3 offers valuable insights as a potent therapeutic lead molecule to combat neurodegeneration even outperforming a well-known non-steroidal anti-inflammatory drug (Aspirin), it also has the potential to use as a promising therapeutic candidate for other mitochondrial oxidative stress related disorders.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":" ","pages":""},"PeriodicalIF":7.1,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681350","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":"Neuroprotective Role of CHCHD2 in Parkinson's Disease: Insights into the GPX4-Related Ferroptosis Pathway.","authors":"Fang Wang, Xuanzhuo Liu, Mingyi Chen, Xiaoxin Xu, Ying Yang, Qiuhong Xu, Huili Zhu, Anding Xu, Mahmoud A Pouladi, Xiaohong Xu","doi":"10.1016/j.freeradbiomed.2024.11.034","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2024.11.034","url":null,"abstract":"<p><p>Parkinson's disease (PD) is the second most prevalent neurodegenerative disease, characterized by pathogenesis involving mitochondrial dysfunction, oxidative stress, and ferroptosis. Unfortunately, there are currently no effective interventions to slow down the progression of PD. The mitochondrial protein coiled-coil-helix-coiled-coil-helix domain containing 2 (CHCHD2), which is implicated in neurodegeneration and serves as a biomarker for PD, has been reported to have neuroprotective effects against oxidative stress, but the potential molecular mechanisms involved remain elusive. In this study, we uncovered a critical mechanism by which CHCHD2 protected neuronal cells against oxidative stress with the ferroptosis pathway playing a pivotal role, as determined through tandem mass tags (TMT)-based proteomic analysis. The overexpression of CHCHD2 was observed to enhance cell viability, reduce levels of lipid peroxidation and reactive oxygen species (ROS), and upregulate the expression of the ferroptosis negative regulatory protein Glutathione peroxidase 4 (GPX4) in PD cells. Conversely, CHCHD2 knockdown led to reduced cell viability, elevated lipid peroxidation, and a decreased expression of GPX4. Additionally, CHCHD2 overexpression ameliorated motor function impairment, reduced α-synuclein levels, and mitigated dopaminergic (DA) neuron loss in the substantia nigra and striatum of PD mice. Importantly, we show that the inhibitory effect of CHCHD2 on ferroptosis in PD is related to the GPX4 signaling pathway. In summary, our study elucidates the neuroprotective role of CHCHD2 in regulating the GPX4-related ferroptosis pathway in PD, providing new targets and ideas for future PD drug development and therapy.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":" ","pages":""},"PeriodicalIF":7.1,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681351","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":"Hydrogen peroxide diffusion across the red blood cell membrane occurs mainly by simple diffusion through the lipid fraction","authors":"Florencia Orrico ,&nbsp;Ana C. Lopez ,&nbsp;Nicolás Silva ,&nbsp;Mélanie Franco ,&nbsp;Isabelle Mouro-Chanteloup ,&nbsp;Ana Denicola ,&nbsp;Mariano A. Ostuni ,&nbsp;Leonor Thomson ,&nbsp;Matias N. Möller","doi":"10.1016/j.freeradbiomed.2024.11.031","DOIUrl":"10.1016/j.freeradbiomed.2024.11.031","url":null,"abstract":"<div><div>Hydrogen peroxide (H₂O₂) is an oxidant produced endogenously by several enzymatic pathways. While it can cause molecular damage, H₂O₂ also plays a role in regulating cell proliferation and survival through redox signaling pathways. In the vascular system, red blood cells (RBCs) are notably efficient at metabolizing H₂O₂. In addition to a robust antioxidant defense, we recently determined that human RBCs also have a high membrane permeability to H₂O₂ that is independent of aquaporin 1 or aquaporin 3. In this work, we sought to further investigate the permeation mechanism of H₂O₂ through the membrane of human RBCs. First, we explored the role of other erythrocytic membrane proteins in H₂O₂ transport, including urea transporter B and ammonia transporter Rh proteins. However, no differences were found in H₂O₂ permeability in RBCs lacking these proteins compared to control RBCs. We then focused on the hypothesis that H₂O₂ diffuses through the lipid bilayer. To test this, we studied H₂O₂ permeability in RBCs from patients with Gaucher disease (GD), which accumulate sphingolipids in the membrane, affecting RBC morphology and deformability. We found that RBCs from GD patients exhibited lower H₂O₂ membrane permeability. In another approach, we treated normal RBCs with hexanol, which fluidizes the lipid fraction of the RBC membrane, and observed an increase in the permeability to H₂O₂. In contrast, hexanol had no effect on the rate of water efflux by aquaporin 1. Together, these results support the hypothesis that H₂O₂ diffusion through the RBC membrane occurs primarily through the lipid fraction.</div></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":"226 ","pages":"Pages 389-396"},"PeriodicalIF":7.1,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647390","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":"SIRT3 alleviates mitochondrial dysfunction and senescence in diabetes-associated periodontitis by deacetylating LRPPRC.","authors":"Hui Tang, Yi Zhou, Yu Ye, Lu Ma, Qian-Xuan Xiao, Jing-Qi Tang, Yan Xu","doi":"10.1016/j.freeradbiomed.2024.11.033","DOIUrl":"10.1016/j.freeradbiomed.2024.11.033","url":null,"abstract":"<p><p>Diabetes-associated periodontitis (DP) is recognized as an inflammatory disease that can lead to teeth loss. Uncontrolled chronic low-grade inflammation-induced senescence impairs the stemness of human periodontal stem cells (hPDLSCs). Sirtuin 3 (SIRT3), an NAD⁺-dependent deacetylase, is pivotal in various biological processes and is closely linked to aging and aging-related diseases. This study aims to explore the mechanism of SIRT3- related senescence and osteogenic differentiation of hPDLSCs under DP and explored the novelty therapeutic targets. Our study revealed that SIRT3 expression was markedly inhibited in periodontal ligament stem cells (PDLSCs) stimulated by high glucose and lipopolysaccharide. Both in vitro and in vivo, reduced SIRT3 expression accelerated cell senescence and impaired osteogenic differentiation of hPDLSCs. We demonstrated that SIRT3 binds to and deacetylates leucine-rich pentatricopeptide repeat-containing protein (LRPPRC), thereby modulating senescence. Additionally, we found that LRPPRC regulates senescence by modulating oxidative phosphorylation and oxidative stress. The activation of SIRT3 by honokiol significantly delayed senescence and promoted alveolar bone regeneration in mice after DP. Our findings indicate that the activation of SIRT3 negatively regulates hPDLSCs senescence by deacetylating LRPPRC, suggesting SIRT3 as a promising therapeutic target for DP.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":" ","pages":""},"PeriodicalIF":7.1,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142667585","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":"AQP1 mediates pancreatic β cell senescence induced by metabolic stress through modulating intracellular H₂O₂ level.","authors":"Qihui Yan, Haifeng Zhang, Yunxiao Ma, Lin Sun, Zhiyue Chen, Yinbei Zhang, Weiying Guo","doi":"10.1016/j.freeradbiomed.2024.11.029","DOIUrl":"10.1016/j.freeradbiomed.2024.11.029","url":null,"abstract":"<p><p>Metabolic stress-induced pancreatic β cell senescence plays a pivotal role in the type 2 diabetes progression, and yet the precise molecular mechanisms remain elusive. Through cellular experiments and bioinformatics analyses, we identified aquaporin 1(AQP1)-mediated transmembrane transport of hydrogen peroxide as a key driver of glucolipotoxicity-induced senescence in MIN6 cells. A PPI network analysis was used to cross-reference 17 differentially expressed genes associated with type 2 diabetes from three independent GEO databases with 188 stress-induced senescence-related genes from CellAge. AQP1 was revealed as a critical molecular nexus connecting diabetes, oxidative stress, and cellular senescence. AQP1 inhibition, through Bacopaside II and si-AQP1, significantly reduced critical senescence markers in MIN6 cells, demonstrated by the reversal of glucolipotoxicity-induced upregulation of p16, p21, and p-γH2A.X, activation of the senescence-associated secretory phenotype genes, and an elevated percentage of senescence-associated-β-galactosidase positive cells. These effects were primarily mediated through oxidative stress MAPK signaling pathway modulation. AQP1 inhibition is crucial in alleviating glucolipotoxicity-induced β cell senescence. It underscores its potential as a molecular target for therapeutic strategies to delay pancreatic β cell senescence by modulating antioxidant pathways during metabolic stress.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":" ","pages":"171-184"},"PeriodicalIF":7.1,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647374","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}