Free Radical Biology and Medicine最新文献

{"title":"Exercise Performance and Health: Role of GLUT4^‡.","authors":"Sean L McGee, Mark Hargreaves","doi":"10.1016/j.freeradbiomed.2024.09.004","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2024.09.004","url":null,"abstract":"<p><p>The glucose transporter GLUT4 is integral for optimal skeletal muscle performance during exercise, as well as for metabolic health. Physiological regulation of GLUT4 translocation during exercise and increased GLUT4 expression following exercise involves multiple, redundant signalling pathways. These include effects of reactive oxygen species (ROS). ROS contribute to GLUT4 translocation that increases skeletal muscle glucose uptake during exercise and stimulate signalling pathways that increase GLUT4 expression. Conversely, ROS can also inhibit GLUT4 translocation and expression in metabolic disease states. The opposing roles of ROS in GLUT4 regulation are ultimately linked to the metabolic state of skeletal muscle and the intricate mechanisms involved give insights into pathways critical for exercise performance and implicated in metabolic health and disease.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142145398","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":"Diabesity alters the protective effects of estrogens on endothelial function through adipose tissue secretome.","authors":"Melanie Raquel Martínez-Cignoni, Agustí González-Vicens, Andrea Morán-Costoya, Emilia Amengual-Cladera, Magdalena Gianotti, Adamo Valle, Ana María Proenza, Isabel Lladó","doi":"10.1016/j.freeradbiomed.2024.09.001","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2024.09.001","url":null,"abstract":"<p><p>Estrogens have a well-known protective role in the development of the metabolic syndrome. Nevertheless, recent epidemiological data question the cardioprotective effect of estrogens in obese and diabetic women. In this context, white adipose tissue (WAT) becomes dysfunctional, which has an impact on the cardiovascular system. The aim of the study was to elucidate the role of 17β-estradiol (E2) in the interplay between adipose tissue and endothelial function in an animal model of diabesity. We used ZDF (fa/fa) female rats subjected to ovariectomy (OVA), OVA+E2 or sham operated, as well as non-obese non-diabetic ZDF (fa/+) rats. Endothelial function and vascular remodeling markers were assessed in the aorta, while mitochondrial function, oxidative stress, and adiponectin production were analyzed in gonadal WAT. Conditioned media from gonadal WAT explants were used to assess the effects of WAT secretome on HUVEC. Additionally, the adiponectin receptor agonist AdipoRON and E2 were utilized to examine potential interactions. Ovariectomy ameliorated the WAT dysfunction associated to the obese and diabetic state and promoted adiponectin secretion, effects that were linked to a reduction of endothelial dysfunction and inflammatory markers in the aorta of OVA rats and in HUVEC treated with OVA-conditioned media. Our findings provide evidence supporting the idea that in the context of obesity and diabetes, ovariectomy improves WAT secretome and positively impacts endothelial function, suggesting a detrimental role for E2. Additionally, our results point to adiponectin as the primary driver of the effects exerted by ovariectomy on the adipovascular axis.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142145396","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":"Dual behaviour of histidine during sensitized photo-oxidation of model compounds and proteins.","authors":"K J Frąckowiak, M T Ignasiak, M Grzechowiak, E Fuentes-Lemus, L F Gamon, T Pędziński, P M Hägglund, M Jaskolski, M J Davies, B Marciniak","doi":"10.1016/j.freeradbiomed.2024.08.040","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2024.08.040","url":null,"abstract":"<p><p>Histidine (His) photo-oxidation has been widely investigated with several transient and stable products characterized, especially for aerobic conditions. Due to its role and structure, His-side chain can be a key player in the quenching of excited states such as the triplet state of the photosensitizer 3-carboxybenzophenone (³CB*). The capacity of His and its derivatives to quench ³CB* under anaerobic conditions are characterized in the current study by laser flash photolysis, with the resulting oxidation products examined by mass spectrometry to determine the reaction mechanism. The latter include adducts of the 3-carboxybenzophenone ketyl radical (CBH^•) to the imidazole ring (Imid-CH₂-CBH), His-His dimers, and other products with lower yields. The data obtained with model compounds are compared to those obtained with more complicated systems, including the peptide Exendin-4, and the protein MtHpt1. The data obtained from transient spectroscopy and product analyses indicate that two CB* quenching mechanisms occur: (i) proton-coupled electron transfer (as reported previously) yielding radicals that can recombine to give His-His dimers and CBH-adducts, and (ii) energy transfer yielding ³His* undergoing further reaction leading to formation of Imidazyl-CH₂-CBH adduct. The latter, unexpected process only occurs when His and its derivatives have a free α-amino group. This process yielded a novel adduct between the imidazole ring and the CBH^• formed by sensitizer reduction.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142145397","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 Elabela-APJ axis attenuates sepsis-induced myocardial dysfunction by reducing pyroptosis by balancing the formation and degradation of autophagosomes.","authors":"Shuai Liu, Fu-Zhong Liu, Jue-Yue Yan, Xing Fang, Zhi-Peng Xu, Hong-Liu Cai, Ying-Jun Yang, Yong-Wei Yu","doi":"10.1016/j.freeradbiomed.2024.09.003","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2024.09.003","url":null,"abstract":"<p><strong>Background: </strong>Sepsis is a life-threatening severe inflammatory reaction caused by the host's dysregulated response to infection. Sepsis-induced myocardial dysfunction (SIMD) has been confirmed to occur in 50% of patients with septic shock. Currently, the pathophysiological mechanism of SIMD is complex, and there is no targeted treatment. Elabela is another endogenous ligand of Aplnr (APJ). The protective effect of APJ on the heart has been proven. Elabela (Ela) has been shown to have a variety of cardiovascular protective effects. However, there are no studies demonstrating the protective effect of Ela-APJ axis on SIMD.</p><p><strong>Materials and methods: </strong>In vivo, C57BL/J mice were injected subcutaneously with 1 mg/kg/d Ela for 2 weeks, and in vitro, AC16 cells were treated with 1 μM Ela for 24 h. A 7-0 thread was used to ligate the distal end of the cecum, followed by puncture with a 20-gauge needle. Once a small amount of fluid leaks out, release the cecum back into the abdominal cavity. We measured the survival rates of the mice, performed ultrasound on their hearts, and evaluated the effects of the treatments. The serum and cell supernatant were extracted to detect myocardial injury markers and pyroptosis-related indicators. Western blotting was used to detect autophagy and pyroptosis-related protein. Molecular docking and other experiments were also used to detect changes in related proteins.</p><p><strong>Results: </strong>In vivo, Ela significantly improved the survival rate of septic mice, improved cardiac function, and reduced the production of myocardial injury markers, oxidative stress and pyroptosis. In vitro, Ela unblocked autophagy flow by affecting TFEB transcription. Autophagy reduces inflammation and oxidative stress by selectively degrading inflammatory bodies and ultimately alleviates pyroptosis.</p><p><strong>Conclusion: </strong>We had demonstrated for the first time that in sepsis, Ela promoted the degradation of inflammasomes, reduced oxidative stress, and inhibited the occurrence of pyroptosis by unblocking autophagy flow.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142145505","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":"Maternal riboflavin deficiency causes embryonic defects by activating ER stress-induced hepatocyte apoptosis pathway.","authors":"Bo Zhang, Ke-Xin Gao, Jun-Ting Cao, Guang-Nan Xing, Zhan-Qing Ji, Zhi-Nan Li, Ya-Ting Li, Jaap Keijer, Ming Xie, Zheng-Kui Zhou, Shui-Sheng Hou, Jing Tang","doi":"10.1016/j.freeradbiomed.2024.09.002","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2024.09.002","url":null,"abstract":"<p><p>Riboflavin deficiency (RD) induces liver damage, abnormal embryonic development, and high mortality. We hypothesized that the phenotype could be rescued by inhibiting ER stress. The objectives of the present study were to investigate the underlying molecular mechanisms of RD-induced embryonic defects using in vitro and in vivo models. Primary duck embryonic hepatocytes were treated with an ER stress inhibitor (4-PBA) or transfected with CHOP siRNA, and cultured in RD medium and riboflavin-sufficient (CON) medium for 8 days. Laying ducks (n = 20 cages/diet, 1 bird/cage) were fed an RD diet or CON diet for 14 wk, and the eggs were collected for hatching. At day 7 of incubation, the fertilized RD eggs were injected with or without 4-PBA into the yolk. RD decreased cell number and cell viability compared to the CON group, induced oxidative stress and apoptosis in primary duck embryonic hepatocytes. However, after being treated with an ER stress inhibitor (4-PBA) or transfected with CHOP siRNA, the apoptosis rate in RD hepatocytes decreased by 60.6% and 86.1%, respectively, being equal to the CON. These results indicated that RD-induced hepatocyte apoptosis is mediated by ER stress and the CHOP pathway. In vivo, RD embryos showed low hatchability, abnormal development, liver damage, ER stress, and apoptosis compared to the CON group. However, 4-PBA administration, as a model of ER stress inhibition, substantially restored embryonic development and alleviated liver damage in the RD group, including ER stress and apoptosis. Notably, hatchability in the RD group increased from 21.7% to 72.7% after 4-PBA treatment, though it remained less than the CON group (87.7%). These results implicated ER stress-CHOP-apoptosis pathway as molecular mechanisms underlying RD-induced abnormal embryonic development and death, this target with potential for therapy or intervention.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142145399","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":"Transcriptomic analysis reveals the mechanism of isorhamnetin in the treatment of diabetes mellitus erectile dysfunction","authors":"","doi":"10.1016/j.freeradbiomed.2024.08.043","DOIUrl":"10.1016/j.freeradbiomed.2024.08.043","url":null,"abstract":"<div><h3>Purpose</h3><p>Exploring the therapeutic effect and mechanism of isorhamnetin in the treatment of DMED.</p></div><div><h3>Methods</h3><p>Using a high glucose environment to induce endothelial cells damage in the corpus cavernosum, and combining with intervention agents such as ferroptosis inhibitors to observe the process of cell damage and repair, evaluating cell status through CCK-8 and DAPI; To establish the STZ-induced diabetes rat model and detect the erectile function and tissue changes; Perform transcriptomic sequencing on rat models and samples treated with isorhamnetin to analyze differentially expressed genes and their GO functions; Identify critical pathways by combining with the ferroptosis database; Flow cytometry was used to detect ROS and mitochondrial membrane potential, and RT-PCR was used to verify gene expression, Seahorse detects mitochondrial oxygen consumption rate, revealing the mechanism of action of isorhamnetin.</p></div><div><h3>Results</h3><p>Ferroptosis inhibitors and isorhamnetin can effectively reverse the damage of corpus cavernosum endothelial cells induced by high glucose and ferroptosis agonists. Isorhamnetin has the ability to reinstate the erectile function of diabetic rats, while enhancing the quantity of endothelial cells and refining the morphology of collagen fibers. Immunohistochemistry revealed that ferroptosis existed in the penis tissue of diabetes rats. Transcriptomic analysis showed that isorhamnetin improves gene expression in DM rats by regulating genes such as GFER, IGHM, GPX4 and HMOX1, involving multiple pathways and biological processes. Flow cytometry and RT-PCR confirmed that isorhamnetin can reduce reactive oxygen species levels, restore essential gene expression, improve mitochondrial membrane potential, and alleviate oxidative stress and ferroptosis. Seahorse detection found that isorhamnetin can restore mitochondrial oxygen consumption rate.</p></div><div><h3>Conclusion</h3><p>Isorhamnetin attenuates high glucose damage to cavernous endothelial cells by inhibiting ferroptosis and oxidative stress, restores erectile function and improves tissue morphology in diabetic rats, and its multi-pathway and multi-targeting regulatory mechanism suggests that it is promising to be an effective drug for the treatment of DMED.</p></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142132285","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":"Systematic analysis of the global characteristics and reciprocal effects of S-nitrosylation and S-persulfidation in the human proteome","authors":"","doi":"10.1016/j.freeradbiomed.2024.08.041","DOIUrl":"10.1016/j.freeradbiomed.2024.08.041","url":null,"abstract":"<div><p>Gasotransmitter-mediated cysteine post-translational modifications, including S-nitrosylation (SNO) and S-persulfidation (SSH), play crucial roles and interact in various biological processes. However, there has been a delay in appreciating the interactional rules between SNO and SSH. Here, all human S-nitrosylated and S-persulfidated proteomic data were curated, and comprehensive analyses from multiple perspectives, including sequence, structure, function, and exact protein impacts (e.g., up-/down-regulation), were performed. Although these two modifications collectively regulated a wide array of proteins to jointly maintain redox homeostasis, they also exhibited intriguing differences. First, SNO tended to be more accessible and functionally clustered in pathways associated with cell damage repair and other protein modifications, such as phosphorylation and ubiquitination. Second, SSH preferentially targeted cysteines in disulfide bonds and modulated tissue development and immune-related pathways. Finally, regardless of whether SNO and SSH occupied the same position of a given protein, their combined effect tended to be suppressive when acting synergistically; otherwise, SNO likely inhibited while SSH activated the target protein. Indeed, a side-by-side comparison of SNO and SSH shed light on their globally reciprocal effects and provided a reference for further research on gasotransmitter-mediated biological effects.</p></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0891584924006361/pdfft?md5=19814a8fa1580d064560c27af95452fc&pid=1-s2.0-S0891584924006361-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142105992","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":"Hydrogen regulated pyroptosis through NLRP3-GSDMD pathway to improve airway mucosal oxidative stress injury induced by endotracheal tube cuff compression","authors":"","doi":"10.1016/j.freeradbiomed.2024.08.035","DOIUrl":"10.1016/j.freeradbiomed.2024.08.035","url":null,"abstract":"<div><p>The cuff of endotracheal tube (ETT) is an indispensable device for establishing an artificial airway, yet cuff-induced compression often causes damage to the airway mucosa. The mechanism of this damage involves mucosal compression ischemia and the oxidative stress injury following reperfusion. Currently, there is a lack of effective strategies to protect the mucosa. Hydrogen, as a natural antioxidant, has demonstrated significant potential in the prevention and treatment of oxidative stress injuries. This study aimed to determine the protective effects of hydrogen on compressed airway mucosa. We found that the damage to the airway mucosa caused by ETT cuff compression was associated with oxidative stress-induced pyroptosis of airway epithelial cells. Inhalation of hydrogen effectively reduced the levels of reactive oxygen species, significantly ameliorating changes in epithelial cell pyroptosis, and this protective effect is linked to the inhibition of the NLRP3-GSDMD pathway. Further cellular studies, involving knockdown and overexpression of NLRP3, clarified that hydrogen exerts its protective effects on the airway mucosa by inhibiting epithelial cell pyroptosis. Additionally, we observed that using hydrogen-rich saline to inflate the ETT cuff in patients under general anesthesia significantly reduced postoperative sore throat. This study confirms that hydrogen effectively enhances tolerance of airway mucosa to oxidative stress injuries, offering a potential preventive and therapeutic strategy for protecting the airway mucosa in patients undergoing endotracheal intubation.</p></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142105989","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":"On the binding of auranofin to Prdx6 and its potential role in cancer cell sensitivity to treatment","authors":"","doi":"10.1016/j.freeradbiomed.2024.08.042","DOIUrl":"10.1016/j.freeradbiomed.2024.08.042","url":null,"abstract":"<div><p>In this study, we demonstrate that ferroptosis is a component of the cell death mechanism induced by auranofin in HT-1080 cells, in contrast to the gold(III) compounds [Au(phen)Cl₂]PF₆ and [Au(bnpy)Cl₂]. Additionally, we identify a potential role of Prdx6 in modulating the sensitivity of A-375 cells to auranofin treatment, whereas the gold(III) compounds evaluated here exhibit Prdx6-independent cytotoxicity. Finally, using mass spectrometry, we show that auranofin binds selectively to the catalytic Cys47 residue of Prdx6 <em>in vitro</em> under acidic conditions. No binding was observed with the C47S mutant or at neutral pH.</p></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142105991","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":"Targeting ALDH2 to augment platinum-based chemosensitivity through ferroptosis in lung adenocarcinoma","authors":"","doi":"10.1016/j.freeradbiomed.2024.08.026","DOIUrl":"10.1016/j.freeradbiomed.2024.08.026","url":null,"abstract":"<div><p>Ferroptosis is a regulated cell death driven by iron-dependent lipid peroxidation and associated with drug resistance in lung adenocarcinoma (LUAD). It's found that aldehyde dehydrogenase 2 (ALDH2), which is highly mutated in East Asian populations, is correlated with response to chemotherapy in LUAD patients. The rs671 variant knock-in, downregulation, and pharmacological inhibition of ALDH2 render LUAD cells more vulnerable to ferroptosis inducers and platinum-based chemotherapy. ALDH2 inhibits ferroptosis through the detoxification of 4-hydroxynonenal and malondialdehyde, the product of lipid peroxidation, as well as the production of NADH at the same time. Besides, ALDH2 deficiency leads to elevated intracellular pH (pHi), thus inhibiting the ERK/CREB1/GPX4 axis. Interestingly, ALDH2 is also regulated by CREB1, and the ALDH2 enzyme activity was decreased with elevated pHi. What's more, the elevated pHi caused by impaired ALDH2 activity promotes the biosynthesis of lipid droplets to counteract ferroptosis. At last, the effect of ALDH2 on ferroptosis and chemosensitivity is confirmed in patient-derived organoids and xenograft models. Collectively, this study demonstrates that ALDH2 deficiency confers sensitivity to platinum through ferroptosis in LUAD, and targeting ALDH2 is a promising new strategy to enhance the sensitivity of platinum-based chemotherapy for the treatment of LUAD patients.</p></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142105993","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}