MitochondrionPub Date : 2024-06-15DOI: 10.1016/j.mito.2024.101921
Cuicui Zhuang , Yang Liu , Herman W. Barkema , Zhaoju Deng , Jian Gao , John P. Kastelic , Bo Han , Jianhai Zhang
{"title":"Escherichia coli infection induces ferroptosis in bovine mammary epithelial cells by activating the Wnt/β-catenin pathway-mediated mitophagy","authors":"Cuicui Zhuang , Yang Liu , Herman W. Barkema , Zhaoju Deng , Jian Gao , John P. Kastelic , Bo Han , Jianhai Zhang","doi":"10.1016/j.mito.2024.101921","DOIUrl":"10.1016/j.mito.2024.101921","url":null,"abstract":"<div><p>Iron overload causes mitochondrial damage, and then activates mitophagy, which may directly trigger and amplify ferroptosis. Our objective was to investigate whether <em>Escherichia coli</em> (<em>E. coli</em>) isolated from clinical bovine mastitis induces ferroptosis in bovine mammary epithelial cells (bMECs) and if so, the underlying regulatory mechanism. <em>E. coli</em> infection caused mitochondrial damage, mitophagy, and ferroptosis. Rapamycin and chloroquine increased and suppressed ferroptosis, respectively, in <em>E. coli</em>-treated bMECs. Moreover, <em>E. coli</em> infection activated the Wnt/β-catenin pathway, but foscenvivint alleviated it. In conclusion, <em>E. coli</em> infection induced ferroptosis through activation of the Wnt/β-catenin pathway-promoted mitophagy, and it also suppressed GPX4 expression.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"78 ","pages":"Article 101921"},"PeriodicalIF":4.4,"publicationDate":"2024-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141391117","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}
MitochondrionPub Date : 2024-06-12DOI: 10.1016/j.mito.2024.101918
Jia-Yi Song , Yong Jia , Hao Han , Xue-Han Yang , Jing Zhang , Qiang Zhang , Su-Shan Wang , Chun-Yan Wang , Li Chen , Ming Zhang
{"title":"Increased expression of SLC25A18 is associated with Alzheimer’s disease and is involved in Aβ42-induced mitochondrial dysfunction and apoptosis in neuronal cells","authors":"Jia-Yi Song , Yong Jia , Hao Han , Xue-Han Yang , Jing Zhang , Qiang Zhang , Su-Shan Wang , Chun-Yan Wang , Li Chen , Ming Zhang","doi":"10.1016/j.mito.2024.101918","DOIUrl":"10.1016/j.mito.2024.101918","url":null,"abstract":"<div><p>Alzheimer’s disease (AD) is currently one of the most serious public health concerns in the world. However, the best approach to treat AD has yet to be discovered, implying that we must continue to work hard to find new AD target genes. In this study, we further analysed Gene Expression Omnibus (GEO) data and discovered that the expression of the Mitochondria glutamate carrier SLC25A18 is associated with AD by screening the differentially expressed genes in different regions of the brains of Alzheimer’s disease patients. To verify the expression of SLC25A18 during Alzheimer’s disease development, we analysed animal models (5×FAD transgenic AD animal model, chemically induced AD animal model, natural ageing animal model), and the results showed that the expression of SLC25A18 was increased in animal models of AD. Further investigation of the different regions found that SLC25A18 expression was elevated in the EC, TeA, and CA3, and expressed in neurons. Next, We found that Aβ42 treatment elevated SLC25A18 expression in Neuro 2A cells. Reducing SLC25A18 expression attenuated mitochondrial dysfunction and neuronal apoptosis caused by Aβ42. Overexpression of SLC25A18 increased ATP and intracellular superoxide anions but decreased mitochondrial membrane potential. The results indicate that SLC25A18 affects mitochondrial function and neuronal apoptosis, and is related to AD, which makes it a potential target for treating brain dysfunction.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"78 ","pages":"Article 101918"},"PeriodicalIF":4.4,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S156772492400076X/pdfft?md5=a6d038576477b989162d7b765a2d4446&pid=1-s2.0-S156772492400076X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141317690","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}
MitochondrionPub Date : 2024-06-12DOI: 10.1016/j.mito.2024.101920
Yizhi Zhong , Siwei Xia , Gaojian Wang , Qinxue Liu , Fengjie Ma , Yijin Yu , Yaping Zhang , Lu Qian , Li Hu , Junran Xie
{"title":"The interplay between mitophagy and mitochondrial ROS in acute lung injury","authors":"Yizhi Zhong , Siwei Xia , Gaojian Wang , Qinxue Liu , Fengjie Ma , Yijin Yu , Yaping Zhang , Lu Qian , Li Hu , Junran Xie","doi":"10.1016/j.mito.2024.101920","DOIUrl":"10.1016/j.mito.2024.101920","url":null,"abstract":"<div><p>Mitochondria orchestrate the production of new mitochondria and the removal of damaged ones to dynamically maintain mitochondrial homeostasis through constant biogenesis and clearance mechanisms. Mitochondrial quality control particularly relies on mitophagy, defined as selective autophagy with mitochondria-targeting specificity. Most ROS are derived from mitochondria, and the physiological concentration of mitochondrial ROS (mtROS) is no longer considered a useless by-product, as it has been proven to participate in immune and autophagy pathway regulation. However, excessive mtROS appears to be a pathogenic factor in several diseases, including acute lung injury (ALI). The interplay between mitophagy and mtROS is complex and closely related to ALI. Here, we review the pathways of mitophagy, the intricate relationship between mitophagy and mtROS, the role of mtROS in the pathogenesis of ALI, and their effects and related progression in ALI induced by different conditions.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"78 ","pages":"Article 101920"},"PeriodicalIF":3.9,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141321214","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}
MitochondrionPub Date : 2024-06-12DOI: 10.1016/j.mito.2024.101919
Chenchen Fan , Yanbei Ren , Wen Zhang , Jing Wen , Wenjia Zhang , Shumeng Lin , Yidong Bai , Tiansheng Zheng , Baigenzhin Abay , Ming Li , Lihong Fan
{"title":"Thyroid hormone enhances efficacy of cisplatin in lung cancer patients via down-regulating GLUT1 expression and reversing the Warburg effect","authors":"Chenchen Fan , Yanbei Ren , Wen Zhang , Jing Wen , Wenjia Zhang , Shumeng Lin , Yidong Bai , Tiansheng Zheng , Baigenzhin Abay , Ming Li , Lihong Fan","doi":"10.1016/j.mito.2024.101919","DOIUrl":"10.1016/j.mito.2024.101919","url":null,"abstract":"<div><p>Cisplatin (CDDP) is a standard non-small cell lung cancer (NSCLC) chemotherapy, but its efficacy is hampered by resistance, partly due to the Warburg effect. This study investigates how thyroid hormones enhance the Warburg effect, increasing sensitivity to cisplatin in lung cancer. Clinical data from advanced NSCLC patients were analyzed based on thyroid hormone levels, categorizing patients into high and low groups. Cellular experiments involved Control, 10uM CDDP, 10uM CDDP + 0.1uM T3, and 10uM CDDP + 0.1uM T4 categories. Parameters were measured in A549 and PC9 lung cancer cells, including proliferation, apoptosis, mitochondrial membrane potential, ROS production, glycolysis enzyme activity, lactic acid level, and ATP content. Gene and protein expressions were assessed using qPCR and Western Blot. Analysis revealed higher FT3 levels correlated with prolonged progression-free survival before chemotherapy (median PFS: high FT3 group = 12.67 months, low FT3 group = 7.03 months, p = 0.01). Cellular experiments demonstrated that thyroid hormones increase lung cancer cell sensitivity to cisplatin, inhibiting proliferation and enhancing efficacy. The mechanism involves thyroid hormones and cisplatin jointly down-regulating MSI1/AKT/GLUT1 expression, reducing lactic acid and glycolysis. This Warburg effect reversal boosts ATP levels, elevates ROS, and decreases MMP, enhancing cisplatin effectiveness in A549 and PC9 cells. In conclusion, elevated free T3 levels in advanced NSCLC patients correlate with prolonged progression-free survival under cisplatin chemotherapy. Cellular experiments reveal that thyroid hormones enhance lung cancer cell sensitivity to cisplatin by reversing the Warburg effect, providing a mechanistic basis for improved therapeutic outcomes.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"78 ","pages":"Article 101919"},"PeriodicalIF":3.9,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141321215","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}
MitochondrionPub Date : 2024-06-06DOI: 10.1016/j.mito.2024.101908
Zeyu Chen , Daniel Rayner , Robert Morton , Laura Banfield , Guillaume Paré , Michael Chong
{"title":"The role of mitochondrial genes in ischemia-reperfusion injury: A systematic review of experimental studies","authors":"Zeyu Chen , Daniel Rayner , Robert Morton , Laura Banfield , Guillaume Paré , Michael Chong","doi":"10.1016/j.mito.2024.101908","DOIUrl":"10.1016/j.mito.2024.101908","url":null,"abstract":"<div><p>Mitochondrial dysfunction contributes to pathological conditions like ischemia–reperfusion (IR) injury. To address the lack of effective therapeutic interventions for IR injury and potential knowledge gaps in the current literature, we systematically reviewed 3800 experimental studies across 5 databases and identified 20 mitochondrial genes impacting IR injury in various organs. Notably, <em>CyPD, Nrf2,</em> and <em>GPX4</em> are well-studied genes consistently influencing IR injury outcomes. Emerging genes like <em>ALDH2, BNIP3,</em> and <em>OPA1</em> are supported by human genetic evidence, thereby warranting further investigation. Findings of this review can inform future research directions and inspire therapeutic advancements.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"78 ","pages":"Article 101908"},"PeriodicalIF":4.4,"publicationDate":"2024-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1567724924000667/pdfft?md5=d2423e2c09b93620a942ba7e3ae8febf&pid=1-s2.0-S1567724924000667-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141288320","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}
MitochondrionPub Date : 2024-06-04DOI: 10.1016/j.mito.2024.101909
Damien Roussel , Nathan Roussel , Yann Voituron , Benjamin Rey
{"title":"Liver mitochondrial coupling efficiency and its relationship to oxidative capacity and adenine nucleotide translocase content: A comparative study among crocodiles, birds and mammals","authors":"Damien Roussel , Nathan Roussel , Yann Voituron , Benjamin Rey","doi":"10.1016/j.mito.2024.101909","DOIUrl":"10.1016/j.mito.2024.101909","url":null,"abstract":"<div><p>The primary objective of this study was to assess whether adenine nucleotide translocase (ANT) content could be associated with phylogenetic disparities in mitochondrial coupling efficiency, within liver mitochondria obtained from rats, crocodiles, and ducklings. Our measurements included mitochondrial membrane conductance, ANT content, and oxidative phosphorylation fluxes at various steady-state rates. We observed significant variations in liver mitochondrial coupling efficiency across the three species. These variations correlated with interspecific differences in mitochondrial oxidative capacity and, to a lesser extent, the ANT content of liver mitochondria. These findings expand upon previous research by highlighting the pivotal role of oxidative capacity and ANT in modulating mitochondrial efficiency on an interspecific scale.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"78 ","pages":"Article 101909"},"PeriodicalIF":4.4,"publicationDate":"2024-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141284232","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}
MitochondrionPub Date : 2024-05-24DOI: 10.1016/j.mito.2024.101906
Moataz Dowaidar
{"title":"Cell-penetrating peptides with nanoparticles hybrid delivery vectors and their uptake pathways","authors":"Moataz Dowaidar","doi":"10.1016/j.mito.2024.101906","DOIUrl":"10.1016/j.mito.2024.101906","url":null,"abstract":"<div><p>Cell-penetrating peptides (CPPs) are molecules that improve the cellular uptake of various molecular payloads that do not easily traverse the cellular membrane. CPPs can be found in pharmaceutical and medical products. The vast majority of cell-penetrating chemicals that are discussed in published research are peptide based. The paper also delves into the various applications of hybrid vectors. Because CPPs are able to carry cargo across the cellular membrane, they are a viable candidate for use as a suitable carrier for a wide variety of cargoes, such as siRNA, nanoparticles, and others. In which we discuss the CPPs, their classification, uptake mechanisms, hybrid vector systems, nanoparticles and their uptake mechanisms, etc. Further in this paper, we discuss CPPs conjugated to Nanoparticles, Combining CPPs with lipids and polymeric Nanoparticles in A Conjugated System, CPPs conjugated to nanoparticles for therapeutic purposes, and potential therapeutic uses of CPPs as delivery molecules. Also discussed the preclinical and clinical use of CPPS, intracellular trafficking of nanoparticles, and activatable and bioconjugated CPPs.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"78 ","pages":"Article 101906"},"PeriodicalIF":4.4,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141140310","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}
MitochondrionPub Date : 2024-05-24DOI: 10.1016/j.mito.2024.101905
Johan L.K. Van Hove , Marisa W. Friederich , Daniella H. Hock , David A. Stroud , Nikeisha J. Caruana , Uwe Christians , Björn Schniedewind , Cole R. Michel , Richard Reisdorph , Edwin D.J. Lopez Gonzalez , Charles Brenner , Tonia E. Donovan , Jessica C. Lee , Kathryn C. Chatfield , Austin A. Larson , Peter R. Baker II , Shawn E. McCandless , Meghan F. Moore Burk
{"title":"ACAD9 treatment with bezafibrate and nicotinamide riboside temporarily stabilizes cardiomyopathy and lactic acidosis","authors":"Johan L.K. Van Hove , Marisa W. Friederich , Daniella H. Hock , David A. Stroud , Nikeisha J. Caruana , Uwe Christians , Björn Schniedewind , Cole R. Michel , Richard Reisdorph , Edwin D.J. Lopez Gonzalez , Charles Brenner , Tonia E. Donovan , Jessica C. Lee , Kathryn C. Chatfield , Austin A. Larson , Peter R. Baker II , Shawn E. McCandless , Meghan F. Moore Burk","doi":"10.1016/j.mito.2024.101905","DOIUrl":"10.1016/j.mito.2024.101905","url":null,"abstract":"<div><p>Pathogenic <em>ACAD9</em> variants cause complex I deficiency. Patients presenting in infancy unresponsive to riboflavin have high mortality. A six-month-old infant presented with riboflavin unresponsive lactic acidosis and life-threatening cardiomyopathy. Treatment with high dose bezafibrate and nicotinamide riboside resulted in marked clinical improvement including reduced lactate and NT-pro-brain type natriuretic peptide levels, with stabilized echocardiographic measures. After a long stable period, the child succumbed from cardiac failure with infection at 10.5 months. Therapy was well tolerated. Peak bezafibrate levels exceeded its EC<sub>50</sub>. The clinical improvement with this treatment illustrates its potential, but weak PPAR agonist activity of bezafibrate limited its efficacy.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"78 ","pages":"Article 101905"},"PeriodicalIF":4.4,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141140945","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}
MitochondrionPub Date : 2024-05-21DOI: 10.1016/j.mito.2024.101903
Lucie J. Lamačová, Jan Trnka
{"title":"Chelating mitochondrial iron and copper: Recipes, pitfalls and promise","authors":"Lucie J. Lamačová, Jan Trnka","doi":"10.1016/j.mito.2024.101903","DOIUrl":"10.1016/j.mito.2024.101903","url":null,"abstract":"<div><p>Iron and copper chelation therapy plays a crucial role in treating conditions associated with metal overload, such as hemochromatosis or Wilson’s disease. However, conventional chelators face challenges in reaching the core of iron and copper metabolism – the mitochondria. Mitochondria-targeted chelators can specifically target and remove metal ions from mitochondria, showing promise in treating diseases linked to mitochondrial dysfunction, including neurodegenerative diseases and cancer. Additionally, they serve as specific mitochondrial metal sensors. However, designing these new molecules presents its own set of challenges. Depending on the chelator’s intended use to prevent or to promote redox cycling of the metals, the chelating moiety must possess different donor atoms and an optimal value of the electrode potential of the chelator–metal complex. Various targeting moieties can be employed for selective delivery into the mitochondria. This review also provides an overview of the current progress in the design of mitochondria-targeted chelators and their biological activity investigation.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"78 ","pages":"Article 101903"},"PeriodicalIF":4.4,"publicationDate":"2024-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141081812","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}
MitochondrionPub Date : 2024-05-21DOI: 10.1016/j.mito.2024.101901
Rafael David Souto de Azevedo , Kivia Vanessa Gomes Falcão , Sinara Monica Vitalino de Almeida , Marlyete Chagas Araújo , Reginaldo Correia Silva-Filho , Maria Bernadete de Souza Maia , Ian Porto Gurgel do Amaral , Ana Catarina Rezende Leite , Ranilson de Souza Bezerra
{"title":"The tissue-specific nature of physiological zebrafish mitochondrial bioenergetics","authors":"Rafael David Souto de Azevedo , Kivia Vanessa Gomes Falcão , Sinara Monica Vitalino de Almeida , Marlyete Chagas Araújo , Reginaldo Correia Silva-Filho , Maria Bernadete de Souza Maia , Ian Porto Gurgel do Amaral , Ana Catarina Rezende Leite , Ranilson de Souza Bezerra","doi":"10.1016/j.mito.2024.101901","DOIUrl":"10.1016/j.mito.2024.101901","url":null,"abstract":"<div><p>Zebrafish are a powerful tool to study a myriad of experimental conditions, including mitochondrial bioenergetics. Considering that mitochondria are different in many aspects depending on the tissue evaluated, in the zebrafish model there is still a lack of this investigation. Especially for juvenile zebrafish. In the present study, we examined whether different tissues from zebrafish juveniles show mitochondrial density- and tissue-specificity comparing brain, liver, heart, and skeletal muscle (SM). The liver and brain complex IV showed the highest O<sub>2</sub> consumption of all ETC in all tissues (10x when compared to other respiratory complexes). The liver showed a higher potential for ROS generation. In this way, the brain and liver showed more susceptibility to O<sub>2</sub><sup><img>−</sup> generation when compared to other tissues. Regarding Ca<sup>2+</sup> transport, the brain showed greater capacity for Ca<sup>2+</sup> uptake and the liver presented low Ca<sup>2+</sup> uptake capacity. The liver and brain were more susceptible to producing <sup><img></sup>NO. The enzymes SOD and Catalase showed high activity in the brain, whereas GPx showed higher activity in the liver and CS in the SM. TEM reveals, as expected, a physiological diverse mitochondrial morphology. The essential differences between zebrafish tissues investigated probably reflect how the mitochondria play a diverse role in systemic homeostasis. This feature may not be limited to normal metabolic functions but also to stress conditions. In summary, mitochondrial bioenergetics in zebrafish juvenile permeabilized tissues showed a tissue-specificity and a useful tool to investigate conditions of redox system imbalance, mainly in the liver and brain.</p></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"77 ","pages":"Article 101901"},"PeriodicalIF":4.4,"publicationDate":"2024-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141081816","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}