Journal of cell science最新文献_第6页

A dual-purification system to isolate mitochondrial subpopulations. 双重纯化系统分离线粒体亚群。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-05-01 Epub Date: 2025-04-14 DOI: 10.1242/jcs.263693

Corey N Cunningham, Jonathan G Van Vranken, Jakeline Larios, Katarina Heyden, Steven P Gygi, Jared Rutter

{"title":"A dual-purification system to isolate mitochondrial subpopulations.","authors":"Corey N Cunningham, Jonathan G Van Vranken, Jakeline Larios, Katarina Heyden, Steven P Gygi, Jared Rutter","doi":"10.1242/jcs.263693","DOIUrl":"10.1242/jcs.263693","url":null,"abstract":"Mitochondria perform diverse functions, including producing ATP through oxidative phosphorylation, synthesizing macromolecule precursors, maintaining redox balance among many others. Given this diversity of functions, we and others have hypothesized that cells maintain specialized subpopulations of mitochondria. To begin addressing this hypothesis, we developed a new dual-purification system to isolate subpopulations of mitochondria for chemical and biochemical analyses. We used APEX2 proximity labeling such that mitochondria were biotinylated based on proximity to another organelle. All mitochondria were isolated by an elutable MitoTag-based affinity precipitation system. Biotinylated mitochondria were then purified using immobilized avidin. We used this system to compare the proteomes of endosome- and lipid droplet-associated mitochondria in U-2 OS cells, which demonstrated that these subpopulations were indistinguishable from one another but were distinct from the global mitochondria proteome. Our results suggest that this purification system could aid in describing subpopulations that contribute to intracellular mitochondrial heterogeneity, and that this heterogeneity might be more substantial than previously imagined.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12045638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615564","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}

引用次数: 0

Mitochondria-plasma membrane contact sites regulate the ER-mitochondria encounter structure. 线粒体-质膜接触位点调节er -线粒体相遇结构。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-05-01 Epub Date: 2025-02-18 DOI: 10.1242/jcs.263685

Jason C Casler, Clare S Harper, Laura L Lackner

{"title":"Mitochondria-plasma membrane contact sites regulate the ER-mitochondria encounter structure.","authors":"Jason C Casler, Clare S Harper, Laura L Lackner","doi":"10.1242/jcs.263685","DOIUrl":"10.1242/jcs.263685","url":null,"abstract":"Cells form multiple, molecularly distinct membrane contact sites (MCSs) between organelles. Despite knowing the molecular identity of several of these complexes, little is known about how MCSs are coordinately regulated in space and time to promote organelle function. Here, we examined two well-characterized mitochondria-endoplasmic reticulum (ER) MCSs - the ER-mitochondria encounter structure (ERMES) and the mitochondria-ER-cortex anchor (MECA) in Saccharomyces cerevisiae. We report that loss of MECA results in a substantial reduction in the number of ERMES contacts. Rather than reducing ERMES protein levels, loss of MECA results in an increase in the size of ERMES contacts. Using live-cell microscopy, we demonstrate that ERMES contacts display several dynamic behaviors, such as de novo formation, fusion and fission, that are altered in the absence of MECA or by changes in growth conditions. Unexpectedly, we find that the mitochondria-plasma membrane (PM) tethering, and not the mitochondria-ER tethering, function of MECA regulates ERMES contacts. Remarkably, synthetic tethering of mitochondria to the PM in the absence of MECA is sufficient to rescue the distribution of ERMES foci. Overall, our work reveals how one MCS can influence the regulation and function of another.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11883241/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059232","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}

引用次数: 0

Origin and evolution of mitochondrial inner membrane composition. 线粒体内膜组成的起源和进化。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-05-01 Epub Date: 2025-04-23 DOI: 10.1242/jcs.263780

Kailash Venkatraman, Nicolas-Frédéric Lipp, Itay Budin

{"title":"Origin and evolution of mitochondrial inner membrane composition.","authors":"Kailash Venkatraman, Nicolas-Frédéric Lipp, Itay Budin","doi":"10.1242/jcs.263780","DOIUrl":"10.1242/jcs.263780","url":null,"abstract":"Unique membrane architectures and lipid building blocks underlie the metabolic and non-metabolic functions of mitochondria. During eukaryogenesis, mitochondria likely arose from an alphaproteobacterial symbiont of an Asgard archaea-related host cell. Subsequently, mitochondria evolved inner membrane folds known as cristae alongside a specialized lipid composition supported by metabolic and transport machinery. Advancements in phylogenetic methods and genomic and metagenomic data have suggested potential origins for cristae-shaping protein complexes, such as the mitochondrial contact site and cristae-organizing system (MICOS). MICOS protein homologs function in the formation of cristae-like intracytoplasmic membranes (ICMs) in diverse extant alphaproteobacteria. The machinery responsible for synthesizing key mitochondrial phospholipids - which cooperate with cristae-shaping proteins to establish inner membrane architecture - could have also evolved from a bacterial ancestor, but its origins have been less explored. In this Review, we examine the current understanding of mitochondrial membrane evolution, highlighting distinctions between prokaryotic and eukaryotic mitochondrial-specific proteins and lipids and their differing roles in shaping cristae and ICM architecture, and propose a model explaining the concurrent specialization of the mitochondrial lipidome and inner membrane structure in eukaryogenesis. We discuss how advancements across a range of disciplines are shedding light on how multiple membrane components co-evolved to support the central functions of eukaryotic mitochondria.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":"138 9","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12136173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144023429","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}

引用次数: 0

ER-mitochondria encounter structure connections determine drug sensitivity and virulence of Cryptococcus neoformans. er -线粒体相遇结构连接决定了新型隐球菌的药物敏感性和毒力。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-05-01 Epub Date: 2025-04-03 DOI: 10.1242/jcs.263558

Deepika Kumari, Mohit Kumar, Naseem A Gaur, Lucky Duhan, Nadezhda Sachivkina, Raman Manoharlal, Ritu Pasrija

{"title":"ER-mitochondria encounter structure connections determine drug sensitivity and virulence of Cryptococcus neoformans.","authors":"Deepika Kumari, Mohit Kumar, Naseem A Gaur, Lucky Duhan, Nadezhda Sachivkina, Raman Manoharlal, Ritu Pasrija","doi":"10.1242/jcs.263558","DOIUrl":"10.1242/jcs.263558","url":null,"abstract":"Cryptococcus neoformans is a common fungal pathogen, causing fatal meningoencephalitis in immunocompromised individuals. The limited availability of antifungals and increasing resistance in pathogens including C. neoformans emphasize the need to find new drugs. Mitochondria have long been associated with drug resistance in fungi. They are connected to the endoplasmic reticulum (ER) via a multiprotein complex, the ER-mitochondria encounter structure (ERMES), which is unique in the fungal kingdom. In this study on C. neoformans, the four subunits of the ERMES complex, namely, Mmm1, Mdm12, Mdm10 and Mdm34, were deleted to generate the strains Δmmm1, Δmdm12, Δmdm10 and Δmdm34, respectively. These mutants had impaired mitochondria and were sensitive to antifungals, including echinocandins, due to lower chitin content. Virulence factors, including capsule formation and melanin production, were debilitated in the mutants. The partner organelle ER was also affected by compromised ERMES contact, as the activity of several ER-synthesized enzymes involved in virulence was impacted. The in vivo studies in Caenorhabditis elegans model of cryptococcosis confirmed the reduced virulence of the mutants. These results indicate that the impairment of the ERMES complex is crucial for the virulence and pathogenesis of C. neoformans.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":"138 9","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772536","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}

引用次数: 0

Pyruvate plus uridine augments mitochondrial respiration and prevents cardiac hypertrophy in zebrafish and H9c2 cells. 丙酮酸加尿苷增强斑马鱼和H9c2细胞的线粒体呼吸和防止心脏肥大。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-05-01 Epub Date: 2025-05-14 DOI: 10.1242/jcs.263653

Soumyajit Mukherjee, Shreya Das, Surajit Das, Samudra Gupta, Subhra Prakash Hui, Arunima Sengupta, Alok Ghosh

{"title":"Pyruvate plus uridine augments mitochondrial respiration and prevents cardiac hypertrophy in zebrafish and H9c2 cells.","authors":"Soumyajit Mukherjee, Shreya Das, Surajit Das, Samudra Gupta, Subhra Prakash Hui, Arunima Sengupta, Alok Ghosh","doi":"10.1242/jcs.263653","DOIUrl":"https://doi.org/10.1242/jcs.263653","url":null,"abstract":"Dysfunction of mitochondrial pyruvate oxidation and aberrant respiratory chain components are common in cardiac defects. However, the precise role of mitochondrial respiration in cardiomyocyte hypertrophy is unclear. Phenylephrine (PE) treatment of rat neonatal H9c2 cardiomyocytes promotes significant hypertrophy with decreased mitochondrial oxygen consumption rate (OCR), membrane potential, respiratory subunit NDUFB8, UQCRC2 and ATP5A (ATP5F1A) expression, and accumulation of reactive oxygen species (ROS). Surprisingly, a 60% reduction in cell survival was observed in PE-treated cells relative to control cells when grown under the respiratory-proficient galactose medium. To revert H9c2 hypertrophy and increase survival, we performed a screening with compounds that boost mitochondrial OCR and scavenge ROS, and identified pyruvate plus uridine as the best hit. As corroboration of the in vitro study, supplementation of pyruvate plus uridine significantly prevented PE-induced cardiac hypertrophy, pericardial edema and bradycardia symptoms in zebrafish embryos. Moreover, pyruvate plus uridine decreased the ventricular and atrial area in cardiomyocyte-specific GFP transgenic Tg (myl7:HRAS-EGFP) lines. Using in vitro and in vivo models, we show that boosting of mitochondrial respiration through pyruvate supplementation and scavenging ROS through uridine supplementation jointly ameliorate cardiac hypertrophy and bradycardia symptoms.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":"138 9","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143997695","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}

引用次数: 0

Mitochondria - the CEO of the cell. 线粒体——细胞的首席执行官。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-05-01 DOI: 10.1242/jcs.263403

Laurie P Lee-Glover, Martin Picard, Timothy E Shutt

引用次数: 0

The Mia40 substrate Mix17 exposes its N-terminus to the cytosolic side of the mitochondrial outer membrane. Mia40底物Mix17将其n端暴露于线粒体外膜的细胞质侧。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-05-01 Epub Date: 2025-04-16 DOI: 10.1242/jcs.263661

Moritz Resch, Johanna S Frickel, Korbinian Dischinger, Rachel Shen Wen Choo, Kai Hell, Max E Harner

{"title":"The Mia40 substrate Mix17 exposes its N-terminus to the cytosolic side of the mitochondrial outer membrane.","authors":"Moritz Resch, Johanna S Frickel, Korbinian Dischinger, Rachel Shen Wen Choo, Kai Hell, Max E Harner","doi":"10.1242/jcs.263661","DOIUrl":"10.1242/jcs.263661","url":null,"abstract":"Mitochondrial architecture and the contacts between the mitochondrial outer and the inner membranes depend on the mitochondrial contact site and cristae-organizing system (MICOS) that is highly conserved from yeast to human. Variants in the mammalian MICOS subunit Mic14 (also known as CHCHD10) have been linked to amyotrophic lateral sclerosis and frontotemporal dementia, indicating the importance of this protein. Mic14 has a yeast ortholog, Mix17, a protein of unknown function, which has not been shown to interact with MICOS so far. As a first step to elucidate the function of Mix17 and its orthologs, we analyzed its interactions, biogenesis and mitochondrial sublocation. We report that Mix17 is not a stable MICOS subunit in yeast. Our data suggest that Mix17 is the first Mia40 substrate in the mitochondrial outer membrane. Unlike all other Mia40 substrates, Mix17 spans the mitochondrial outer membrane and exposes its N-terminus to the cytosol. The insertion of Mix17 into the mitochondrial outer membrane is likely to be mediated by its interaction with Tom40, the pore of the TOM complex. Moreover, we show that the exposure of Mix17 to the cytosolic side of the mitochondrial membrane depends on its N-terminus.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12045630/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648589","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}

引用次数: 0

Fis1 regulates mitochondrial morphology, bioenergetics and removal of mitochondrial DNA damage in irradiated glioblastoma cells. Fis1调节辐照胶质母细胞瘤细胞的线粒体形态、生物能量学和mtDNA损伤的去除。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-05-01 Epub Date: 2025-01-28 DOI: 10.1242/jcs.263459

Yuli Buckley, Maria S K Stoll, Charles L Hoppel, Jason A Mears

{"title":"Fis1 regulates mitochondrial morphology, bioenergetics and removal of mitochondrial DNA damage in irradiated glioblastoma cells.","authors":"Yuli Buckley, Maria S K Stoll, Charles L Hoppel, Jason A Mears","doi":"10.1242/jcs.263459","DOIUrl":"10.1242/jcs.263459","url":null,"abstract":"In response to external stress, mitochondrial dynamics is often disrupted, but the associated physiologic changes are often uncharacterized. In many cancers, including glioblastoma (GBM), mitochondrial dysfunction has been observed. Understanding how mitochondrial dynamics and physiology contribute to treatment resistance will lead to more targeted and effective therapeutics. This study aims to uncover how mitochondria in GBM cells adapt to and resist ionizing radiation (IR), a component of the standard of care for GBM. Using several approaches, we investigated how mitochondrial dynamics and physiology adapt to radiation stress, and we uncover a novel role for Fis1, a pro-fission protein, in regulating the stress response through mitochondrial DNA (mtDNA) maintenance and altered mitochondrial bioenergetics. Importantly, our data demonstrate that increased fission in response to IR leads to removal of mtDNA damage and more efficient oxygen consumption through altered electron transport chain (ETC) activities in intact mitochondria. These findings demonstrate a key role for Fis1 in targeting damaged mtDNA for degradation and regulating mitochondrial bioenergetics through altered dynamics.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11828467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864233","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}

引用次数: 0

Mitochondrial fission - changing perspectives for future progress. 线粒体裂变——改变未来进展的前景。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-05-01 Epub Date: 2025-03-19 DOI: 10.1242/jcs.263640

Sukrut C Kamerkar, Ao Liu, Henry N Higgs

{"title":"Mitochondrial fission - changing perspectives for future progress.","authors":"Sukrut C Kamerkar, Ao Liu, Henry N Higgs","doi":"10.1242/jcs.263640","DOIUrl":"10.1242/jcs.263640","url":null,"abstract":"Mitochondrial fission is important for many aspects of cellular homeostasis, including mitochondrial distribution, stress response, mitophagy, mitochondrially derived vesicle production and metabolic regulation. Several decades of research has revealed much about fission, including identification of a key division protein - the dynamin Drp1 (also known as DNM1L) - receptors for Drp1 on the outer mitochondrial membrane (OMM), including Mff, MiD49 and MiD51 (also known as MIEF2 and MIEF1, respectively) and Fis1, and important Drp1 regulators, including post-translational modifications, actin filaments and the phospholipid cardiolipin. In addition, it is now appreciated that other organelles, including the endoplasmic reticulum, lysosomes and Golgi-derived vesicles, can participate in mitochondrial fission. However, a more holistic understanding of the process is lacking. In this Review, we address three questions that highlight knowledge gaps. First, how do we quantify mitochondrial fission? Second, how does the inner mitochondrial membrane (IMM) divide? Third, how many 'types' of fission exist? We also introduce a model that integrates multiple regulatory factors in mammalian mitochondrial fission. In this model, three possible pathways (cellular stimulation, metabolic switching or mitochondrial dysfunction) independently initiate Drp1 recruitment at the fission site, followed by a shared second step in which Mff mediates subsequent assembly of a contractile Drp1 ring. We conclude by discussing some perplexing issues in fission regulation, including the effects of Drp1 phosphorylation and the multiple Drp1 isoforms.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":"138 9","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12136174/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657032","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}

引用次数: 0

Vps41 functions as a molecular ruler for HOPS tethering complex-mediated membrane fusion. Vps41是调控hopstethering complex function的分子标尺。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-04-15 Epub Date: 2025-04-25 DOI: 10.1242/jcs.263788

Caroline König, Dmitry Shvarev, Jieqiong Gao, Eduard Haar, Nicole Susan, Kathrin Auffarth, Lars Langemeyer, Arne Moeller, Christian Ungermann

{"title":"Vps41 functions as a molecular ruler for HOPS tethering complex-mediated membrane fusion.","authors":"Caroline König, Dmitry Shvarev, Jieqiong Gao, Eduard Haar, Nicole Susan, Kathrin Auffarth, Lars Langemeyer, Arne Moeller, Christian Ungermann","doi":"10.1242/jcs.263788","DOIUrl":"10.1242/jcs.263788","url":null,"abstract":"Fusion at the lysosome (or the yeast vacuole) requires the conserved hexameric HOPS tethering complex. In the yeast Saccharomyces cerevisiae, HOPS binds to the vacuolar Rab7-like GTPase Ypt7 via its subunits Vps41 and Vps39 and supports fusion by promoting SNARE assembly. In contrast to its sister complex CORVET, the Ypt7-interacting domain of Vps41 in the HOPS complex is connected to the core by a long, extended α-solenoid domain. Here, we show that this solenoid acts as a molecular ruler to position the Ypt7-interacting region of Vps41 relative to the core of HOPS to support function. Mutant complexes with a shortened or extended α-solenoid region in Vps41 still tethered membranes, but failed to efficiently support their fusion. In vivo, Vps41 mutants grew poorly and showed defects in vacuolar morphology, endolysosomal sorting and autophagy. Importantly, when a length-compensating linker was inserted instead of the shortened α-solenoid domain, these defects were rescued. This suggests that the Rab-specific Vps41 subunit requires the exact length of the α-solenoid domain but not the α-solenoid architecture for functionality, suggesting a revised model of how HOPS supports fusion.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752874","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}

引用次数: 0