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Decoding the influence of mitochondrial Ca2+ regulation on neurodegenerative disease progression
Mitochondrial Communications Pub Date : 2025-01-01 DOI: 10.1016/j.mitoco.2025.01.001
Jianxu Sun , Ge Gao , Sitong Wang , Hongmei Liu , Tie-Shan Tang
{"title":"Decoding the influence of mitochondrial Ca2+ regulation on neurodegenerative disease progression","authors":"Jianxu Sun ,&nbsp;Ge Gao ,&nbsp;Sitong Wang ,&nbsp;Hongmei Liu ,&nbsp;Tie-Shan Tang","doi":"10.1016/j.mitoco.2025.01.001","DOIUrl":"10.1016/j.mitoco.2025.01.001","url":null,"abstract":"<div><div>Mitochondria are pivotal hubs in maintaining cellular homeostasis, encompassing vital processes such as bioenergetics, redox regulation, Ca<sup>2+</sup> signaling, and programmed cell death. Ca<sup>2+</sup> is a key second messenger within cells, paramount in numerous critical biological processes. The maintenance of mitochondrial calcium homeostasis relies on a delicate balance between Ca<sup>2+</sup> uptake and efflux. At the mitochondrial level, Ca<sup>2+</sup> serves a dual function, participating in essential physiological processes such as ATP production and the regulation of mitochondrial metabolisms and contributing to pathophysiological events, including cell death and cancer metastasis. Alterations in mitochondrial Ca<sup>2+</sup> (Ca<sup>2+</sup><sub>mito</sub>) levels influence cellular activity and functionality. The regulation of mitochondrial Ca<sup>2+</sup> homeostasis involves the collaborative participation of the mitochondrial Ca<sup>2+</sup> transporter and the mitochondria-endoplasmic reticulum contact sites (MERCS). This review provides a comprehensive overview of current knowledge regarding the regulation of mitochondrial Ca<sup>2+</sup> homeostasis and its implications in both physiological processes and neurodegenerative disorders. Moreover, we highlight potential opportunities and challenges in developing therapeutic interventions that target mitochondrial Ca<sup>2+</sup> homeostasis and its regulators, such as novel drug delivery systems and specific calcium-modulating agents.</div></div>","PeriodicalId":100931,"journal":{"name":"Mitochondrial Communications","volume":"3 ","pages":"Pages 1-15"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143139404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Tissue-specific knockdown of OMM protein via GFP nanobody-mediated degradation 通过 GFP 纳米抗体介导的降解,特异性敲除组织中的 OMM 蛋白
Mitochondrial Communications Pub Date : 2024-01-01 DOI: 10.1016/j.mitoco.2024.07.003
Xiaojie Wang , Qiyue Zhang , Suhong Xu
{"title":"Tissue-specific knockdown of OMM protein via GFP nanobody-mediated degradation","authors":"Xiaojie Wang ,&nbsp;Qiyue Zhang ,&nbsp;Suhong Xu","doi":"10.1016/j.mitoco.2024.07.003","DOIUrl":"10.1016/j.mitoco.2024.07.003","url":null,"abstract":"<div><p>Mitochondria, with their diverse morphologies across tissues, hint at a unique function based on location. For instance, outer mitochondrial membrane (OMM) proteins are critical for various mitochondrial activities, including regulating mitochondrial dynamics, ion homeostasis, and protein translocation. This study introduces a green fluorescent protein (GFP) nanobody-mediated protein degradation (G-DEG) system to investigate tissue-specific mitochondrial functions in <em>Caenorhabditis elegans</em> and potential other model systems. G-DEG combines CRISPR-Cas9 GFP knock-in with ZIF-1-mediated protein degradation, leveraging the high specificity of antigen–antibody recognition for precise manipulation across species. We demonstrate the G-DEG system by targeting FZO-1, a mammalian homolog of MAN1/2, which is essential for mitochondrial fusion. Our protocol includes CRISPR-Cas9-mediated <em>fzo-1</em>:GFP knock-in and the construction of tissue-specific GFP nanobody degradation plasmids for the epidermis, muscle, and neurons. Injection of these plasmids into wild-type <em>C. elegans</em> and subsequent crossbreeding with the <em>fzo-1</em>:GFP knock-in strain allows for effective FZO-1 targeting, providing tissue-specific insights into mitochondrial protein function. Overall, G-DEG emerges as a powerful and versatile tool for tissue-specific knockdown of OMM proteins, paving the way for advanced studies on their diverse biological functions.</p></div>","PeriodicalId":100931,"journal":{"name":"Mitochondrial Communications","volume":"2 ","pages":"Pages 85-89"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590279224000087/pdfft?md5=f5d2d52b3e5d9bb6460686031c07f0e6&pid=1-s2.0-S2590279224000087-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141961581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Single-cell mitochondrial DNA sequencing: Methodologies and applications 单细胞线粒体 DNA 测序:方法与应用
Mitochondrial Communications Pub Date : 2024-01-01 DOI: 10.1016/j.mitoco.2024.10.001
Guoqiang Zhou , Zhenglong Gu , Jin Xu
{"title":"Single-cell mitochondrial DNA sequencing: Methodologies and applications","authors":"Guoqiang Zhou ,&nbsp;Zhenglong Gu ,&nbsp;Jin Xu","doi":"10.1016/j.mitoco.2024.10.001","DOIUrl":"10.1016/j.mitoco.2024.10.001","url":null,"abstract":"<div><div>Mitochondria play a pivotal role in cellular energetics, metabolism, and various regulatory processes. Their dysregulation is implicated in numerous diseases. Traditional population-level mitochondrial DNA (mtDNA) sequencing often obscures crucial information from individual cells, leading to a limited understanding of mitochondrial genetics. In contrast, single-cell mtDNA sequencing enables the precise detection and characterization of mtDNA mutations at the individual cell level, providing a nuanced view of mitochondrial heteroplasmy and its dynamics. This review aims to provide a comprehensive overview of current single-cell mtDNA sequencing methodologies and their applications in advancing our understanding of mitochondrial genetics.</div></div>","PeriodicalId":100931,"journal":{"name":"Mitochondrial Communications","volume":"2 ","pages":"Pages 107-113"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142571269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Nature conference on mitochondria and immunity: Uncovering Mitochondria–Immunity crosstalk and fostering global scientific exchanges
Mitochondrial Communications Pub Date : 2024-01-01 DOI: 10.1016/j.mitoco.2024.12.002
Juan Liu, Yanjun Li, Yushan Zhu, Quan Chen
{"title":"Nature conference on mitochondria and immunity: Uncovering Mitochondria–Immunity crosstalk and fostering global scientific exchanges","authors":"Juan Liu,&nbsp;Yanjun Li,&nbsp;Yushan Zhu,&nbsp;Quan Chen","doi":"10.1016/j.mitoco.2024.12.002","DOIUrl":"10.1016/j.mitoco.2024.12.002","url":null,"abstract":"","PeriodicalId":100931,"journal":{"name":"Mitochondrial Communications","volume":"2 ","pages":"Pages A1-A6"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143143974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Lipid transfer at mitochondrial membrane contact sites
Mitochondrial Communications Pub Date : 2024-01-01 DOI: 10.1016/j.mitoco.2024.11.002
Qingzhu Chu , Wei-Ke Ji
{"title":"Lipid transfer at mitochondrial membrane contact sites","authors":"Qingzhu Chu ,&nbsp;Wei-Ke Ji","doi":"10.1016/j.mitoco.2024.11.002","DOIUrl":"10.1016/j.mitoco.2024.11.002","url":null,"abstract":"<div><div>Mitochondria are semiautonomous organelles that are actively shaped into an extended reticular network that is not connected to the endomembrane system via vesicular transport. Instead, active lipid exchange occurs between mitochondria and other organelles, such as the endoplasmic reticulum (ER) and lipid droplets (LDs), at mitochondrial membrane contact sites (MCSs), where the two organelles are juxtaposed with each other at a distance of 10–30 nm. Recent advances have led to an increasing understanding of the molecular mechanism that mediates the transfer of different lipid species between these organelles. Here, we highlight advances that demonstrate the role of lipid transfer proteins at ER–mitochondrial and LD–mitochondrial MCSs. Importantly, we summarize the fundamental questions on this topic that remain unanswered.</div></div>","PeriodicalId":100931,"journal":{"name":"Mitochondrial Communications","volume":"2 ","pages":"Pages 123-128"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143143975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Innovative methods for isolating highly purified mitochondria essential for biomedical studies 分离生物医学研究必需的高纯度线粒体的创新方法
Mitochondrial Communications Pub Date : 2024-01-01 DOI: 10.1016/j.mitoco.2024.09.002
Yan Huang , Xiangwaner Jin , Yi Zhang , Yanan Li, Jinming Liu, Yanjun Li
{"title":"Innovative methods for isolating highly purified mitochondria essential for biomedical studies","authors":"Yan Huang ,&nbsp;Xiangwaner Jin ,&nbsp;Yi Zhang ,&nbsp;Yanan Li,&nbsp;Jinming Liu,&nbsp;Yanjun Li","doi":"10.1016/j.mitoco.2024.09.002","DOIUrl":"10.1016/j.mitoco.2024.09.002","url":null,"abstract":"<div><div>Mitochondria, being multifunctional and highly complex organelles, possess unique structures and exhibit heterogeneity. In recent decades, the isolation and purification of functional mitochondria have been instrumental for mitochondrial research. As mitochondrial research, including omics, advances, there is a growing demand for the isolation of highly purified mitochondria or individual mitochondria. This paper provides a comprehensive overview of the evolution of mitochondrial purification methods and introduces two innovative and improved techniques for isolating mitochondria from mouse cerebral cortex and in vitro cultured cells. The first method utilizes self-prepared magnetic beads conjugated with anti-TOMM20 antibody for the immunoisolation of highly purified intact mitochondria. The second method utilizes flow cytometry to isolate single mitochondria based on fluorescent protein labeling, allowing for the isolation of mitochondria from a highly heterogeneous population. We provide detailed protocols that aim to benefit the rapidly growing mitochondria research community in assessing mitochondrial function, especially at the single-organelle level.</div></div>","PeriodicalId":100931,"journal":{"name":"Mitochondrial Communications","volume":"2 ","pages":"Pages 90-99"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142423696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","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 lipid metabolism in metastatic breast cancer 转移性乳腺癌的线粒体脂质代谢
Mitochondrial Communications Pub Date : 2024-01-01 DOI: 10.1016/j.mitoco.2024.07.001
Bhuban Ruidas
{"title":"Mitochondrial lipid metabolism in metastatic breast cancer","authors":"Bhuban Ruidas","doi":"10.1016/j.mitoco.2024.07.001","DOIUrl":"10.1016/j.mitoco.2024.07.001","url":null,"abstract":"<div><p>The significance of mitochondrial lipid metabolism in cancer stemness, survival, and proliferation, particularly in the context of metastasis, has garnered significant attention. Warburg's hypothesis posits that cancer cells primarily rely on aerobic glycolysis for survival due to mitochondrial dysfunction. However, recent evidence has challenged this perspective, emphasizing the direct involvement of mitochondria in cancer's rapid progression. Metabolic rearrangements, a hallmark of metastatic cancer, fulfill heightened energy demands during rapid proliferation, primarily through mitochondrial oxidative phosphorylation and lipid metabolism, even under hypoxic conditions. Moreover, lipid metabolism is elevated throughout the progression of metastatic cancer to meet crucial energy needs. However, the relative importance of mitochondrial lipid metabolism and aerobic glycolysis in highly aggressive cancers remains poorly defined, and further investigation could enhance treatment outcomes in cases of metastatic progression. In this context, a comprehensive understanding of mitochondrial lipid metabolism in metastatic breast cancer patients could potentially lead to significant breakthroughs in improving therapies, especially for triple-negative breast cancer.</p></div>","PeriodicalId":100931,"journal":{"name":"Mitochondrial Communications","volume":"2 ","pages":"Pages 58-66"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590279224000063/pdfft?md5=50183d4ee164426611eb75a5606347dd&pid=1-s2.0-S2590279224000063-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141843364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The mitochondria chronicles of melatonin and ATP: Guardians of phase separation 褪黑素和 ATP 的线粒体编年史:相分离的守护者
Mitochondrial Communications Pub Date : 2024-01-01 DOI: 10.1016/j.mitoco.2024.07.002
Doris Loh , Russel J. Reiter
{"title":"The mitochondria chronicles of melatonin and ATP: Guardians of phase separation","authors":"Doris Loh ,&nbsp;Russel J. Reiter","doi":"10.1016/j.mitoco.2024.07.002","DOIUrl":"10.1016/j.mitoco.2024.07.002","url":null,"abstract":"<div><p>Phase separation is a thermodynamic process used by all living organisms since the origin of life to rapidly assemble and disassemble membraneless condensates in response to changes in exogenous and endogenous stress conditions. For ∼4.5 billion years, living organisms in the three major domains of life depended upon the high chemical potential of adenosine triphosphate (ATP) to harness nonequilibrium chemical reactions that govern the formation and suppression of membraneless organelles via phase separation. Melatonin enhances the unique chemistry of ATP in water, promoting the solubilization via the adenosine moiety effect, supporting the survival of early organisms in an anoxic environment. Eukaryotes, including dinoflagellates and plants, can produce melatonin in extreme levels under stress as compensation for inadequate ATP for optimal regulation of survival responses dependent upon phase separation. The production of ATP and melatonin in mitochondria enables the fine-tuning of dynamics that modulate phase separation of proteins associated with ATP production, biogenesis and degradation, membrane dynamics, gene transcription, mitophagy, unfolded protein response, and apoptosis/survival responses in mitochondria. Exogenous melatonin application enhances mitochondrial ATP production and synergy, attenuating aberrant phase separation and associated mitochondrial dysfunction and disease.</p></div>","PeriodicalId":100931,"journal":{"name":"Mitochondrial Communications","volume":"2 ","pages":"Pages 67-84"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590279224000075/pdfft?md5=7d5edc08bd32f09b779eb9636af81ee8&pid=1-s2.0-S2590279224000075-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141846938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Antioxidants targeting mitochondria function in kidney diseases 针对肾脏疾病线粒体功能的抗氧化剂
Mitochondrial Communications Pub Date : 2024-01-01 DOI: 10.1016/j.mitoco.2024.03.002
Ana Karina Aranda-Rivera , Alfredo Cruz-Gregorio , Isabel Amador-Martínez , Estefani Yaquelin Hernández-Cruz , Edilia Tapia , José Pedraza-Chaverri
{"title":"Antioxidants targeting mitochondria function in kidney diseases","authors":"Ana Karina Aranda-Rivera ,&nbsp;Alfredo Cruz-Gregorio ,&nbsp;Isabel Amador-Martínez ,&nbsp;Estefani Yaquelin Hernández-Cruz ,&nbsp;Edilia Tapia ,&nbsp;José Pedraza-Chaverri","doi":"10.1016/j.mitoco.2024.03.002","DOIUrl":"https://doi.org/10.1016/j.mitoco.2024.03.002","url":null,"abstract":"<div><p>Kidney diseases are a growing health problem worldwide, causing millions of deaths. Acute kidney injury (AKI) commonly evolves into chronic kidney disease (CKD) and fibrosis, which is a feature of CKD predisposing to end-stage renal disease. Thus, treatments that avoid this transition are urgently necessary. Mitochondria are the hub energy house of the renal cells, which provides energy in adenosine triphosphate (ATP) form, commonly obtained from β-oxidation through fatty acids degradation into the mitochondrial matrix. Mitochondria are plastic organelles that constantly change according to the cell's energy requirements. For this, mitochondria carry out biogenesis, fission, fusion, and mitophagy/autophagy, processes highly regulated to maintain mitochondrial bioenergetics and homeostasis. Alterations in one or more of these processes might cause detrimental consequences that affect cell function. In this sense, it is widely accepted that mitochondrial dysfunction associated with oxidative stress plays a crucial role in developing kidney diseases. Therefore, antioxidants that target mitochondria might be an excellent strategy to ameliorate mitochondrial dysfunction, and selecting one or another antioxidant could depend on AKI or CKD requirements. This review focuses on potent antioxidants such as sulforaphane (SFN), <em>N</em>-acetyl cysteine (NAC), resveratrol, curcumin, quercetin, and α-mangostin in the improvement of mitochondrial function in kidney pathologies.</p></div>","PeriodicalId":100931,"journal":{"name":"Mitochondrial Communications","volume":"2 ","pages":"Pages 21-37"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S259027922400004X/pdfft?md5=5869184899ade6f79d140563bae21bc8&pid=1-s2.0-S259027922400004X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140327839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Photobleaching and phototoxicity of mitochondria in live cell fluorescent super-resolution microscopy 活细胞荧光超分辨率显微镜中线粒体的光漂白和光毒性
Mitochondrial Communications Pub Date : 2024-01-01 DOI: 10.1016/j.mitoco.2024.03.001
Chia-Hung Lee , Douglas C. Wallace , Peter J. Burke
{"title":"Photobleaching and phototoxicity of mitochondria in live cell fluorescent super-resolution microscopy","authors":"Chia-Hung Lee ,&nbsp;Douglas C. Wallace ,&nbsp;Peter J. Burke","doi":"10.1016/j.mitoco.2024.03.001","DOIUrl":"10.1016/j.mitoco.2024.03.001","url":null,"abstract":"<div><p>Photobleaching and phototoxicity can induce detrimental effects on cell viability and compromise the integrity of collected data, particularly in studies utilizing super-resolution microscopes. Given the involvement of multiple factors, it is currently challenging to propose a single set of standards for assessing the potential of phototoxicity. The objective of this paper is to present empirical data on the effects of photobleaching and phototoxicity on mitochondria during super-resolution imaging of mitochondrial structure and function using Airyscan and the fluorescent structure dyes Mitotracker green (MTG), 10-N-nonyl acridine orange (NAO), and voltage dye Tetramethylrhodamine, Ethyl Ester (TMRE). We discern two related phenomena. First, phototoxicity causes a transformation of mitochondria from tubular to spherical shape, accompanied by a reduction in the number of cristae. Second, phototoxicity impacts the mitochondrial membrane potential. Through these parameters, we discovered that upon illumination, NAO is much more phototoxic to mitochondria compared to MTG or TMRE and that these parameters can be used to evaluate the relative phototoxicity of various mitochondrial dye-illumination combinations during mitochondrial imaging.</p></div>","PeriodicalId":100931,"journal":{"name":"Mitochondrial Communications","volume":"2 ","pages":"Pages 38-47"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590279224000038/pdfft?md5=96dab14e2fc33e7b9392f96865841292&pid=1-s2.0-S2590279224000038-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140275628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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