Cardiovascular Research最新文献

筛选
英文 中文
TGF-β signalling: the Dr. Jekyll and Mr. Hyde of the aortic aneurysms. TGF-β 信号:主动脉瘤的 "杰基尔博士 "和 "海德先生"。
IF 10.2 1区 医学
Cardiovascular Research Pub Date : 2024-11-19 DOI: 10.1093/cvr/cvae245
Sara Perrotta, Daniela Carnevale, Giuseppe Lembo
{"title":"TGF-β signalling: the Dr. Jekyll and Mr. Hyde of the aortic aneurysms.","authors":"Sara Perrotta, Daniela Carnevale, Giuseppe Lembo","doi":"10.1093/cvr/cvae245","DOIUrl":"https://doi.org/10.1093/cvr/cvae245","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":""},"PeriodicalIF":10.2,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142675217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
C-C motif chemokine receptor-2 blockade ameliorates pulmonary hypertension in rats and synergizes with a pulmonary vasodilator. C-C motif趋化因子受体-2阻断剂可改善大鼠肺动脉高压,并与肺血管扩张剂协同作用。
IF 10.2 1区 医学
Cardiovascular Research Pub Date : 2024-11-18 DOI: 10.1093/cvr/cvae244
Naoki Tsuboya, Hirofumi Sawada, Yoshihide Mitani, Hironori Oshita, Kazunobu Ohya, Mami Takeoka, Jane Chanda Kabwe, Yoshiki Miyasaka, Hiromasa Ito, Noriko Yodoya, Hiroyuki Ohashi, Junko Maruyama, Ryuji Okamoto, Tomoji Mashimo, Kaoru Dohi, Yuhei Nishimura, Kazuo Maruyama, Masahiro Hirayama
{"title":"C-C motif chemokine receptor-2 blockade ameliorates pulmonary hypertension in rats and synergizes with a pulmonary vasodilator.","authors":"Naoki Tsuboya, Hirofumi Sawada, Yoshihide Mitani, Hironori Oshita, Kazunobu Ohya, Mami Takeoka, Jane Chanda Kabwe, Yoshiki Miyasaka, Hiromasa Ito, Noriko Yodoya, Hiroyuki Ohashi, Junko Maruyama, Ryuji Okamoto, Tomoji Mashimo, Kaoru Dohi, Yuhei Nishimura, Kazuo Maruyama, Masahiro Hirayama","doi":"10.1093/cvr/cvae244","DOIUrl":"https://doi.org/10.1093/cvr/cvae244","url":null,"abstract":"<p><strong>Aims: </strong>We investigated whether the disruption of C-C motif chemokine receptor (CCR) 2 may attenuate the development of pulmonary arterial hypertension (PAH) in any rat models with the reversal of the associated pro-inflammatory state and vascular dysfunction, and synergize with a conventional pulmonary vasodilator.</p><p><strong>Methods and results: </strong>Using Ccr2(-/-) rats generated by CRISPR/Cas9, we investigated pulmonary hypertension (PH) in Ccr2(+/+) or Ccr2(-/-) rats treated with monocrotaline (MCT), SU5416/hypoxia (SuHx) and chronic hypoxia (CH). Ccr2(-/-) decreased the right ventricular systolic pressure, an index of right ventricular hypertrophy and mortality rate, and reversed increased expression of inflammatory cytokines/chemokines (interleukin-6, tumor necrosis factor-α, C-C motif chemokine receptor (CCL)-2, interleukin-1β, transforming growth factor-β) in rats 3weeks after MCT injection, but not in SuHx or CH models. Consistently, Ccr2(-/-) decreased indices of pulmonary vascular diseases (PVD) and perivascular macrophage infiltration, as well as reversed impaired bone morphogenetic protein receptor type 2 signaling, increased endothelial apoptosis and impaired nitric oxide signaling and decreased phosphodiesterase-5 (PDE5) expression in lungs in MCT-treated rats. Gene expression of receptors for prostaglandin I2 and endothelin was not changed by Ccr2(-/-) in MCT-treated rats. In cultured pulmonary arterial smooth muscle cells (PASMCs), Ccr2(-/-) suppressed CCL2-induced hyperproliferation and dedifferentiation as well as reversed CCL2-induced decrease in PDE5 expression. The whole-genome RNA sequencing analysis identified differentially expressed genes in CCL2-stimulated Ccr2(-/-) PASMCs, which are related to regulation of cellular differentiation and contraction. Based on studies in rats and cultured PASMCs, we investigated whether a PDE5 inhibitor, tadalafil, synergizes with Ccr2(-/-). Tadalafil administration ameliorated PH and PVDs in MCT-treated Ccr2(-/-) rats but not in Ccr2(+/+) rats. Tadalafil further improved survival in MCT-treated Ccr2(-/-) rats.</p><p><strong>Conclusion: </strong>The present findings demonstrated that CCR2 disruption ameliorated PAH in MCT-treated rats, which was associated with the reversal of dysregulated inflammatory pathways and vascular dysfunction and synergized with tadalafil. These findings suggest that CCR2 may be a therapeutic target in intractable PAH patients with a certain CCR2-related inflammatory phenotype and refractory to conventional pulmonary vasodilators.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":""},"PeriodicalIF":10.2,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142646878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Inflammation and heart failure: are we facing a "hedgehog's dilemma"? 炎症与心力衰竭:我们是否面临 "刺猬的困境"?
IF 10.2 1区 医学
Cardiovascular Research Pub Date : 2024-11-16 DOI: 10.1093/cvr/cvae246
Stefano Ministrini, Giovanni G Camici
{"title":"Inflammation and heart failure: are we facing a \"hedgehog's dilemma\"?","authors":"Stefano Ministrini, Giovanni G Camici","doi":"10.1093/cvr/cvae246","DOIUrl":"https://doi.org/10.1093/cvr/cvae246","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":""},"PeriodicalIF":10.2,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Advancing cardiovascular risk assessment. 推进心血管风险评估。
IF 10.2 1区 医学
Cardiovascular Research Pub Date : 2024-11-13 DOI: 10.1093/cvr/cvae234
Christos P Kotanidis, Brittany Weber
{"title":"Advancing cardiovascular risk assessment.","authors":"Christos P Kotanidis, Brittany Weber","doi":"10.1093/cvr/cvae234","DOIUrl":"https://doi.org/10.1093/cvr/cvae234","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":""},"PeriodicalIF":10.2,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Inflammaging, a targetable pathway for preventing cardiovascular diseases 炎症--预防心血管疾病的目标途径
IF 10.8 1区 医学
Cardiovascular Research Pub Date : 2024-11-12 DOI: 10.1093/cvr/cvae240
Juan Francisco Aranda, Cristina M Ramírez, María Mittelbrunn
{"title":"Inflammaging, a targetable pathway for preventing cardiovascular diseases","authors":"Juan Francisco Aranda, Cristina M Ramírez, María Mittelbrunn","doi":"10.1093/cvr/cvae240","DOIUrl":"https://doi.org/10.1093/cvr/cvae240","url":null,"abstract":"Inflammaging, characterized by persistent chronic inflammation in older adults, has emerged as a critical factor linked to age-related diseases such as cardiovascular diseases (CVDs), metabolic disorders, and cognitive decline, which collectively contribute to the leading causes of death globally. Elevated levels of cytokines, chemokines, and others inflammatory mediators characterize inflammaging and serve as indicators of biological age. Among the causes of inflammaging, deterioration of the immune system, mitochondrial dysfunction, dysbiosis, accumulation of DAMPs, together with genetic or epigenetic factors, contribute to inflammaging not only in CVD but also in other age-related conditions. This review examines the causes and consequences of inflammaging, particularly its implications for atherosclerosis and heart failure with preserved ejection fraction (HFpEF) and explores potential strategies to mitigate it in the onset of CVD.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"95 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142601208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Regulation of blood pressure by METTL3 via RUNX1b-eNOS pathway in endothelial cells in mice 小鼠内皮细胞中的 METTL3 通过 RUNX1b-eNOS 通路调节血压
IF 10.8 1区 医学
Cardiovascular Research Pub Date : 2024-11-12 DOI: 10.1093/cvr/cvae242
Yanhong Zhang, Xiaoxiao Yang, Mei Lan, Ze Yuan, Shuai Li, Yangping Liu, Cha Han, Ding Ai, Yang Yang, Yi Zhu, Bochuan Li
{"title":"Regulation of blood pressure by METTL3 via RUNX1b-eNOS pathway in endothelial cells in mice","authors":"Yanhong Zhang, Xiaoxiao Yang, Mei Lan, Ze Yuan, Shuai Li, Yangping Liu, Cha Han, Ding Ai, Yang Yang, Yi Zhu, Bochuan Li","doi":"10.1093/cvr/cvae242","DOIUrl":"https://doi.org/10.1093/cvr/cvae242","url":null,"abstract":"Aims Endothelial cells regulate vascular tone to control the blood pressure (BP) by producing both relaxing and contracting factors. Previously, we identified methyltransferase-like 3 (METTL3), a primary N6-methyladenosine (m6A) methyltransferase, as a key player in alleviating endothelial atherogenic progression. However, its involvement in BP regulation remains unclear. Methods and results To evaluate the role of METTL3 in vivo, mice with EC specific METTL3 deficiency (EC-Mettl3KO) with or without Ang II infusion were used to create a hypertensive model. Functional and MeRIP sequencing analysis were performed to explore the mechanism of METTL3-mediated hypertension. We observed a reduction in endothelial METTL3 activity by Ang II in vitro and in vivo. Endothelial METTL3-deficient mice exhibited higher BP than controls, with no gender disparity observed. The subsequent study primarily conducted in male mice. Through m6A sequencing and functional analysis, we identified m6A modification of various RUNX1 monomers resulted in endothelial dysfunction. Mutations in the 3′UTR region of RUNX1b abolished its luciferase reporter activity, and enhanced eNOS promoter luciferase reporter activity with or without METTL3 overexpression. Overexpression of METTL3 by adeno-associated virus reduced Ang II-induced BP elevation. Conclusion This study reveals that METTL3 alleviates hypertension through m6A-dependent stabilization of RUNX1b mRNA, leading to upregulation of eNOS, thus underscoring the pivotal role of RNA transcriptomics in the regulation of hypertension.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"80 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142601201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
miR-24-3p secreted as extracellular vesicle cargo by cardiomyocytes inhibits fibrosis in human cardiac microtissues 心肌细胞作为细胞外囊泡货物分泌的 miR-24-3p 可抑制人类心脏微组织的纤维化
IF 10.8 1区 医学
Cardiovascular Research Pub Date : 2024-11-11 DOI: 10.1093/cvr/cvae243
Giorgia Senesi, Alessandra M Lodrini, Shafeeq Mohammed, Simone Mosole, Jesper Hjortnaes, Rogier J A Veltrop, Bela Kubat, Davide Ceresa, Sara Bolis, Andrea Raimondi, Tiziano Torre, Paolo Malatesta, Marie-José Goumans, Francesco Paneni, Giovanni G Camici, Lucio Barile, Carolina Balbi, Giuseppe Vassalli
{"title":"miR-24-3p secreted as extracellular vesicle cargo by cardiomyocytes inhibits fibrosis in human cardiac microtissues","authors":"Giorgia Senesi, Alessandra M Lodrini, Shafeeq Mohammed, Simone Mosole, Jesper Hjortnaes, Rogier J A Veltrop, Bela Kubat, Davide Ceresa, Sara Bolis, Andrea Raimondi, Tiziano Torre, Paolo Malatesta, Marie-José Goumans, Francesco Paneni, Giovanni G Camici, Lucio Barile, Carolina Balbi, Giuseppe Vassalli","doi":"10.1093/cvr/cvae243","DOIUrl":"https://doi.org/10.1093/cvr/cvae243","url":null,"abstract":"Background and Aims Cardiac fibrosis in response to injury leads to myocardial stiffness and heart failure. At the cellular level, fibrosis is triggered by the conversion of cardiac fibroblasts (CF) into extracellular matrix–producing myofibroblasts. miR-24-3p regulates this process in animal models. Here, we investigated whether miR-24-3p plays similar roles in human models. Methods and Results Gain– and loss–of–function experiments were performed using human induced pluripotent stem cell–derived cardiomyocytes (hCM) and primary hCF under normoxic or ischaemia–simulating conditions. hCM–derived extracellular vesicles (EVs) were added to hCF. Similar experiments were performed using three-dimensional human cardiac microtissues and ex vivo–cultured human cardiac slices. hCF transfection with miR-24-3p mimic prevented TGFβ1–mediated induction of FURIN, CCND1 and SMAD4—miR-24-3p target genes participating in TGFβ1–dependent fibrinogenesis —, regulating hCF–to–myofibroblast conversion. hCM secreted miR-24-3p as EV cargo. hCM–derived EVs modulated hCF activation. Ischaemia–simulating conditions induced miR-24-3p depletion in hCM-EVs and microtissues. Similarly, hypoxia downregulated miR-24-3p in cardiac slices. Analyses of clinical samples revealed decreased miR-24-3p levels in circulating EVs in acute myocardial infarction (AMI) patients, compared with healthy subjects. Post-mortem RNAScope analysis showed miR-24-3p downregulation in myocardium from AMI patients, compared with patients who died from noncardiac diseases. Berberin, a plant–derived agent with miR-24-3p–stimulatory activity, increased miR-24-3p contents in hCM-EVs, downregulated FURIN, CCND1 and SMAD4, and inhibited fibrosis in cardiac microtissues. Conclusions These findings suggest that hCM may control hCF activation through miR-24-3p secreted as EV cargo. Ischaemia impairs this mechanism, favouring fibrosis.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"29 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142599703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Correction to: Modulation of lncRNA links endothelial glycocalyx to vascular dysfunction of tyrosine kinase inhibitor. Correction to:lncRNA的调节将内皮糖萼与酪氨酸激酶抑制剂的血管功能障碍联系起来。
IF 10.2 1区 医学
Cardiovascular Research Pub Date : 2024-11-06 DOI: 10.1093/cvr/cvae233
{"title":"Correction to: Modulation of lncRNA links endothelial glycocalyx to vascular dysfunction of tyrosine kinase inhibitor.","authors":"","doi":"10.1093/cvr/cvae233","DOIUrl":"https://doi.org/10.1093/cvr/cvae233","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":""},"PeriodicalIF":10.2,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142589605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Epitranscriptomic regulation of cardiac fibrosis via YTHDF1-dependent PIEZO2 mRNA m6A modification. 通过 YTHDF1 依赖性 PIEZO2 mRNA m6A 修饰对心脏纤维化的外转录组调控
IF 10.2 1区 医学
Cardiovascular Research Pub Date : 2024-11-05 DOI: 10.1093/cvr/cvae239
Ji-Fei Ding, Bin Tu, Kai Song, Zhen-Yu Liu, Li-Chan Lin, Zhi-Yan Liu, Yan Shi, Jing-Jing Yang, Jian-Yuan Zhao, Hui Tao
{"title":"Epitranscriptomic regulation of cardiac fibrosis via YTHDF1-dependent PIEZO2 mRNA m6A modification.","authors":"Ji-Fei Ding, Bin Tu, Kai Song, Zhen-Yu Liu, Li-Chan Lin, Zhi-Yan Liu, Yan Shi, Jing-Jing Yang, Jian-Yuan Zhao, Hui Tao","doi":"10.1093/cvr/cvae239","DOIUrl":"https://doi.org/10.1093/cvr/cvae239","url":null,"abstract":"<p><strong>Background: </strong>Mechanosensitive ion channels play a key role in heart development, physiology, and disease. However, little is known about the molecular mechanisms of the mechanosensitive nonselective cationic channel Piezo family in cardiac fibrosis.</p><p><strong>Methods and results: </strong>Mice were treated with ISO/Ang-II/TAC to induce cardiac fibrosis. AAV9 carrying POSTN promoter-driven small hairpin RNA targeting YTHDF1, and Piezo2 were administered to ISO mice to investigate their roles in cardiac fibrosis. RNA-seq, single-cell sequencing, and histological and biochemical analyses were performed to determine the mechanism by which YTHDF1 regulates Piezo2 expression in cardiac fibrosis. Piezo2 was reconstituted in YTHDF1-deficient cardiac fibroblasts and mouse hearts to study its effects on cardiac fibroblast autophagy and fibrosis. Piezo2 but not Piezo1 expression increased in experimental cardiac fibrosis and TGF-β1-induced cardiac fibroblasts. Fibroblast-specific Piezo2 deficiency ameliorated fibroblast activation and autophagy and inhibited cardiac fibrosis. Mechanistically, Piezo2 upregulation was associated with elevated m6A mRNA levels. Site-specific m6A modifications at peak_26355 were crucial for regulating the binding of YTHDF1 to Piezo2 mRNA and inducing Piezo2 translation. Notably, Piezo2 epitranscriptomic repression ameliorated experimental cardiac fibrosis.</p><p><strong>Conclusions: </strong>We demonstrated a novel epitranscriptomic mechanism through which YTHDF1 recognizes Piezo2 and controls cardiac fibroblast autophagy and fibrosis through m6A-dependent modulation. Our findings provide new insights for the development of preventive measures for cardiac fibrosis.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":""},"PeriodicalIF":10.2,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Physiological and pathological ventricular hypertrophy: a role for cavin-2 mediated Akt regulation. 生理性和病理性心室肥大:Cavin-2 介导的 Akt 调节作用
IF 10.2 1区 医学
Cardiovascular Research Pub Date : 2024-11-05 DOI: 10.1093/cvr/cvae184
Raffaele Coppini, Lucrezia Giammarino, Elisabetta Cerbai
{"title":"Physiological and pathological ventricular hypertrophy: a role for cavin-2 mediated Akt regulation.","authors":"Raffaele Coppini, Lucrezia Giammarino, Elisabetta Cerbai","doi":"10.1093/cvr/cvae184","DOIUrl":"10.1093/cvr/cvae184","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"1499-1500"},"PeriodicalIF":10.2,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信