Nature cardiovascular research最新文献_第9页

Transcriptional pausing as a molecular mechanism of sprouting angiogenesis 转录暂停是萌芽血管生成的分子机制。

IF 9.4

Nature cardiovascular research Pub Date : 2024-10-07 DOI: 10.1038/s44161-024-00547-4

Inês Cebola, Graeme M. Birdsey, Anna M. Randi

引用次数: 0

Semaglutide may reduce cardiovascular disease and heart failure 塞马鲁肽可减少心血管疾病和心力衰竭。

IF 9.4

Nature cardiovascular research Pub Date : 2024-10-04 DOI: 10.1038/s44161-024-00556-3

Michelle Korda

引用次数: 0

Chronic inflammation after ischemic stroke induces maladaptive cardiac remodeling 缺血性中风后的慢性炎症会诱发适应不良的心脏重塑。

IF 9.4

Nature cardiovascular research Pub Date : 2024-10-01 DOI: 10.1038/s44161-024-00554-5

Andrea Tavosanis

引用次数: 0

Evolution of cardiac genomic elements in humans and non-human primates 人类和非人灵长类动物心脏基因组元素的进化。

IF 9.4

Nature cardiovascular research Pub Date : 2024-10-01 DOI: 10.1038/s44161-024-00552-7

引用次数: 0

RNF20-mediated transcriptional pausing and VEGFA splicing orchestrate vessel growth RNF20 介导的转录暂停和 VEGFA 剪接协调了血管的生长。

IF 9.4

Nature cardiovascular research Pub Date : 2024-09-25 DOI: 10.1038/s44161-024-00546-5

Nalan Tetik-Elsherbiny, Adel Elsherbiny, Aadhyaa Setya, Johannes Gahn, Yongqin Tang, Purnima Gupta, Yanliang Dou, Heike Serke, Thomas Wieland, Alexandre Dubrac, Joerg Heineke, Michael Potente, Julio Cordero, Roxana Ola, Gergana Dobreva

{"title":"RNF20-mediated transcriptional pausing and VEGFA splicing orchestrate vessel growth","authors":"Nalan Tetik-Elsherbiny, Adel Elsherbiny, Aadhyaa Setya, Johannes Gahn, Yongqin Tang, Purnima Gupta, Yanliang Dou, Heike Serke, Thomas Wieland, Alexandre Dubrac, Joerg Heineke, Michael Potente, Julio Cordero, Roxana Ola, Gergana Dobreva","doi":"10.1038/s44161-024-00546-5","DOIUrl":"10.1038/s44161-024-00546-5","url":null,"abstract":"Signal-responsive gene expression is essential for vascular development, yet the mechanisms integrating signaling inputs with transcriptional activities are largely unknown. Here we show that RNF20, the primary E3 ubiquitin ligase for histone H2B, plays a multifaceted role in sprouting angiogenesis. RNF20 mediates RNA polymerase (Pol II) promoter-proximal pausing at genes highly paused in endothelial cells, involved in VEGFA signaling, stress response, cell cycle control and mRNA splicing. It also orchestrates large-scale mRNA processing events that alter the bioavailability and function of critical pro-angiogenic factors, such as VEGFA. Mechanistically, RNF20 restricts ERG-dependent Pol II pause release at highly paused genes while binding to Notch1 to promote H2B monoubiquitination at Notch target genes and Notch-dependent gene expression. This balance is crucial, as loss of Rnf20 leads to uncontrolled tip cell specification. Our findings highlight the pivotal role of RNF20 in regulating VEGF–Notch signaling circuits during vessel growth, underscoring its potential for therapeutic modulation of angiogenesis. Tetik-Elsherbiny et al. demonstrate that the E3 ubiquitin ligase RNF20 mediates RNA polymerase II promoter-proximal pausing and alternative splicing, regulating the bioavailability and signaling of pro-angiogenic factors and angiogenesis.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 10","pages":"1199-1216"},"PeriodicalIF":9.4,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s44161-024-00546-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142333948","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

Measured and genetically predicted protein levels and cardiovascular diseases in UK Biobank and China Kadoorie Biobank 英国生物库和中国嘉道理生物库中测量和基因预测的蛋白质水平与心血管疾病。

IF 9.4

Nature cardiovascular research Pub Date : 2024-09-25 DOI: 10.1038/s44161-024-00545-6

Lars Lind, Mohsen Mazidi, Robert Clarke, Derrick A. Bennett, Rui Zheng

{"title":"Measured and genetically predicted protein levels and cardiovascular diseases in UK Biobank and China Kadoorie Biobank","authors":"Lars Lind, Mohsen Mazidi, Robert Clarke, Derrick A. Bennett, Rui Zheng","doi":"10.1038/s44161-024-00545-6","DOIUrl":"10.1038/s44161-024-00545-6","url":null,"abstract":"Several large-scale studies have measured plasma levels of the proteome in individuals with cardiovascular diseases (CVDs)1–7. However, since the majority of such proteins are interrelated2, it is difficult for observational studies to distinguish which proteins are likely to be of etiological relevance. Here we evaluate whether plasma levels of 2,919 proteins measured in 52,164 UK Biobank participants are associated with incident myocardial infarction, ischemic stroke or heart failure. Of those proteins, 126 were associated with all three CVD outcomes and 118 were associated with at least one CVD in the China Kadoorie Biobank. Mendelian randomization and colocalization analyses indicated that genetically determined levels of 47 and 18 proteins, respectively, were associated with CVDs, including FGF5, PROCR and FURIN. While the majority of protein–CVD observational associations were noncausal, these three proteins showed evidence to support potential causality and are therefore promising targets for drug treatment for CVD outcomes. Lind et al. investigate the causal relationship between plasma proteins and cardiovascular disease outcomes in patients of European and Chinese descent, identifying FGF5, PROCR and FURIN as promising targets for the development of new drugs.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 10","pages":"1189-1198"},"PeriodicalIF":9.4,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s44161-024-00545-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142333947","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

Evolution of translational control and the emergence of genes and open reading frames in human and non-human primate hearts 翻译控制的进化以及人类和非人灵长类动物心脏中基因和开放阅读框的出现。

IF 9.4

Nature cardiovascular research Pub Date : 2024-09-24 DOI: 10.1038/s44161-024-00544-7

Jorge Ruiz-Orera, Duncan C. Miller, Johannes Greiner, Carolin Genehr, Aliki Grammatikaki, Susanne Blachut, Jeanne Mbebi, Giannino Patone, Anna Myronova, Eleonora Adami, Nikita Dewani, Ning Liang, Oliver Hummel, Michael B. Muecke, Thomas B. Hildebrandt, Guido Fritsch, Lisa Schrade, Wolfram H. Zimmermann, Ivanela Kondova, Sebastian Diecke, Sebastiaan van Heesch, Norbert Hübner

{"title":"Evolution of translational control and the emergence of genes and open reading frames in human and non-human primate hearts","authors":"Jorge Ruiz-Orera, Duncan C. Miller, Johannes Greiner, Carolin Genehr, Aliki Grammatikaki, Susanne Blachut, Jeanne Mbebi, Giannino Patone, Anna Myronova, Eleonora Adami, Nikita Dewani, Ning Liang, Oliver Hummel, Michael B. Muecke, Thomas B. Hildebrandt, Guido Fritsch, Lisa Schrade, Wolfram H. Zimmermann, Ivanela Kondova, Sebastian Diecke, Sebastiaan van Heesch, Norbert Hübner","doi":"10.1038/s44161-024-00544-7","DOIUrl":"10.1038/s44161-024-00544-7","url":null,"abstract":"Evolutionary innovations can be driven by changes in the rates of RNA translation and the emergence of new genes and small open reading frames (sORFs). In this study, we characterized the transcriptional and translational landscape of the hearts of four primate and two rodent species through integrative ribosome and transcriptomic profiling, including adult left ventricle tissues and induced pluripotent stem cell-derived cardiomyocyte cell cultures. We show here that the translational efficiencies of subunits of the mitochondrial oxidative phosphorylation chain complexes IV and V evolved rapidly across mammalian evolution. Moreover, we discovered hundreds of species-specific and lineage-specific genomic innovations that emerged during primate evolution in the heart, including 551 genes, 504 sORFs and 76 evolutionarily conserved genes displaying human-specific cardiac-enriched expression. Overall, our work describes the evolutionary processes and mechanisms that have shaped cardiac transcription and translation in recent primate evolution and sheds light on how these can contribute to cardiac development and disease. Ruiz-Orera et al. used comparative transcriptomics and translatomics to analyze the cardiac evolution in primates and discovered species-specific and lineage-specific genomic innovations that might contribute to cardiac development and disease.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 10","pages":"1217-1235"},"PeriodicalIF":9.4,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s44161-024-00544-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142333946","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

Cardiac NAD+ depletion in mice promotes hypertrophic cardiomyopathy and arrhythmias prior to impaired bioenergetics 小鼠心脏的 NAD+ 缺乏会在生物能受损之前导致肥厚型心肌病和心律失常。

IF 9.4

Nature cardiovascular research Pub Date : 2024-09-18 DOI: 10.1038/s44161-024-00542-9

Khanh V. Doan, Timothy S. Luongo, Thato T. Ts’olo, Won Dong Lee, David W. Frederick, Sarmistha Mukherjee, Gabriel K. Adzika, Caroline E. Perry, Ryan B. Gaspar, Nicole Walker, Megan C. Blair, Nicole Bye, James G. Davis, Corey D. Holman, Qingwei Chu, Lin Wang, Joshua D. Rabinowitz, Daniel P. Kelly, Thomas P. Cappola, Kenneth B. Margulies, Joseph A. Baur

{"title":"Cardiac NAD+ depletion in mice promotes hypertrophic cardiomyopathy and arrhythmias prior to impaired bioenergetics","authors":"Khanh V. Doan, Timothy S. Luongo, Thato T. Ts’olo, Won Dong Lee, David W. Frederick, Sarmistha Mukherjee, Gabriel K. Adzika, Caroline E. Perry, Ryan B. Gaspar, Nicole Walker, Megan C. Blair, Nicole Bye, James G. Davis, Corey D. Holman, Qingwei Chu, Lin Wang, Joshua D. Rabinowitz, Daniel P. Kelly, Thomas P. Cappola, Kenneth B. Margulies, Joseph A. Baur","doi":"10.1038/s44161-024-00542-9","DOIUrl":"10.1038/s44161-024-00542-9","url":null,"abstract":"Nicotinamide adenine dinucleotide (NAD+) is an essential co-factor in metabolic reactions and co-substrate for signaling enzymes. Failing human hearts display decreased expression of the major NAD+ biosynthetic enzyme nicotinamide phosphoribosyltransferase (Nampt) and lower NAD+ levels, and supplementation with NAD+ precursors is protective in preclinical models. Here we show that Nampt loss in adult cardiomyocytes caused depletion of NAD+ along with marked metabolic derangements, hypertrophic remodeling and sudden cardiac deaths, despite unchanged ejection fraction, endurance and mitochondrial respiratory capacity. These effects were directly attributable to NAD+ loss as all were ameliorated by restoring cardiac NAD+ levels with the NAD+ precursor nicotinamide riboside (NR). Electrocardiograms revealed that loss of myocardial Nampt caused a shortening of QT intervals with spontaneous lethal arrhythmias causing sudden cardiac death. Thus, changes in NAD+ concentration can have a profound influence on cardiac physiology even at levels sufficient to maintain energetics. Doan et al. show that loss of cardiac NAD+ is sufficient to drive metabolic derangements, hypertrophic remodeling and lethal arrhythmias in adult mouse hearts, despite maintenance of ejection fraction and bioenergetics.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 10","pages":"1236-1248"},"PeriodicalIF":9.4,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142247373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Success in heart regeneration depends on endocardial innate immune signaling 心脏再生的成功取决于心内膜先天性免疫信号的传递

IF 9.4

Nature cardiovascular research Pub Date : 2024-09-13 DOI: 10.1038/s44161-024-00539-4

Kazu Kikuchi

引用次数: 0

Identifying a gene-regulatory network that drives fibromuscular dysplasia 确定驱动纤维肌发育不良的基因调控网络

IF 9.4

Nature cardiovascular research Pub Date : 2024-09-13 DOI: 10.1038/s44161-024-00534-9

引用次数: 0