Nature cardiovascular research最新文献_第2页

Inhibition of endothelial cell proliferation as a potential therapeutic approach in hereditary hemorrhagic telangectasia 将抑制内皮细胞增殖作为遗传性出血性毛细血管扩张症的一种潜在治疗方法。

IF 9.4

Nature cardiovascular research Pub Date : 2024-11-01 DOI: 10.1038/s44161-024-00557-2

Nicolas Ricard, Sabine Bailly

引用次数: 0

Macrophage GPNMB-mediated cardiac repair 巨噬细胞 GPNMB 介导的心脏修复

IF 9.4

Nature cardiovascular research Pub Date : 2024-10-25 DOI: 10.1038/s44161-024-00559-0

Jennifer J. Hill

引用次数: 0

Bone-marrow macrophage-derived GPNMB protein binds to orphan receptor GPR39 and plays a critical role in cardiac repair 骨髓巨噬细胞衍生的 GPNMB 蛋白与孤儿受体 GPR39 结合，在心脏修复中发挥关键作用。

IF 9.4

Nature cardiovascular research Pub Date : 2024-10-25 DOI: 10.1038/s44161-024-00555-4

Sivakumar Ramadoss, Juan Qin, Bo Tao, Nathan E. Thomas, Edward Cao, Rimao Wu, Daniel R. Sandoval, Ann Piermatteo, Kaare V. Grunddal, Feiyang Ma, Shen Li, Baiming Sun, Yonggang Zhou, Jijun Wan, Matteo Pellegrini, Birgitte Holst, Aldons J. Lusis, Philip L.S.M. Gordts, Arjun Deb

{"title":"Bone-marrow macrophage-derived GPNMB protein binds to orphan receptor GPR39 and plays a critical role in cardiac repair","authors":"Sivakumar Ramadoss, Juan Qin, Bo Tao, Nathan E. Thomas, Edward Cao, Rimao Wu, Daniel R. Sandoval, Ann Piermatteo, Kaare V. Grunddal, Feiyang Ma, Shen Li, Baiming Sun, Yonggang Zhou, Jijun Wan, Matteo Pellegrini, Birgitte Holst, Aldons J. Lusis, Philip L.S.M. Gordts, Arjun Deb","doi":"10.1038/s44161-024-00555-4","DOIUrl":"10.1038/s44161-024-00555-4","url":null,"abstract":"Glycoprotein nonmetastatic melanoma protein B (GPNMB) is a type I transmembrane protein initially identified in nonmetastatic melanomas and has been associated with human heart failure; however, its role in cardiac injury and function remains unclear. Here we show that GPNMB expression is elevated in failing human and mouse hearts after myocardial infarction (MI). Lineage tracing and bone-marrow transplantation reveal that bone-marrow-derived macrophages are the main source of GPNMB in injured hearts. Using genetic loss-of-function models, we demonstrate that GPNMB deficiency leads to increased mortality, cardiac rupture and rapid post-MI left ventricular dysfunction. Conversely, increasing circulating GPNMB levels through viral delivery improves heart function after MI. Single-cell transcriptomics show that GPNMB enhances myocyte contraction and reduces fibroblast activation. Additionally, we identified GPR39 as a receptor for circulating GPNMB, with its absence negating the beneficial effects. These findings highlight a pivotal role of macrophage-derived GPNMBs in post-MI cardiac repair through GPR39 signaling. Ramadoss et al. show that bone-marrow-derived macrophages contribute to heart repair following myocardial infarction by secreting GPNMB, which binds to the orphan receptor GPR39 to improve myocyte contractility and reduce fibroblast activation.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 11","pages":"1356-1373"},"PeriodicalIF":9.4,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142516782","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

Hypoxia sensing in resident cardiac macrophages regulates monocyte fate specification following ischemic heart injury 缺血性心脏损伤后，常驻心脏巨噬细胞的缺氧感知调节单核细胞的命运分化。

IF 9.4

Nature cardiovascular research Pub Date : 2024-10-21 DOI: 10.1038/s44161-024-00553-6

Farid F. Kadyrov, Andrew L. Koenig, Junedh M. Amrute, Hao Dun, Wenjun Li, Carla J. Weinheimer, Jessica M. Nigro, Attila Kovacs, Andrea L. Bredemeyer, Steven Yang, Shibali Das, Vinay R. Penna, Alekhya Parvathaneni, Lulu Lai, Niklas Hartmann, Benjamin J. Kopecky, Daniel Kreisel, Kory J. Lavine

{"title":"Hypoxia sensing in resident cardiac macrophages regulates monocyte fate specification following ischemic heart injury","authors":"Farid F. Kadyrov, Andrew L. Koenig, Junedh M. Amrute, Hao Dun, Wenjun Li, Carla J. Weinheimer, Jessica M. Nigro, Attila Kovacs, Andrea L. Bredemeyer, Steven Yang, Shibali Das, Vinay R. Penna, Alekhya Parvathaneni, Lulu Lai, Niklas Hartmann, Benjamin J. Kopecky, Daniel Kreisel, Kory J. Lavine","doi":"10.1038/s44161-024-00553-6","DOIUrl":"10.1038/s44161-024-00553-6","url":null,"abstract":"Myocardial infarction initiates cardiac remodeling and is central to heart failure pathogenesis. Following myocardial ischemia–reperfusion injury, monocytes enter the heart and differentiate into diverse subpopulations of macrophages. Here we show that deletion of Hif1α, a hypoxia response transcription factor, in resident cardiac macrophages led to increased remodeling and overrepresentation of macrophages expressing arginase 1 (Arg1). Arg1+ macrophages displayed an inflammatory gene signature and may represent an intermediate state of monocyte differentiation. Lineage tracing of Arg1+ macrophages revealed a monocyte differentiation trajectory consisting of multiple transcriptionally distinct states. We further showed that deletion of Hif1α in resident cardiac macrophages resulted in arrested progression through this trajectory and accumulation of an inflammatory intermediate state marked by persistent Arg1 expression. Depletion of the Arg1+ trajectory accelerated cardiac remodeling following ischemic injury. Our findings unveil distinct trajectories of monocyte differentiation and identify hypoxia sensing as an important determinant of monocyte differentiation following myocardial infarction. Kadyrov et al. reveal that the hypoxia sensing through HIF1A is an important regulator of monocyte-derived macrophage differentiation, which determines the extent of inflammation and cardiac remodeling after injury.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 11","pages":"1337-1355"},"PeriodicalIF":9.4,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142482515","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

CCL2-mediated endothelial injury drives cardiac dysfunction in long COVID CCL2 介导的内皮损伤导致长 COVID 的心脏功能障碍

IF 9.4

Nature cardiovascular research Pub Date : 2024-10-14 DOI: 10.1038/s44161-024-00543-8

Dilip Thomas, Chikage Noishiki, Sadhana Gaddam, David Wu, Amit Manhas, Yu Liu, Dipti Tripathi, Nimish Kathale, Shaunak S. Adkar, Jaishree Garhyan, Chun Liu, Baohui Xu, Elsie G. Ross, Ronald L. Dalman, Kevin C. Wang, Anthony E. Oro, Karim Sallam, Jason T. Lee, Joseph C. Wu, Nazish Sayed

{"title":"CCL2-mediated endothelial injury drives cardiac dysfunction in long COVID","authors":"Dilip Thomas, Chikage Noishiki, Sadhana Gaddam, David Wu, Amit Manhas, Yu Liu, Dipti Tripathi, Nimish Kathale, Shaunak S. Adkar, Jaishree Garhyan, Chun Liu, Baohui Xu, Elsie G. Ross, Ronald L. Dalman, Kevin C. Wang, Anthony E. Oro, Karim Sallam, Jason T. Lee, Joseph C. Wu, Nazish Sayed","doi":"10.1038/s44161-024-00543-8","DOIUrl":"10.1038/s44161-024-00543-8","url":null,"abstract":"Evidence linking the endothelium to cardiac injury in long coronavirus disease (COVID) is well documented, but the underlying mechanisms remain unknown. Here we show that cytokines released by endothelial cells (ECs) contribute to long-COVID-associated cardiac dysfunction. Using thrombotic vascular tissues from patients with long COVID and induced pluripotent stem cell-derived ECs (iPSC-ECs), we modeled endotheliitis and observed similar dysfunction and cytokine upregulation, notably CCL2. Cardiac organoids comprising iPSC-ECs and iPSC-derived cardiomyocytes showed cardiac dysfunction after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) exposure, driven by CCL2. Profiling of chromatin accessibility and gene expression at a single-cell resolution linked CCL2 to ‘phenotype switching’ and cardiac dysfunction, validated by high-throughput proteomics. Disease modeling of cardiac organoids and exposure of human ACE2 transgenic mice to SARS-CoV-2 spike proteins revealed that CCL2-induced oxidative stress promoted post-translational modification of cardiac proteins, leading to cardiac dysfunction. These findings suggest that EC-released cytokines contribute to cardiac dysfunction in long COVID, highlighting the importance of early vascular health monitoring in patients with long COVID. Thomas, Noishiki, Gaddam et al. used thrombotic vascular tissues and iPSC-derived cardiac organoids to show that COVID-19-induced endotheliitis and cytokine release disrupt endothelial–cardiomyocyte crosstalk and contribute to cardiac dysfunction in long COVID.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 10","pages":"1249-1265"},"PeriodicalIF":9.4,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142435943","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

Endothelial cells as paracrine mediators of long COVID 内皮细胞是长 COVID 的旁分泌介质

IF 9.4

Nature cardiovascular research Pub Date : 2024-10-14 DOI: 10.1038/s44161-024-00551-8

Simon R. Foster, James E. Hudson

引用次数: 0

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