Nature cardiovascular research最新文献_第8页

Engineered human heart tissue reveals pathogenicity of autoantibodies in systemic lupus erythematosus 工程人体心脏组织揭示了自身抗体在系统性红斑狼疮中的致病性。

IF 9.4

Nature cardiovascular research Pub Date : 2024-08-29 DOI: 10.1038/s44161-024-00535-8

Madeleine W. Cunningham

引用次数: 0

The effect of cardiovascular medicine on sports doping 心血管医学对体育兴奋剂的影响。

IF 9.4

Nature cardiovascular research Pub Date : 2024-08-29 DOI: 10.1038/s44161-024-00536-7

Gerburg Schwaerzer

引用次数: 0

Participation of ventricular trabeculae in neonatal cardiac regeneration leads to ectopic recruitment of Purkinje-like cells 心室小梁参与新心肌再生导致了浦肯野样细胞的异位招募。

IF 9.4

Nature cardiovascular research Pub Date : 2024-08-28 DOI: 10.1038/s44161-024-00530-z

Lucie Boulgakoff, Rachel Sturny, Veronika Olejnickova, David Sedmera, Robert G. Kelly, Lucile Miquerol

{"title":"Participation of ventricular trabeculae in neonatal cardiac regeneration leads to ectopic recruitment of Purkinje-like cells","authors":"Lucie Boulgakoff, Rachel Sturny, Veronika Olejnickova, David Sedmera, Robert G. Kelly, Lucile Miquerol","doi":"10.1038/s44161-024-00530-z","DOIUrl":"10.1038/s44161-024-00530-z","url":null,"abstract":"Unlike adult mammals, newborn mice can regenerate a functional heart after myocardial infarction; however, the precise origin of the newly formed cardiomyocytes and whether the distal part of the conduction system (the Purkinje fiber (PF) network) is properly formed in regenerated hearts remains unclear. PFs, as well as subendocardial contractile cardiomyocytes, are derived from trabeculae, transient myocardial ridges on the inner ventricular surface. Here, using connexin 40-driven genetic tracing, we uncover a substantial participation of the trabecular lineage in myocardial regeneration through dedifferentiation and proliferation. Concomitantly, regeneration disrupted PF network maturation, resulting in permanent PF hyperplasia and impaired ventricular conduction. Proliferation assays, genetic impairment of PF recruitment, lineage tracing and clonal analysis revealed that PF network hyperplasia results from excessive recruitment of PFs due to increased trabecular fate plasticity. These data indicate that PF network hyperplasia is a consequence of trabeculae participation in myocardial regeneration. Boulgakoff et al. show that during cardiac regeneration, ventricular trabeculae participate in the repair of the contractile myocardium resulting in an excessive production of immature Purkinje fibers forming a hyperplastic PF network and altered ventricular conduction.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 9","pages":"1140-1157"},"PeriodicalIF":9.4,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142094273","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

Cardioprotective effects of glatiramer acetate after ischemic myocardial injury 缺血性心肌损伤后醋酸格拉替雷的心脏保护作用

IF 9.4

Nature cardiovascular research Pub Date : 2024-08-26 DOI: 10.1038/s44161-024-00517-w

Ulrich Hofmann, Stefan Frantz

引用次数: 0

Repurposing of glatiramer acetate to treat cardiac ischemia in rodent models 在啮齿动物模型中重新利用醋酸格拉替雷治疗心肌缺血。

IF 9.4

Nature cardiovascular research Pub Date : 2024-08-26 DOI: 10.1038/s44161-024-00524-x

Gal Aviel, Jacob Elkahal, Kfir Baruch Umansky, Hanna Bueno-Levy, Zachary Petrover, Yulia Kotlovski, Daria Lendengolts, David Kain, Tali Shalit, Lingling Zhang, Shoval Miyara, Matthias P. Kramer, Yifat Merbl, Stav Kozlovski, Ronen Alon, Rina Aharoni, Ruth Arnon, David Mishali, Uriel Katz, Dean Nachman, Rabea Asleh, Offer Amir, Eldad Tzahor, Rachel Sarig

{"title":"Repurposing of glatiramer acetate to treat cardiac ischemia in rodent models","authors":"Gal Aviel, Jacob Elkahal, Kfir Baruch Umansky, Hanna Bueno-Levy, Zachary Petrover, Yulia Kotlovski, Daria Lendengolts, David Kain, Tali Shalit, Lingling Zhang, Shoval Miyara, Matthias P. Kramer, Yifat Merbl, Stav Kozlovski, Ronen Alon, Rina Aharoni, Ruth Arnon, David Mishali, Uriel Katz, Dean Nachman, Rabea Asleh, Offer Amir, Eldad Tzahor, Rachel Sarig","doi":"10.1038/s44161-024-00524-x","DOIUrl":"10.1038/s44161-024-00524-x","url":null,"abstract":"Myocardial injury may ultimately lead to adverse ventricular remodeling and development of heart failure (HF), which is a major cause of morbidity and mortality worldwide. Given the slow pace and substantial costs of developing new therapeutics, drug repurposing is an attractive alternative. Studies of many organs, including the heart, highlight the importance of the immune system in modulating injury and repair outcomes. Glatiramer acetate (GA) is an immunomodulatory drug prescribed for patients with multiple sclerosis. Here, we report that short-term GA treatment improves cardiac function and reduces scar area in a mouse model of acute myocardial infarction and a rat model of ischemic HF. We provide mechanistic evidence indicating that, in addition to its immunomodulatory functions, GA exerts beneficial pleiotropic effects, including cardiomyocyte protection and enhanced angiogenesis. Overall, these findings highlight the potential repurposing of GA as a future therapy for a myriad of heart diseases. Sarig and Tzahor et al. show that the multiple sclerosis drug glatiramer acetate improves cardiac function and reduces scar area in rodent models of acute myocardial infarction and ischemic heart failure.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 9","pages":"1049-1066"},"PeriodicalIF":9.4,"publicationDate":"2024-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142115648","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

Author Correction: GPR15-mediated T cell recruitment during acute viral myocarditis facilitated virus elimination and improved outcome 作者更正：急性病毒性心肌炎期间GPR15介导的T细胞招募有助于病毒清除并改善预后

IF 9.4

Nature cardiovascular research Pub Date : 2024-08-23 DOI: 10.1038/s44161-024-00540-x

Bastian Stoffers, Hanna Wolf, Lucas Bacmeister, Svenja Kupsch, Tamara Vico, Timoteo Marchini, Maria A. Brehm, Isabell Yan, P. Moritz Becher, Armin Ardeshirdavani, Felicitas Escher, Sangwon V. Kim, Karin Klingel, Paulus Kirchhof, Stefan Blankenberg, Tanja Zeller, Dennis Wolf, Ingo Hilgendorf, Dirk Westermann, Diana Lindner

引用次数: 0

Epicardial adipose tissue resident memory T cells in atrial fibrillation 心房颤动中的心外膜脂肪组织常驻记忆 T 细胞

IF 9.4

Nature cardiovascular research Pub Date : 2024-08-23 DOI: 10.1038/s44161-024-00528-7

Federica Ruggeri, Vasiliki Papadopoulou, Marinos Kallikourdis

引用次数: 0

Tissue-resident memory T cells in epicardial adipose tissue comprise transcriptionally distinct subsets that are modulated in atrial fibrillation 心外膜脂肪组织中的组织驻留记忆 T 细胞由转录不同的亚群组成，这些亚群在心房颤动中受到调节

IF 9.4

Nature cardiovascular research Pub Date : 2024-08-23 DOI: 10.1038/s44161-024-00532-x

Vishal Vyas, Balraj Sandhar, Jack M. Keane, Elizabeth G. Wood, Hazel Blythe, Aled Jones, Eriomina Shahaj, Silvia Fanti, Jack Williams, Nasrine Metic, Mirjana Efremova, Han Leng Ng, Gayathri Nageswaran, Suzanne Byrne, Niklas Feldhahn, Federica Marelli-Berg, Benny Chain, Andrew Tinker, Malcolm C. Finlay, M. Paula Longhi

{"title":"Tissue-resident memory T cells in epicardial adipose tissue comprise transcriptionally distinct subsets that are modulated in atrial fibrillation","authors":"Vishal Vyas, Balraj Sandhar, Jack M. Keane, Elizabeth G. Wood, Hazel Blythe, Aled Jones, Eriomina Shahaj, Silvia Fanti, Jack Williams, Nasrine Metic, Mirjana Efremova, Han Leng Ng, Gayathri Nageswaran, Suzanne Byrne, Niklas Feldhahn, Federica Marelli-Berg, Benny Chain, Andrew Tinker, Malcolm C. Finlay, M. Paula Longhi","doi":"10.1038/s44161-024-00532-x","DOIUrl":"10.1038/s44161-024-00532-x","url":null,"abstract":"Atrial fibrillation (AF) is the most common sustained arrhythmia and carries an increased risk of stroke and heart failure. Here we investigated how the immune infiltrate of human epicardial adipose tissue (EAT), which directly overlies the myocardium, contributes to AF. Flow cytometry analysis revealed an enrichment of tissue-resident memory T (TRM) cells in patients with AF. Cellular indexing of transcriptomes and epitopes by sequencing (CITE-seq) and single-cell T cell receptor (TCR) sequencing identified two transcriptionally distinct CD8+ TRM cells that are modulated in AF. Spatial transcriptomic analysis of EAT and atrial tissue identified the border region between the tissues to be a region of intense inflammatory and fibrotic activity, and the addition of TRM populations to atrial cardiomyocytes demonstrated their ability to differentially alter calcium flux as well as activate inflammatory and apoptotic signaling pathways. This study identified EAT as a reservoir of TRM cells that can directly modulate vulnerability to cardiac arrhythmia. Vyas et al. show that epicardial adipose tissue is a reservoir for a subpopulation of tissue-resident memory T cells that can increase the vulnerability of the heart to atrial fibrillation.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 9","pages":"1067-1082"},"PeriodicalIF":9.4,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s44161-024-00532-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142231154","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

An engineered human cardiac tissue model reveals contributions of systemic lupus erythematosus autoantibodies to myocardial injury 工程人体心脏组织模型揭示了系统性红斑狼疮自身抗体对心肌损伤的作用。

IF 9.4

Nature cardiovascular research Pub Date : 2024-08-15 DOI: 10.1038/s44161-024-00525-w

Sharon Fleischer, Trevor R. Nash, Manuel A. Tamargo, Roberta I. Lock, Gabriela Venturini, Margaretha Morsink, Pamela L. Graney, Vanessa Li, Morgan J. Lamberti, Martin Liberman, Youngbin Kim, Daniel N. Tavakol, Richard Z. Zhuang, Jaron Whitehead, Richard A. Friedman, Rajesh K. Soni, Jonathan G. Seidman, Christine E. Seidman, Laura Geraldino-Pardilla, Robert Winchester, Gordana Vunjak-Novakovic

{"title":"An engineered human cardiac tissue model reveals contributions of systemic lupus erythematosus autoantibodies to myocardial injury","authors":"Sharon Fleischer, Trevor R. Nash, Manuel A. Tamargo, Roberta I. Lock, Gabriela Venturini, Margaretha Morsink, Pamela L. Graney, Vanessa Li, Morgan J. Lamberti, Martin Liberman, Youngbin Kim, Daniel N. Tavakol, Richard Z. Zhuang, Jaron Whitehead, Richard A. Friedman, Rajesh K. Soni, Jonathan G. Seidman, Christine E. Seidman, Laura Geraldino-Pardilla, Robert Winchester, Gordana Vunjak-Novakovic","doi":"10.1038/s44161-024-00525-w","DOIUrl":"10.1038/s44161-024-00525-w","url":null,"abstract":"Systemic lupus erythematosus (SLE) is a heterogenous autoimmune disease that affects multiple organs, including the heart. The mechanisms of myocardial injury in SLE remain poorly understood. In this study, we engineered human cardiac tissues and cultured them with IgG from patients with SLE, with and without myocardial involvement. IgG from patients with elevated myocardial inflammation exhibited increased binding to apoptotic cells within cardiac tissues subjected to stress, whereas IgG from patients with systolic dysfunction exhibited enhanced binding to the surface of live cardiomyocytes. Functional assays and RNA sequencing revealed that, in the absence of immune cells, IgG from patients with systolic dysfunction altered cellular composition, respiration and calcium handling. Phage immunoprecipitation sequencing (PhIP-seq) confirmed distinctive IgG profiles between patient subgroups. Coupling IgG profiling with cell surfaceome analysis identified four potential pathogenic autoantibodies that may directly affect the myocardium. Overall, these insights may improve patient risk stratification and inform the development of new therapeutic strategies. Using engineered cardiac tissues, Fleischer, Nash et al. found that patients with lupus-mediated cardiac damage have unique autoantibodies that can independently alter tissue function. They also identified autoantibodies associated with heart injury.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 9","pages":"1123-1139"},"PeriodicalIF":9.4,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s44161-024-00525-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142082861","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

Dampening the immune response protects vascular integrity and reduces lung damage in respiratory syndromes 抑制免疫反应，保护血管完整性，减少呼吸综合征对肺部的损伤

IF 9.4

Nature cardiovascular research Pub Date : 2024-08-12 DOI: 10.1038/s44161-024-00527-8

Andrea Tavosanis

引用次数: 0