Nature cardiovascular research最新文献_第4页

Saving KLF2/4 from γ-protocadherin to reduce vascular inflammation and atherosclerosis 从γ-原粘连蛋白中拯救 KLF2/4，减少血管炎症和动脉粥样硬化。

IF 9.4

Nature cardiovascular research Pub Date : 2024-09-04 DOI: 10.1038/s44161-024-00523-y

Christian Park, Kyung In Baek, Hanjoong Jo

引用次数: 0

Endothelial γ-protocadherins inhibit KLF2 and KLF4 to promote atherosclerosis 内皮γ-原粘连蛋白抑制KLF2和KLF4，从而促进动脉粥样硬化。

IF 9.4

Nature cardiovascular research Pub Date : 2024-09-04 DOI: 10.1038/s44161-024-00522-z

Divyesh Joshi, Brian G. Coon, Raja Chakraborty, Hanqiang Deng, Ziyu Yang, Muhammad Usman Babar, Pablo Fernandez-Tussy, Emily Meredith, John Attanasio, Nikhil Joshi, James G. Traylor Jr., Anthony Wayne Orr, Carlos Fernandez-Hernando, Stephania Libreros, Martin A. Schwartz

{"title":"Endothelial γ-protocadherins inhibit KLF2 and KLF4 to promote atherosclerosis","authors":"Divyesh Joshi, Brian G. Coon, Raja Chakraborty, Hanqiang Deng, Ziyu Yang, Muhammad Usman Babar, Pablo Fernandez-Tussy, Emily Meredith, John Attanasio, Nikhil Joshi, James G. Traylor Jr., Anthony Wayne Orr, Carlos Fernandez-Hernando, Stephania Libreros, Martin A. Schwartz","doi":"10.1038/s44161-024-00522-z","DOIUrl":"10.1038/s44161-024-00522-z","url":null,"abstract":"Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of mortality worldwide. Laminar shear stress from blood flow, sensed by vascular endothelial cells, protects from ASCVD by upregulating the transcription factors KLF2 and KLF4, which induces an anti-inflammatory program that promotes vascular resilience. Here we identify clustered γ-protocadherins as therapeutically targetable, potent KLF2 and KLF4 suppressors whose upregulation contributes to ASCVD. Mechanistic studies show that γ-protocadherin cleavage results in translocation of the conserved intracellular domain to the nucleus where it physically associates with and suppresses signaling by the Notch intracellular domain. γ-Protocadherins are elevated in human ASCVD endothelium; their genetic deletion or antibody blockade protects from ASCVD in mice without detectably compromising host defense against bacterial or viral infection. These results elucidate a fundamental mechanism of vascular inflammation and reveal a method to target the endothelium rather than the immune system as a protective strategy in ASCVD. Joshi et al. show that γ-protocadherins suppress the anti-inflammatory KLF2 and KLF4 pathway and that targeting them is a viable therapeutic strategy to protect against atherosclerosis.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 9","pages":"1035-1048"},"PeriodicalIF":9.4,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s44161-024-00522-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142134664","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

α-Ketoglutarate promotes cardiomyocyte proliferation and heart regeneration after myocardial infarction α-酮戊二酸促进心肌细胞增殖和心肌梗死后的心脏再生

IF 9.4

Nature cardiovascular research Pub Date : 2024-09-02 DOI: 10.1038/s44161-024-00531-y

Yu Shi, Miao Tian, Xiaofang Zhao, Luxun Tang, Feng Wang, Hao Wu, Qiao Liao, Hongmei Ren, Wenbin Fu, Shuo Zheng, Pedro A. Jose, Liangpeng Li, Chunyu Zeng

{"title":"α-Ketoglutarate promotes cardiomyocyte proliferation and heart regeneration after myocardial infarction","authors":"Yu Shi, Miao Tian, Xiaofang Zhao, Luxun Tang, Feng Wang, Hao Wu, Qiao Liao, Hongmei Ren, Wenbin Fu, Shuo Zheng, Pedro A. Jose, Liangpeng Li, Chunyu Zeng","doi":"10.1038/s44161-024-00531-y","DOIUrl":"10.1038/s44161-024-00531-y","url":null,"abstract":"The neonatal mammalian heart can regenerate following injury through cardiomyocyte proliferation but loses this potential by postnatal day 7. Stimulating adult cardiomyocytes to reenter the cell cycle remains unclear. Here we show that cardiomyocyte proliferation depends on its metabolic state. Given the connection between the tricarboxylic acid cycle and cell proliferation, we analyzed these metabolites in mouse hearts from postnatal day 0.5 to day 7 and found that α-ketoglutarate ranked highest among the decreased metabolites. Injection of α-ketoglutarate extended the window of cardiomyocyte proliferation during heart development and promoted heart regeneration after myocardial infarction by inducing adult cardiomyocyte proliferation. This was confirmed in Ogdh-siRNA-treated mice with increased α-ketoglutarate levels. Mechanistically, α-ketoglutarate decreases H3K27me3 deposition at the promoters of cell cycle genes in cardiomyocytes. Thus, α-ketoglutarate promotes cardiomyocyte proliferation through JMJD3-dependent demethylation, offering a potential approach for treating myocardial infarction. Yu Shi et al. show that the citric acid cycle metabolite α-ketoglutarate promotes cardiomyocyte proliferation during heart development and promotes heart regeneration after myocardial infarction.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 9","pages":"1083-1097"},"PeriodicalIF":9.4,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142121286","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

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