首页 > 最新文献

Nature cardiovascular research最新文献

英文 中文
Multiview deep learning improves detection of major cardiac conditions from echocardiography. 多视图深度学习改进了超声心动图对主要心脏疾病的检测。
IF 10.8 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2026-03-01 Epub Date: 2026-03-17 DOI: 10.1038/s44161-026-00786-7
Joshua P Barrios, Minhaj U Ansari, Jeffrey E Olgin, Sean Abreau, Jacques Delfrate, Elodie L Langlais, Robert Avram, Geoffrey H Tison

Medical imaging often captures multiple two-dimensional views of three-dimensional anatomic structures, but most artificial intelligence (AI) models analyze two-dimensional data. Here we show that integrating multiple imaging views using a single AI model can improve diagnostic performance. We developed a deep neural network (DNN) architecture that combines information from multiple video views simultaneously. Using echocardiogram data from the University of California, San Francisco, and the Montreal Heart Institute, we applied our multiview DNN approach for three primary demonstration tasks: detecting any left or right ventricular abnormality, diastolic dysfunction, and substantial valvular regurgitation. Across various tasks, our multiview DNNs improved discrimination as measured by the area under the receiver operating characteristic curve by 0.06-0.09 compared to DNNs trained on any single view. This demonstrates that AI models that can combine information from multiple imaging views simultaneously can better capture complex anatomy and physiology for certain tasks, underscoring the value of a multiview paradigm for AI in medical imaging.

医学成像通常捕获三维解剖结构的多个二维视图,但大多数人工智能(AI)模型分析二维数据。本文表明,使用单个AI模型集成多个成像视图可以提高诊断性能。我们开发了一个深度神经网络(DNN)架构,同时结合来自多个视频视图的信息。利用来自加州大学旧金山分校和蒙特利尔心脏研究所的超声心动图数据,我们将我们的多视点DNN方法应用于三个主要演示任务:检测任何左心室或右心室异常、舒张功能障碍和严重的瓣膜反流。在各种任务中,与在任何单一视图上训练的dnn相比,我们的多视图dnn通过接收器工作特征曲线下的面积来测量识别率,提高了0.06-0.09。这表明,可以同时结合来自多个成像视图的信息的人工智能模型可以更好地捕获复杂的解剖和生理,以完成某些任务,强调了人工智能在医学成像中的多视图范式的价值。
{"title":"Multiview deep learning improves detection of major cardiac conditions from echocardiography.","authors":"Joshua P Barrios, Minhaj U Ansari, Jeffrey E Olgin, Sean Abreau, Jacques Delfrate, Elodie L Langlais, Robert Avram, Geoffrey H Tison","doi":"10.1038/s44161-026-00786-7","DOIUrl":"10.1038/s44161-026-00786-7","url":null,"abstract":"<p><p>Medical imaging often captures multiple two-dimensional views of three-dimensional anatomic structures, but most artificial intelligence (AI) models analyze two-dimensional data. Here we show that integrating multiple imaging views using a single AI model can improve diagnostic performance. We developed a deep neural network (DNN) architecture that combines information from multiple video views simultaneously. Using echocardiogram data from the University of California, San Francisco, and the Montreal Heart Institute, we applied our multiview DNN approach for three primary demonstration tasks: detecting any left or right ventricular abnormality, diastolic dysfunction, and substantial valvular regurgitation. Across various tasks, our multiview DNNs improved discrimination as measured by the area under the receiver operating characteristic curve by 0.06-0.09 compared to DNNs trained on any single view. This demonstrates that AI models that can combine information from multiple imaging views simultaneously can better capture complex anatomy and physiology for certain tasks, underscoring the value of a multiview paradigm for AI in medical imaging.</p>","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 3","pages":"234-245"},"PeriodicalIF":10.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12995717/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147476651","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
Ventricular assist device unloading reverses microvascular senescence in single ventricle disease. 心室辅助装置卸载逆转单心室疾病微血管衰老。
IF 10.8 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2026-03-01 Epub Date: 2026-03-04 DOI: 10.1038/s44161-026-00790-x
Xiao Li, Diwakar Turaga, Yi Zhao, Chang-Ru Tsai, Richard Gang Li, Yuka Morikawa, Hanna J Tadros, Md Abdul Hassan Samee, Iki Adachi, James F Martin

Individuals with hypoplastic left heart syndrome (HLHS) have an underdeveloped left ventricle and require surgery to reconfigure blood flow for survival. Here we profiled the HLHS right-ventricular microenvironment by single-nucleus RNA sequencing and spatial transcriptomics at birth (before heart failure), after surgery with heart failure and after ventricular assist device (VAD) unloading (reduced hypoxia and volume overload). We show that HLHS cardiomyocytes, both within the heart and when derived from induced pluripotent stem cells, are intrinsically senescent. The HLHS myocardium contained a senescent microvascular niche with endothelial cells, pericytes and YAP-high fibroblasts, consistent with hypoxic and mechanical stress. This senescent niche is similar to adult myocardial infarction but not pediatric dilated cardiomyopathy with heart failure, pointing to a prominent role of hypoxia in senescence. The microvascular senescent niche was improved by VAD, providing insight into the potential to reverse cardiac cell states that lead to heart failure.

患有左心发育不全综合征(HLHS)的个体左心室发育不全,需要手术来重新配置血流以维持生存。在这里,我们通过单核RNA测序和空间转录组学分析了HLHS在出生时(心力衰竭前)、心力衰竭手术后和心室辅助装置(VAD)卸载后(缺氧和容量过载减少)的右心室微环境。我们发现,无论是在心脏内还是从诱导多能干细胞中提取的HLHS心肌细胞,本质上都是衰老的。HLHS心肌包含一个衰老的微血管生态位,内皮细胞、周细胞和yap高的成纤维细胞,与缺氧和机械应力一致。这种衰老生态位与成人心肌梗死相似,但与儿童扩张型心肌病合并心力衰竭不同,这表明缺氧在衰老中起着突出作用。VAD改善了微血管衰老生态位,为逆转导致心力衰竭的心脏细胞状态提供了潜在的见解。
{"title":"Ventricular assist device unloading reverses microvascular senescence in single ventricle disease.","authors":"Xiao Li, Diwakar Turaga, Yi Zhao, Chang-Ru Tsai, Richard Gang Li, Yuka Morikawa, Hanna J Tadros, Md Abdul Hassan Samee, Iki Adachi, James F Martin","doi":"10.1038/s44161-026-00790-x","DOIUrl":"10.1038/s44161-026-00790-x","url":null,"abstract":"<p><p>Individuals with hypoplastic left heart syndrome (HLHS) have an underdeveloped left ventricle and require surgery to reconfigure blood flow for survival. Here we profiled the HLHS right-ventricular microenvironment by single-nucleus RNA sequencing and spatial transcriptomics at birth (before heart failure), after surgery with heart failure and after ventricular assist device (VAD) unloading (reduced hypoxia and volume overload). We show that HLHS cardiomyocytes, both within the heart and when derived from induced pluripotent stem cells, are intrinsically senescent. The HLHS myocardium contained a senescent microvascular niche with endothelial cells, pericytes and YAP-high fibroblasts, consistent with hypoxic and mechanical stress. This senescent niche is similar to adult myocardial infarction but not pediatric dilated cardiomyopathy with heart failure, pointing to a prominent role of hypoxia in senescence. The microvascular senescent niche was improved by VAD, providing insight into the potential to reverse cardiac cell states that lead to heart failure.</p>","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":" ","pages":"262-280"},"PeriodicalIF":10.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147357936","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
Strategies to improve regional representation in heart failure randomized controlled clinical trials. 提高心力衰竭随机对照临床试验区域代表性的策略。
IF 10.8 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2026-03-01 Epub Date: 2026-03-05 DOI: 10.1038/s44161-026-00779-6
Guillaume Baudry, Luca Monzo, Rebecca A V Newton, Guowei Li, Mark C Petrie, Nicolas Girerd, Alexandre Mebazaa, Diego Araiza Garaygordobil, Ana Mocumbi, Katja Rohwedder, Javed Butler, Lawrence Mbuagbaw, Faiez Zannad, Harriette G C Van Spall

The regional enrollment of participants in pivotal randomized controlled trials (RCTs) often does not represent the regional distribution of cardiovascular diseases. Over the past four decades, trials have enrolled participants primarily from North America and Europe, limiting the global generalizability of findings. In this Perspective, we review the evolution of regional participation in RCTs, using heart failure as a case study to assess temporal trends, current gaps in representativeness and opportunities for improvement. We assess the regulatory, logistical and financial barriers to clinical trial enrollment in underrepresented regions. We examine the manner in which global regions have been classified in trials, and propose a standardized regional classification system for reporting and subgroup analysis. To improve regional representativeness, we suggest targeted strategies that address barriers faced at the national, regulatory, sponsor or funder, institution and patient level. We also recommend the use of a representativeness index during trial planning and site selection to enhance regional representativeness. Expanding trial participation beyond historically dominant regions could be a key step in improving trial efficiency, external validity and global health equity.

关键随机对照试验(RCTs)参与者的区域入组通常不能代表心血管疾病的区域分布。在过去的40年里,试验主要招募了来自北美和欧洲的参与者,限制了研究结果的全球普遍性。在这一视角下,我们回顾了区域参与随机对照试验的演变,以心力衰竭为案例研究来评估时间趋势、当前代表性的差距和改进的机会。我们评估了在代表性不足地区临床试验入组的监管、后勤和财务障碍。我们研究了全球地区在试验中分类的方式,并提出了一种标准化的区域分类系统,用于报告和亚组分析。为了提高区域代表性,我们提出了有针对性的策略,以解决在国家、监管机构、赞助商或资助者、机构和患者层面面临的障碍。我们还建议在试验规划和选址过程中使用代表性指数,以增强区域代表性。将试验参与扩大到历史上占主导地位的地区以外,可能是提高试验效率、外部有效性和全球卫生公平性的关键一步。
{"title":"Strategies to improve regional representation in heart failure randomized controlled clinical trials.","authors":"Guillaume Baudry, Luca Monzo, Rebecca A V Newton, Guowei Li, Mark C Petrie, Nicolas Girerd, Alexandre Mebazaa, Diego Araiza Garaygordobil, Ana Mocumbi, Katja Rohwedder, Javed Butler, Lawrence Mbuagbaw, Faiez Zannad, Harriette G C Van Spall","doi":"10.1038/s44161-026-00779-6","DOIUrl":"10.1038/s44161-026-00779-6","url":null,"abstract":"<p><p>The regional enrollment of participants in pivotal randomized controlled trials (RCTs) often does not represent the regional distribution of cardiovascular diseases. Over the past four decades, trials have enrolled participants primarily from North America and Europe, limiting the global generalizability of findings. In this Perspective, we review the evolution of regional participation in RCTs, using heart failure as a case study to assess temporal trends, current gaps in representativeness and opportunities for improvement. We assess the regulatory, logistical and financial barriers to clinical trial enrollment in underrepresented regions. We examine the manner in which global regions have been classified in trials, and propose a standardized regional classification system for reporting and subgroup analysis. To improve regional representativeness, we suggest targeted strategies that address barriers faced at the national, regulatory, sponsor or funder, institution and patient level. We also recommend the use of a representativeness index during trial planning and site selection to enhance regional representativeness. Expanding trial participation beyond historically dominant regions could be a key step in improving trial efficiency, external validity and global health equity.</p>","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":" ","pages":"183-192"},"PeriodicalIF":10.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147367518","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
A blood biomarker to specifically identify idiopathic pulmonary arterial hypertension. 一种专门识别特发性肺动脉高压的血液生物标志物。
IF 10.8 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2026-03-01 DOI: 10.1038/s44161-026-00789-4
Merve Keles, Martin R Wilkins, Allan Lawrie
{"title":"A blood biomarker to specifically identify idiopathic pulmonary arterial hypertension.","authors":"Merve Keles, Martin R Wilkins, Allan Lawrie","doi":"10.1038/s44161-026-00789-4","DOIUrl":"10.1038/s44161-026-00789-4","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":" ","pages":"178-180"},"PeriodicalIF":10.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147313218","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
Targeting immunometabolic pathways with AZD1656 alleviates inflammation and metabolic dysfunction in type 2 diabetic cardiomyopathy AZD1656靶向免疫代谢途径可减轻2型糖尿病心肌病的炎症和代谢功能障碍
IF 10.8 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2026-02-23 DOI: 10.1038/s44161-025-00769-0
Stephanie Anderson, Anja Karlstaedt, Megan Young, Loucia Karatzia, Fenn Cullen, Jianmin Chen, Caroline E. O’Riordan, Michael R. Barnes, Zorana Štaka, Lauren J. Albee, Conor Garrod-Ketchley, Sanushi Dambure, Hiran A. Prag, Filip Cvetko, Jack J. J. J. Miller, Christoph Thiemermann, Andrew J. M. Lewis, Michael P. Murphy, David M. Smith, Sian M. Henson, Damian J. Tyler, Dunja Aksentijevic
Type 2 diabetes (T2D) precipitates diabetic cardiomyopathy (dbCM), a condition characterized by chronic inflammation, metabolic dysregulation and impaired cardiac performance. Here we show that the glucokinase activator AZD1656, originally developed for glycemic control but later identified to have immunomodulatory effects, reverses cardiac dysfunction and metabolic remodeling in dbCM. In obese, hyperglycemic db/db mice with diastolic dysfunction, 6 weeks of AZD1656 treatment improved myocardial performance, reduced infarct size and enhanced post-ischaemic recovery. Integrated metabolic, functional and histological analyses revealed restoration of mitochondrial metabolism and attenuation of fibrosis. Mechanistically, AZD1656 remodeled the cardiac immune landscape by promoting infiltration of regulatory T cells. These findings demonstrate a link between cardiac inflammation and metabolic remodeling in dbCM and highlight that modulation of immune cells and metabolism can protect the diabetic heart. Targeting immunometabolic pathways may therefore offer a therapeutic strategy to alleviate cardiac dysfunction and reduce infarct vulnerability in T2D. Anderson et al. demonstrate that the glucokinase activator AZD1656 reduces inflammation and reverses cardiac dysfunction and metabolic remodeling in mice with diabetic cardiomyopathy.
2型糖尿病(T2D)沉淀为糖尿病性心肌病(dbCM),以慢性炎症、代谢失调和心脏功能受损为特征。本研究表明,葡萄糖激酶激活剂AZD1656最初是为血糖控制而开发的,但后来被发现具有免疫调节作用,可逆转dbCM的心功能障碍和代谢重塑。在患有舒张功能障碍的肥胖、高血糖db/db小鼠中,6周AZD1656治疗可改善心肌功能,减少梗死面积,增强缺血后恢复。综合代谢、功能和组织学分析显示线粒体代谢恢复和纤维化减弱。从机制上讲,AZD1656通过促进调节性T细胞的浸润来重塑心脏免疫景观。这些发现证明了dbCM中心脏炎症和代谢重塑之间的联系,并强调了免疫细胞和代谢的调节可以保护糖尿病心脏。因此,靶向免疫代谢途径可能提供一种缓解心功能障碍和降低T2D梗死易感性的治疗策略。Anderson等人证明,葡萄糖激酶激活剂AZD1656可以减轻糖尿病性心肌病小鼠的炎症,逆转心功能障碍和代谢重塑。
{"title":"Targeting immunometabolic pathways with AZD1656 alleviates inflammation and metabolic dysfunction in type 2 diabetic cardiomyopathy","authors":"Stephanie Anderson,&nbsp;Anja Karlstaedt,&nbsp;Megan Young,&nbsp;Loucia Karatzia,&nbsp;Fenn Cullen,&nbsp;Jianmin Chen,&nbsp;Caroline E. O’Riordan,&nbsp;Michael R. Barnes,&nbsp;Zorana Štaka,&nbsp;Lauren J. Albee,&nbsp;Conor Garrod-Ketchley,&nbsp;Sanushi Dambure,&nbsp;Hiran A. Prag,&nbsp;Filip Cvetko,&nbsp;Jack J. J. J. Miller,&nbsp;Christoph Thiemermann,&nbsp;Andrew J. M. Lewis,&nbsp;Michael P. Murphy,&nbsp;David M. Smith,&nbsp;Sian M. Henson,&nbsp;Damian J. Tyler,&nbsp;Dunja Aksentijevic","doi":"10.1038/s44161-025-00769-0","DOIUrl":"10.1038/s44161-025-00769-0","url":null,"abstract":"Type 2 diabetes (T2D) precipitates diabetic cardiomyopathy (dbCM), a condition characterized by chronic inflammation, metabolic dysregulation and impaired cardiac performance. Here we show that the glucokinase activator AZD1656, originally developed for glycemic control but later identified to have immunomodulatory effects, reverses cardiac dysfunction and metabolic remodeling in dbCM. In obese, hyperglycemic db/db mice with diastolic dysfunction, 6 weeks of AZD1656 treatment improved myocardial performance, reduced infarct size and enhanced post-ischaemic recovery. Integrated metabolic, functional and histological analyses revealed restoration of mitochondrial metabolism and attenuation of fibrosis. Mechanistically, AZD1656 remodeled the cardiac immune landscape by promoting infiltration of regulatory T cells. These findings demonstrate a link between cardiac inflammation and metabolic remodeling in dbCM and highlight that modulation of immune cells and metabolism can protect the diabetic heart. Targeting immunometabolic pathways may therefore offer a therapeutic strategy to alleviate cardiac dysfunction and reduce infarct vulnerability in T2D. Anderson et al. demonstrate that the glucokinase activator AZD1656 reduces inflammation and reverses cardiac dysfunction and metabolic remodeling in mice with diabetic cardiomyopathy.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 2","pages":"138-154"},"PeriodicalIF":10.8,"publicationDate":"2026-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-025-00769-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147269049","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
Targeting immunometabolism for the treatment of diabetic cardiomyopathy 靶向免疫代谢治疗糖尿病性心肌病
IF 10.8 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2026-02-23 DOI: 10.1038/s44161-025-00771-6
Takuma Takada, Jamie Francisco, Sebastiano Sciarretta, Junichi Sadoshima
Aberrant immunometabolic signaling promotes cardiac remodeling in type 2 diabetes. Targeting this axis by enhancing the migratory capacity of regulatory T cells improves diabetic cardiomyopathy.
异常免疫代谢信号促进2型糖尿病患者心脏重构通过增强调节性T细胞的迁移能力靶向该轴可改善糖尿病性心肌病。
{"title":"Targeting immunometabolism for the treatment of diabetic cardiomyopathy","authors":"Takuma Takada,&nbsp;Jamie Francisco,&nbsp;Sebastiano Sciarretta,&nbsp;Junichi Sadoshima","doi":"10.1038/s44161-025-00771-6","DOIUrl":"10.1038/s44161-025-00771-6","url":null,"abstract":"Aberrant immunometabolic signaling promotes cardiac remodeling in type 2 diabetes. Targeting this axis by enhancing the migratory capacity of regulatory T cells improves diabetic cardiomyopathy.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 2","pages":"91-93"},"PeriodicalIF":10.8,"publicationDate":"2026-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147269042","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
A reduced TBX5-dependent gene regulatory network links atrial fibrillation and heart failure 减少tbx5依赖性基因调控网络连接心房颤动和心力衰竭
IF 10.8 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2026-02-23 DOI: 10.1038/s44161-025-00775-2
Sonja Lazarevic, Carlos Perez-Cervantes, Zhezhen Wang, Kaitlyn M. Shen, Margaret Gadek, Junhua Xiao, Naoko Yamaguchi, Johnathon M. Hall, Yildiz Koca, Douglas J. Chapski, Manuel Rosa-Garrido, Marcello Rubino, Rangarajan D. Nadadur, Timothy A. McKinsey, Thomas M. Vondriska, Alexander J. Ruthenburg, Sebastian Pott, David S. Park, Ivan P. Moskowitz
Atrial fibrillation (AF) and heart failure (HF) frequently coexist and worsen one another’s outcomes. To investigate shared molecular mechanisms, we compared atrial gene regulatory networks (GRNs) in the mouse Tbx5 conditional knockout (Tbx5 cKO) AF model and the transverse aortic constriction (TAC) HF model. Here we show highly correlated changes in atrial transcriptional and genomic profiles, including downregulated atrial Tbx5 expression in both mouse and human HF. More than 100 transcription factor genes were coordinately dysregulated in the atria of the Tbx5 cKO and TAC models. The wild-type atrial TBX5-driven GRN, including Klf15, a repressor of cardiomyocyte hypertrophy, was disrupted in Tbx5 cKO and TAC models. Conversely, a disease-specific network featuring Sox9 emerged in activated fibroblasts of Tbx5 cKO and TAC models. Our results identify coordinated disruption of TBX5-dependent atrial gene regulation in AF and HF, suggesting that a shared genomic injury response may underlie the reciprocal risk between these conditions. Lazarevic et al. reveal a shared loss of a TBX5-dependent atrial gene network in cardiomyocytes and a disease-specific network gain in activated fibroblasts across atrial fibrillation and heart failure models.
心房颤动(AF)和心力衰竭(HF)经常共存,并使彼此的预后恶化。为了探讨共同的分子机制,我们比较了小鼠Tbx5条件敲除(Tbx5 cKO) AF模型和横断主动脉缩窄(TAC) HF模型中的心房基因调控网络(grn)。在这里,我们显示了心房转录和基因组谱的高度相关变化,包括小鼠和人类HF中心房Tbx5表达的下调。在Tbx5 cKO和TAC模型中,超过100个转录因子基因在心房中协同失调。野生型心房Tbx5驱动的GRN,包括抑制心肌细胞肥厚的Klf15,在Tbx5 cKO和TAC模型中被破坏。相反,在Tbx5 cKO和TAC模型的活化成纤维细胞中出现了以Sox9为特征的疾病特异性网络。我们的研究结果确定了房颤和心衰中tbx5依赖性心房基因调控的协同破坏,表明共同的基因组损伤反应可能是这些疾病相互风险的基础。Lazarevic等人揭示了在心房颤动和心力衰竭模型中,心肌细胞中tbx5依赖性心房基因网络的共同缺失和活化成纤维细胞中疾病特异性网络的获得。
{"title":"A reduced TBX5-dependent gene regulatory network links atrial fibrillation and heart failure","authors":"Sonja Lazarevic,&nbsp;Carlos Perez-Cervantes,&nbsp;Zhezhen Wang,&nbsp;Kaitlyn M. Shen,&nbsp;Margaret Gadek,&nbsp;Junhua Xiao,&nbsp;Naoko Yamaguchi,&nbsp;Johnathon M. Hall,&nbsp;Yildiz Koca,&nbsp;Douglas J. Chapski,&nbsp;Manuel Rosa-Garrido,&nbsp;Marcello Rubino,&nbsp;Rangarajan D. Nadadur,&nbsp;Timothy A. McKinsey,&nbsp;Thomas M. Vondriska,&nbsp;Alexander J. Ruthenburg,&nbsp;Sebastian Pott,&nbsp;David S. Park,&nbsp;Ivan P. Moskowitz","doi":"10.1038/s44161-025-00775-2","DOIUrl":"10.1038/s44161-025-00775-2","url":null,"abstract":"Atrial fibrillation (AF) and heart failure (HF) frequently coexist and worsen one another’s outcomes. To investigate shared molecular mechanisms, we compared atrial gene regulatory networks (GRNs) in the mouse Tbx5 conditional knockout (Tbx5 cKO) AF model and the transverse aortic constriction (TAC) HF model. Here we show highly correlated changes in atrial transcriptional and genomic profiles, including downregulated atrial Tbx5 expression in both mouse and human HF. More than 100 transcription factor genes were coordinately dysregulated in the atria of the Tbx5 cKO and TAC models. The wild-type atrial TBX5-driven GRN, including Klf15, a repressor of cardiomyocyte hypertrophy, was disrupted in Tbx5 cKO and TAC models. Conversely, a disease-specific network featuring Sox9 emerged in activated fibroblasts of Tbx5 cKO and TAC models. Our results identify coordinated disruption of TBX5-dependent atrial gene regulation in AF and HF, suggesting that a shared genomic injury response may underlie the reciprocal risk between these conditions. Lazarevic et al. reveal a shared loss of a TBX5-dependent atrial gene network in cardiomyocytes and a disease-specific network gain in activated fibroblasts across atrial fibrillation and heart failure models.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 2","pages":"96-117"},"PeriodicalIF":10.8,"publicationDate":"2026-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147269047","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
Smart stents as self-powered guardians against restenosis 智能支架作为防止再狭窄的自供电监护人。
IF 10.8 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2026-02-16 DOI: 10.1038/s44161-026-00778-7
Amir Lotfi
A smart magnetoelastic stent has now been developed to prevent in-stent restenosis after implantation.
现在已经开发出一种智能磁弹性支架,以防止植入后支架内再狭窄。
{"title":"Smart stents as self-powered guardians against restenosis","authors":"Amir Lotfi","doi":"10.1038/s44161-026-00778-7","DOIUrl":"10.1038/s44161-026-00778-7","url":null,"abstract":"A smart magnetoelastic stent has now been developed to prevent in-stent restenosis after implantation.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 2","pages":"94-95"},"PeriodicalIF":10.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146208182","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
Self-powered in-stent restenosis diagnosis via magnetoelastic stents 自供电支架内再狭窄的磁弹性支架诊断。
IF 10.8 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2026-02-16 DOI: 10.1038/s44161-025-00773-4
Guorui Chen, Wi Jin Kim, Youcheng Yang, Yan-Ruide Li, Jing Tian, Junkai Zhang, Xun Zhao, Kamryn Scott, Lily G. Defelice, Zeyang Liu, Jing Xu, Tzuchun Chung, Jarod Carol, Yihao Zhou, Anthony C. Wang, Olujimi A. Ajijola, Paul S. Weiss, Wei Wang, Song Li, Geoffrey P. Colby, Jun Chen
Widely used in millions of atherosclerosis treatments, conventional metal stents, although pervasive, only provide mechanical support to narrowed arteries. However, many patients experience in-stent restenosis after implantation. Here we developed smart magnetoelastic stents that preserve mechanical functionality while enabling self-powered hemodynamic monitoring for continuous and timely diagnosis of in-stent restenosis. Using a clinical catheter, the smart stent is deployed in the swine carotid artery for in vivo hemodynamic sensing, enabling effective detection of induced stenosis through artificial intelligence-assisted signal interpretation. In vivo and in vitro studies demonstrate the biosafety of the smart stent through immune profiling, human cytokine analysis and single-cell RNA sequencing. These results underscore the smart stent’s potential for seamless integration into biological systems as a reliable diagnostic tool. This platform technology could potentially revolutionize current stent technology and contribute to improved strategies for managing atherosclerosis. Chen et al. developed a self-powered smart magnetoelastic stent for real-time hemodynamic monitoring and stenosis detection.
传统的金属支架虽然广泛应用于动脉粥样硬化治疗,但它只能为狭窄的动脉提供机械支持。然而,许多患者在植入后出现支架内再狭窄。在这里,我们开发了智能磁弹性支架,既能保持机械功能,又能实现自供电血流动力学监测,从而连续及时地诊断支架内再狭窄。使用临床导管,智能支架部署在猪颈动脉内进行体内血流动力学传感,通过人工智能辅助信号解读有效检测诱发性狭窄。体内和体外研究通过免疫分析、人类细胞因子分析和单细胞RNA测序证明了智能支架的生物安全性。这些结果强调了智能支架作为一种可靠的诊断工具无缝集成到生物系统中的潜力。该平台技术可能会彻底改变目前的支架技术,并有助于改善动脉粥样硬化管理策略。
{"title":"Self-powered in-stent restenosis diagnosis via magnetoelastic stents","authors":"Guorui Chen,&nbsp;Wi Jin Kim,&nbsp;Youcheng Yang,&nbsp;Yan-Ruide Li,&nbsp;Jing Tian,&nbsp;Junkai Zhang,&nbsp;Xun Zhao,&nbsp;Kamryn Scott,&nbsp;Lily G. Defelice,&nbsp;Zeyang Liu,&nbsp;Jing Xu,&nbsp;Tzuchun Chung,&nbsp;Jarod Carol,&nbsp;Yihao Zhou,&nbsp;Anthony C. Wang,&nbsp;Olujimi A. Ajijola,&nbsp;Paul S. Weiss,&nbsp;Wei Wang,&nbsp;Song Li,&nbsp;Geoffrey P. Colby,&nbsp;Jun Chen","doi":"10.1038/s44161-025-00773-4","DOIUrl":"10.1038/s44161-025-00773-4","url":null,"abstract":"Widely used in millions of atherosclerosis treatments, conventional metal stents, although pervasive, only provide mechanical support to narrowed arteries. However, many patients experience in-stent restenosis after implantation. Here we developed smart magnetoelastic stents that preserve mechanical functionality while enabling self-powered hemodynamic monitoring for continuous and timely diagnosis of in-stent restenosis. Using a clinical catheter, the smart stent is deployed in the swine carotid artery for in vivo hemodynamic sensing, enabling effective detection of induced stenosis through artificial intelligence-assisted signal interpretation. In vivo and in vitro studies demonstrate the biosafety of the smart stent through immune profiling, human cytokine analysis and single-cell RNA sequencing. These results underscore the smart stent’s potential for seamless integration into biological systems as a reliable diagnostic tool. This platform technology could potentially revolutionize current stent technology and contribute to improved strategies for managing atherosclerosis. Chen et al. developed a self-powered smart magnetoelastic stent for real-time hemodynamic monitoring and stenosis detection.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 2","pages":"155-167"},"PeriodicalIF":10.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146208088","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
CXCR6 signaling as a key mediator of CD8+ T cell-driven ICI myocarditis CXCR6信号作为CD8+ T细胞驱动的ICI心肌炎的关键介质。
IF 10.8 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2026-02-09 DOI: 10.1038/s44161-026-00784-9
Elisa Martini
{"title":"CXCR6 signaling as a key mediator of CD8+ T cell-driven ICI myocarditis","authors":"Elisa Martini","doi":"10.1038/s44161-026-00784-9","DOIUrl":"10.1038/s44161-026-00784-9","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 2","pages":"86-86"},"PeriodicalIF":10.8,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146151391","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
期刊
Nature cardiovascular research
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
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
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1