Nature cardiovascular research最新文献_第4页

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

Nature cardiovascular research Pub 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

{"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":"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. Li, Turaga and colleagues reveal intrinsic cardiomyocyte senescence and a hypoxic, mechanically stressed microvascular niche in hypoplastic left heart syndrome right ventricles and demonstrate that ventricular assist device therapy can alleviate these senescent states.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 3","pages":"262-280"},"PeriodicalIF":10.8,"publicationDate":"2026-03-04","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

Attenuation of epicardial activation and myofibroblast abundance via the Fbln2–Nupr1b axis stimulates cardiac regeneration in zebrafish 通过Fbln2-Nupr1b轴减弱心外膜激活和肌成纤维细胞丰度刺激斑马鱼心脏再生。

IF 10.8

Nature cardiovascular research Pub Date : 2026-03-03 DOI: 10.1038/s44161-026-00785-8

Gülsüm Kayman Kürekçi, Gursimran Kaur Bajwa, Shaoqiu Zhang, Séverine Leclerc, Emilie de Chantal, Darrell Belke, Gregor Andelfinger, Justin F. Deniset, Rubén Marín-Juez

{"title":"Attenuation of epicardial activation and myofibroblast abundance via the Fbln2–Nupr1b axis stimulates cardiac regeneration in zebrafish","authors":"Gülsüm Kayman Kürekçi, Gursimran Kaur Bajwa, Shaoqiu Zhang, Séverine Leclerc, Emilie de Chantal, Darrell Belke, Gregor Andelfinger, Justin F. Deniset, Rubén Marín-Juez","doi":"10.1038/s44161-026-00785-8","DOIUrl":"10.1038/s44161-026-00785-8","url":null,"abstract":"After injury, the adult human heart fails to regenerate and forms a persistent fibrotic scar. By contrast, fibrosis is transient in the injured zebrafish heart, facilitating cell recruitment and providing regenerative cues. The mechanisms that restrain excessive fibrosis while enabling regeneration remain poorly understood. Here we show that fibulin-2 (Fbln2) regulates specific populations of activated epicardial cells to balance the response to cardiac injury. Using genetic tools for Fbln2 dosage, we find that attenuation of epicardial activation stimulates regenerative programs. Mechanistically, we identify epicardial nuclear protein 1b (Nupr1b) as an Fbln2 effector. Using gain- and loss-of-function approaches, we show that Nupr1b controls epicardial myofibroblast abundance. Notably, epicardial-specific overexpression of nupr1b rescued fbln2 mutant phenotypes. These findings shed light on how modulation of epicardial cell state transitions through Fbln2–Nupr1b signaling regulates regenerative responses after cardiac injury. Kayman Kürekçi et al. show that fibulin-2 regulates epicardial cell activation through nuclear protein 1b signaling to balance fibrosis and regeneration after cardiac injury, and modulating this pathway can enhance heart regeneration in zebrafish.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 3","pages":"218-233"},"PeriodicalIF":10.8,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12995719/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147349884","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

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

Nature cardiovascular research Pub Date : 2026-02-26 DOI: 10.1038/s44161-026-00789-4

Merve Keles, Martin R. Wilkins, Allan Lawrie

引用次数: 0

Genetic studies of aortic stenosis provide a broader view of narrowed valves 主动脉狭窄的遗传学研究为狭窄的瓣膜提供了更广阔的视野。

IF 10.8

Nature cardiovascular research Pub Date : 2026-02-23 DOI: 10.1038/s44161-026-00787-6

Mihir M. Sanghvi, Patricia B. Munroe

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

Nature cardiovascular research 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

{"title":"Targeting immunometabolic pathways with AZD1656 alleviates inflammation and metabolic dysfunction in type 2 diabetic cardiomyopathy","authors":"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","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

Nature cardiovascular research Pub Date : 2026-02-23 DOI: 10.1038/s44161-025-00771-6

Takuma Takada, Jamie Francisco, Sebastiano Sciarretta, Junichi Sadoshima

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

Nature cardiovascular research 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

{"title":"A reduced TBX5-dependent gene regulatory network links atrial fibrillation and heart failure","authors":"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","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

Nature cardiovascular research Pub Date : 2026-02-16 DOI: 10.1038/s44161-026-00778-7

Amir Lotfi

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

Nature cardiovascular research 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

{"title":"Self-powered in-stent restenosis diagnosis via magnetoelastic stents","authors":"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","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

Nature cardiovascular research Pub Date : 2026-02-09 DOI: 10.1038/s44161-026-00784-9

Elisa Martini

引用次数: 0