Pub Date : 2026-03-01Epub Date: 2026-03-17DOI: 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.
{"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}
Pub Date : 2026-03-01Epub Date: 2026-03-04DOI: 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.
{"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}
Pub Date : 2026-03-01Epub Date: 2026-03-05DOI: 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.
{"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}
Pub Date : 2026-03-01DOI: 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}
Pub Date : 2026-02-23DOI: 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.
{"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}
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.
{"title":"Targeting immunometabolism for the treatment of diabetic cardiomyopathy","authors":"Takuma Takada, Jamie Francisco, Sebastiano Sciarretta, 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}
Pub Date : 2026-02-23DOI: 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.
{"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}
Pub Date : 2026-02-16DOI: 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}
Pub Date : 2026-02-16DOI: 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.
{"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}
Pub Date : 2026-02-09DOI: 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}