Nature cardiovascular research最新文献

{"title":"Smartwatches capture early functional decline in heart failure","authors":"Elisa Martini","doi":"10.1038/s44161-026-00811-9","DOIUrl":"10.1038/s44161-026-00811-9","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 4","pages":"282-282"},"PeriodicalIF":10.8,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147693980","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}

{"title":"A wave of fetal hematopoiesis stemming from the hemogenic endothelium of vitelline and umbilical arteries","authors":"","doi":"10.1038/s44161-026-00797-4","DOIUrl":"10.1038/s44161-026-00797-4","url":null,"abstract":"How fetal and adult hematopoietic programs are organized in the embryo has remained a long-standing question. Using lineage tracing in mice, we identified a subset of specialized fetal blood progenitors that originate from the hemogenic endothelium of the embryonic vitelline and umbilical arteries. These fetal hematopoietic cells underlie a previously unrecognized developmental wave of hematopoiesis.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 4","pages":"289-290"},"PeriodicalIF":10.8,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147640767","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}

{"title":"Fetal-restricted hematopoietic progenitors arise from hemogenic endothelium in vitelline and umbilical arteries","authors":"Cristiana Barone, Giulia Quattrini, Alessandro Muratore, Giorgio Anselmi, Yurim Park, Naeema T. Mehmood, Elena Morganti, Roberto Orsenigo, Filipa Timóteo-Ferreira, Anna Cazzola, Arianna Patelli, Thea Milanesi, Bianca Nesti, Francisca Soares-da-Silva, Matthew Nicholls, Gloria Zambelli, Mario Mauri, Silvia Bombelli, Sofia De Marco, Deborah D’Aliberti, Silvia Spinelli, Veronica Bonalume, Alison Domingues, Mahdieh Naghavi Alhosseini, Gianluca Sala, Arianna Colonna, Elisabetta D’Errico, Cristina D’Orlando, Cristina Bianchi, Roberto A. Perego, Raffaella Meneveri, Ana Cumano, Silvia Brunelli, Marella F. T. R. De Bruijn, Andrea Ditadi, Alessandro Fantin, Rocco Piazza, Emanuele Azzoni","doi":"10.1038/s44161-026-00793-8","DOIUrl":"10.1038/s44161-026-00793-8","url":null,"abstract":"Embryonic hematopoiesis involves successive waves of progenitors from distinct anatomical sites, but the origins and contributions of early hematopoietic stem and progenitor cells (HSPCs) remain incompletely defined. Here we use genetic fate mapping in mice to temporally label hemogenic endothelium (HE) subsets and track their progeny. We show that a wave of fetal-restricted HSPCs arises from HE in the vitelline and umbilical arteries between embryonic days 8.5 and 9.5, preceding the emergence of definitive hematopoietic stem cells. Lineage tracing, single-cell transcriptomic analyses and functional assays revealed that these progenitors are transient and distinct from erythro-myeloid progenitors, contribute extensively to fetal lympho-myelopoiesis but decline postnatally. Our findings reveal a previously unrecognized early HE wave as a key source of fetal-restricted HSPCs, refining the spatial–temporal understanding of layered hematopoiesis and informing developmental origins of blood cell diversity. Barone et al. identify a fetal-restricted wave of hematopoietic progenitors that emerge from the hemogenic endothelium before hematopoietic stem cells and substantially contribute to embryonic lympho-myelopoiesis.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 4","pages":"308-327"},"PeriodicalIF":10.8,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-026-00793-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147640788","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}

{"title":"Spastin-mediated severing of glutamylated microtubules controls cardiomyocyte coupling","authors":"Jiayin Zhang, Xiaozhi Huang, Zhichao Wu, Jinxiu Liang, Shuo Chen, Chen Xu, Xinjian Wang, Ranran Cao, Xue Ji, Zijian Feng, Tao Lin, Xuyun Li, Xinyang Hu, Wei Zhu, Peidong Han","doi":"10.1038/s44161-026-00800-y","DOIUrl":"10.1038/s44161-026-00800-y","url":null,"abstract":"Cardiac ischemia–reperfusion injury frequently induces malignant arrhythmias because of connexin 43 (Cx43) mislocalization and impaired cardiomyocyte coupling; yet, effective therapies targeting this mechanism remain scarce. Here we show that ischemic cardiomyopathy in humans and ischemia–reperfusion in mice promote the accumulation and stabilization of glutamylated microtubules, disrupting targeted Cx43 trafficking. This remodeling of the glutamylated microtubule network is mediated by the microtubule-severing enzyme spastin. Spastin overexpression in cardiomyocytes reduced microtubule density, whereas its deficiency caused accumulation of glutamylated, stabilized microtubules. Although cardiomyocyte-specific spastin knockout mice displayed normal cardiac structure and function at baseline, they were highly susceptible to stress-induced malignant arrhythmias. Mechanistically, spastin deficiency impaired microtubule plus end dynamics and Cx43 transport. Notably, genetic or pharmacological reduction of microtubule glutamylation before ischemia–reperfusion preserved Cx43 localization and mitigated oxidative stress-induced injury. Together, these findings identify microtubule glutamylation as a key regulator of cardiac electrical stability and a promising therapeutic target in ischemia–reperfusion injury. Zhang et al. demonstrate that cardiac ischemia–reperfusion injury leads to the accumulation of glutamylated microtubules, which disrupts connexin 43 trafficking and promotes arrhythmias. They further show that targeting microtubule glutamylation or spastin preserves electrical stability and protects the heart from injury.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 4","pages":"366-382"},"PeriodicalIF":10.8,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147635370","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}

{"title":"A single intramuscular injection of self-amplifying Nppa RNA provides cardiac protection in preclinical models of myocardial infarction","authors":"Gerburg Schwaerzer","doi":"10.1038/s44161-026-00810-w","DOIUrl":"10.1038/s44161-026-00810-w","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 4","pages":"281-281"},"PeriodicalIF":10.8,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147617196","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}

{"title":"Large-scale identification of protein biomarkers and therapeutic targets in heart and brain disease","authors":"Chao Wu, Dantong Li, Sumeet A. Khetarpal, Zixun Yuan, Shengyuan Huang, Justin Ralph Baldovino Guerra, Chunyu Li, Qiulian Zhou, Meixi Quan, Jiaqi He, Meng Wang, Huiying Liang, Anthony Rosenzweig","doi":"10.1038/s44161-026-00799-2","DOIUrl":"10.1038/s44161-026-00799-2","url":null,"abstract":"Neurological complications frequently impact morbidity, mortality and quality of life in patients with cardiovascular disease, yet the biological mediators connecting cardiovascular and neurological disease are poorly understood. Here we leverage data from 53,014 individuals with plasma proteomic profiles and 50,228 with cardiac and brain magnetic resonance imaging from the UK Biobank to identify circulating proteins correlated with imaging-derived phenotypes (IDPs); 404 and 76 proteins were associated with cardiac or brain IDPs, and 37 with both. Expression analyses suggested these proteins largely originate from fibroblasts, smooth muscle cells, and macrophages in the arterial vasculature. Pathway analyses highlighted cytokine and vasculature-related processes for cardiac IDPs-associated proteins and extracellular matrix pathways in brain IDPs-associated proteins. Mendelian randomization and genetic colocalization supported causal roles for over 63% of these proteins in disease pathogenesis. Over 90% of the proposed candidates have not previously been established as clinical biomarkers or therapeutic targets and represent a catalog for further research. Wu et al. identify circulating proteins associated with cardiovascular and neurological imaging traits and diseases, and validate GDF15 as a shared determinant of heart and brain pathologies in mice.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 4","pages":"351-365"},"PeriodicalIF":10.8,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147610907","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}

{"title":"LIFE-Preserved enables long-term risk prediction in patients with heart failure with preserved ejection fraction","authors":"Andrea Tavosanis","doi":"10.1038/s44161-026-00809-3","DOIUrl":"10.1038/s44161-026-00809-3","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 4","pages":"283-283"},"PeriodicalIF":10.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147596676","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}

{"title":"Cardiovascular PIEZO discovery continues apace to reveal myocardial nerves feeling posture and blood loss","authors":"David J. Beech","doi":"10.1038/s44161-026-00802-w","DOIUrl":"10.1038/s44161-026-00802-w","url":null,"abstract":"The idea of myocardial mechanical reflexes was previously considered, but it struggled to gain traction in mainstream thinking. New research shows PIEZO2 ion channels conferring vagal force sensing in atrial and ventricular myocardium to protect the circulation as blood volume changes with gravity and injury.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 4","pages":"286-288"},"PeriodicalIF":10.8,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147517353","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}

{"title":"Decentralized clinical trials in cardiovascular disease : A primer for clinical trialists","authors":"Guillaume Baudry, Prashanth Kulkarni, Tor Biering-Sørensen, Adam D. DeVore, Charles Michael Gibson, Christopher B. Granger, Harriette G. C. Van Spall","doi":"10.1038/s44161-026-00788-5","DOIUrl":"10.1038/s44161-026-00788-5","url":null,"abstract":"Decentralized clinical trials (DCTs) move trial activities—such as recruitment, consent, delivery of the intervention, data collection and assessment of outcomes—away from traditional research sites to the homes or communities of patients. This participant-centered approach is accomplished through the use of digital health technology, remote monitoring, electronic data capture, and home- or community-based procedures. The advantage of DCTs may include broader trial recruitment pools with greater representativeness, reduced participant burden, greater operational efficiency and the ability to generate evidence in real-world settings. These features are particularly relevant in cardiovascular disease, which imposes a disproportionate population burden in regions where clinical trial centers are lacking. In this Perspective, we outline the essential components of the DCT ecosystem, discuss how DCTs can address key challenges in cardiovascular disease research, and using case examples, highlight operational and regulatory considerations in designing fully or partially (hybrid) decentralized trials. We also review the potential risks of DCTs and propose mitigation strategies to ensure high-quality, safe and reliable trial execution. Baudry et al. review the main components and operational considerations for running decentralized clinical trials, outline their specific advantages for the cardiovascular field, and propose strategies to mitigate their downsides and ensure their quality.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 3","pages":"193-203"},"PeriodicalIF":10.8,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147476645","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}

{"title":"Multi-view deep learning for echocardiogram interpretation","authors":"Mostafa A. Al-Alusi","doi":"10.1038/s44161-026-00780-z","DOIUrl":"10.1038/s44161-026-00780-z","url":null,"abstract":"Deep learning can identify cardiac abnormalities from echocardiogram videos, but previous work has predominantly used 2D video clips from a single cross-section of the heart. Research now shows that more complex approaches that integrate information from several echocardiographic views can improve deep learning prediction of cardiac abnormalities.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 3","pages":"172-174"},"PeriodicalIF":10.8,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147476588","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}