Nature cardiovascular research最新文献

{"title":"Publisher Correction: Genome-wide association study of coronary flow reserve assessed by cardiac perfusion PET suggests a role for NF-κB pathway","authors":"Rasika Venkatesh, Tess Cherlin, Nicole Wayne, Rachit Kumar, Lindsay Guare, Venkata P. Singamneni, Brett Irving, Scott Dudek, Penn Medicine BioBank, Michael G. Levin, Shefali Setia-Verma, Marie A. Guerraty","doi":"10.1038/s44161-026-00846-y","DOIUrl":"10.1038/s44161-026-00846-y","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 8","pages":"777-777"},"PeriodicalIF":12.6,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-026-00846-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148383302","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":"Loss of STMP1 impairs mitochondrial structure and links inflammaging to heart failure","authors":"Andrea Tavosanis","doi":"10.1038/s44161-026-00842-2","DOIUrl":"10.1038/s44161-026-00842-2","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 7","pages":"590-590"},"PeriodicalIF":12.6,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148364649","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":"HeartMap charts new territory in cardiac disease biology","authors":"David W. Staudt, Mark Mercola","doi":"10.1038/s44161-026-00835-1","DOIUrl":"10.1038/s44161-026-00835-1","url":null,"abstract":"Single-cell and single-nuclei transcriptomics reveal cell type-specific expression in heart disease, but inter-study variation and low power limit comparisons. A study now presents HeartMap, an atlas of 2.4 million cells from healthy and diseased hearts, enabling robust disease, cell-type and patient-subgroup analyses.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 7","pages":"591-592"},"PeriodicalIF":12.6,"publicationDate":"2026-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148341227","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":"An integrated cell atlas of 2.4 million cardiac cells across 209 individuals in health and disease","authors":"Yesh Datar, Mark Chaffin, Bridget Simonson, Alex Mandia, Patrick T. Ellinor","doi":"10.1038/s44161-026-00831-5","DOIUrl":"10.1038/s44161-026-00831-5","url":null,"abstract":"Cardiovascular disease remains the leading cause of global mortality. Understanding its complexity requires dissecting the heartʼs cellular landscape. Here we present HeartMap, a comprehensive single-nucleus RNA sequencing atlas of the adult human heart. This resource integrates data from nine studies, encompassing over 2.4 million nuclei, 209 individuals, eight anatomical regions and seven disease and healthy states. After rigorous data harmonization and method comparison of batch correction methods, we characterized transcriptional diversity across 14 cell types. To demonstrate the utility of HeartMap, we identified robust disease-associated gene signatures in dilated cardiomyopathy by comparing multiple studies. Notably, we identified distinct activated fibroblast populations, enriched for COL22A1 or TNC, that display variable prevalence across cardiomyopathies. HeartMap provides a valuable tool for exploring cardiac disease at the single-cell level, facilitating both fundamental research and potential therapeutic development. Datar et al. integrate multiple single-nucleus RNA sequencing datasets to generate a unified atlas of cardiovascular diseases, including ischemic and non-ischemic cardiomyopathies, myocardial infarction and coronary artery disease, and highlight the differential activation of fibroblast subsets across conditions.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 7","pages":"624-637"},"PeriodicalIF":12.6,"publicationDate":"2026-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-026-00831-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148341238","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":"Interim results of the Heart-2 clinical trial testing the safety and efficacy of VERVE-102 therapy","authors":"Elisa Martini","doi":"10.1038/s44161-026-00840-4","DOIUrl":"10.1038/s44161-026-00840-4","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 7","pages":"589-589"},"PeriodicalIF":12.6,"publicationDate":"2026-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148321092","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":"Publisher Correction: Genetic perspectives on the comorbidity of anxiety and mood disorders with cardiovascular disease","authors":"Eco J. C. de Geus, Jorien L. Treur, Brenda W. J. H. Penninx","doi":"10.1038/s44161-026-00838-y","DOIUrl":"10.1038/s44161-026-00838-y","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 7","pages":"659-659"},"PeriodicalIF":12.6,"publicationDate":"2026-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-026-00838-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148310580","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":"Author Correction: 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 Abul Hassan Samee, Iki Adachi, James F. Martin","doi":"10.1038/s44161-026-00839-x","DOIUrl":"10.1038/s44161-026-00839-x","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 7","pages":"658-658"},"PeriodicalIF":12.6,"publicationDate":"2026-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-026-00839-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148310556","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":"Proteomics reveals spatial and molecular heterogeneities in advanced atherosclerotic carotid artery plaques","authors":"Ankit Sinha, Nadja Sachs, Elena Kratz, Jessica Pauli, Sophia Steigerwald, Vincent Albrecht, Thierry M. Nordmann, Enes Ugur, Edwin H. Rodriguez, Marie-Luise Engl, Patricia Skowronek, Denys Oliinyk, Andreas Metousis, Moritz von Scheidt, Michael Wierer, Hanna Winter, Heribert Schunkert, Daniela Branzan, Lars Maegdefessel, Matthias Mann","doi":"10.1038/s44161-026-00827-1","DOIUrl":"10.1038/s44161-026-00827-1","url":null,"abstract":"Atherosclerotic plaque rupture is a major cause of cerebrovascular events, yet the molecular determinants underlying vulnerability-related plaque morphology, including fibrous-cap thickness, remain incompletely defined. Using histomorphology-guided spatial proteomics, here we delineate molecular programs associated with plaque cap phenotype across discrete plaque subregions. In 112 carotid endarterectomy specimens, differences between thin-cap and thick-cap plaques were predominantly localized to the necrotic core and fibrous cap. These differences were enriched for processes related to inflammation, lipid handling, extracellular matrix remodeling and ossification/calcification, and supported the presence of proteome-based plaque subtypes. PCSK9 was among the proteins most strongly associated with thin-cap plaques. Consistently, an in vitro model of necrotic core-like oxidative and inflammatory stress increased PCSK9 secretion in primary vascular smooth muscle cells. Together, these findings localize molecular programs associated with cap phenotype to plaque compartments and provide a framework for spatially informed biomarker discovery in advanced carotid atherosclerosis. Atherosclerotic plaque rupture underlies many cerebrovascular events, yet the molecular determinants of vulnerable plaque morphology remain poorly defined. Using histomorphology-guided spatial proteomics of 112 carotid plaques, Sinha et al. show that cap thickness-associated molecular programs are spatially confined to the fibrous cap and necrotic core, link thin-cap plaques to inflammatory and lipid handling pathways, and identify PCSK9 as a compartment-specific marker induced by oxidative and inflammatory stress in vascular smooth muscle cells.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 7","pages":"605-623"},"PeriodicalIF":12.6,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-026-00827-1.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148303996","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":"Deciphering molecular heterogeneity of carotid plaques using spatial proteomics","authors":"","doi":"10.1038/s44161-026-00828-0","DOIUrl":"10.1038/s44161-026-00828-0","url":null,"abstract":"We applied an ultra-sensitive, histomorphology-guided spatial proteomics workflow to advanced atherosclerotic carotid plaques to define molecular changes associated with minimum fibrous-cap thickness. Our analyses identified distinct plaque subtypes and showed that thin-cap plaques are enriched for inflammatory, lipid-processing, extracellular matrix remodeling and calcification-related programs concentrated in the necrotic core and fibrous cap.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 7","pages":"595-596"},"PeriodicalIF":12.6,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148303947","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":"Titin cleavage alters the myocardial elastic network and remodels the heart","authors":"","doi":"10.1038/s44161-026-00834-2","DOIUrl":"10.1038/s44161-026-00834-2","url":null,"abstract":"Proteolytic cleavage of the giant elastic protein titin causes the heart to lose elastic recoil, leading to a restrictive phenotype, impaired ventricular filling, disrupted cell–matrix connectivity, and immediate fibroblast activation followed by fibrosis. These findings identify titin-based restoring forces as essential regulators of cardiac mechanical homeostasis.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 7","pages":"593-594"},"PeriodicalIF":12.6,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148303950","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}