Nature cardiovascular research最新文献

{"title":"27-hydroxycholesterol and endothelial cell immune memory link maternal hypercholesterolemia with atherosclerosis in the offspring.","authors":"Chieko Mineo, Philip W Shaul","doi":"10.1038/s44161-025-00631-3","DOIUrl":"10.1038/s44161-025-00631-3","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":" ","pages":"350-352"},"PeriodicalIF":9.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143733458","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":"Epigenetic silencing of PCSK9 enables durable reduction of low-density lipoprotein cholesterol.","authors":"Elisa Martini","doi":"10.1038/s44161-025-00644-y","DOIUrl":"10.1038/s44161-025-00644-y","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":" ","pages":"347"},"PeriodicalIF":9.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143812965","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":"Single-cell RNA sequencing reveals sex differences in the subcellular composition and associated gene-regulatory network activity of human carotid plaques.","authors":"Katyayani Sukhavasi, Giuseppe Mocci, Lijiang Ma, Chani J Hodonsky, Ernest Diez Benevante, Lars Muhl, Jianping Liu, Sonja Gustafsson, Byambajav Buyandelger, Simon Koplev, Urban Lendahl, Michael Vanlandewijck, Prosanta Singha, Tiit Örd, Mustafa Beter, Ilakya Selvarajan, Johanna P Laakkonen, Marika Väli, Hester M den Ruijter, Mete Civelek, Ke Hao, Arno Ruusalepp, Christer Betsholtz, Heli Järve, Jason C Kovacic, Clint L Miller, Casey Romanoski, Minna U Kaikkonen, Johan L M Björkegren","doi":"10.1038/s44161-025-00628-y","DOIUrl":"https://doi.org/10.1038/s44161-025-00628-y","url":null,"abstract":"<p><p>Carotid stenosis causes ischemic stroke in both sexes, but the clinical presentation and plaque characteristics differ. Here we run deep single-cell sequencing of 7,690 human carotid plaque cells from male and female patients. While we found no sex differences in major cell types, we identified a predominance of the osteogenic phenotype in smooth muscle cells, immunomodulating macrophages (MPs) and endothelial cells (ECs) undergoing endothelial-to-mesenchymal transition in females. In males, we found smooth muscle cells with the chondrocytic phenotype, MPs involved in tissue remodeling and ECs with angiogenic activity. Sex-biased subcellular clusters were integrated with tissue-specific gene-regulatory networks (GRNs) from the Stockholm-Tartu Atherosclerosis Reverse Network Engineering Task study. We identified GRN195 involved in angiogenesis and T cell-mediated cytotoxicity in male ECs, while in females, we found GRN33 and GRN122 related to TREM2^-/TREM1⁺ MPs and endothelial-to-mesenchymal transition. The impact of GRN195 on EC proliferation in males was functionally validated, providing evidence for potential therapy targets for atherosclerosis that are sex specific.</p>","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 4","pages":"412-432"},"PeriodicalIF":9.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11994450/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144060183","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":"The immune checkpoint regulator CD40 potentiates myocardial inflammation.","authors":"Jesus Jimenez, Junedh Amrute, Pan Ma, Xiaoran Wang, Shibali Das, Raymond Dai, Yohei Komaru, Andreas Herrlich, Matthias Mack, Kory J Lavine","doi":"10.1038/s44161-025-00633-1","DOIUrl":"https://doi.org/10.1038/s44161-025-00633-1","url":null,"abstract":"<p><p>Immune checkpoint therapeutics including CD40 agonists have tremendous promise to elicit antitumor responses in patients resistant to current therapies. Conventional immune checkpoint inhibitors (PD-1, PD-L1 and CTLA-4 antagonists) are associated with serious adverse cardiac events including life-threatening myocarditis. However, little is known regarding the potential for CD40 agonists to trigger myocardial inflammation or myocarditis. Here we leverage genetic mouse models, single-cell sequencing and cell depletion studies to show that an anti-CD40 agonist antibody reshapes the cardiac immune landscape through activation of CCR2⁺ macrophages and subsequent recruitment of effector memory CD8⁺ T cells. We identify a positive feedback loop between CCR2⁺ macrophages (positive for the chemokine receptor CCR2) and CD8⁺ T cells driven by IL-12b, TNF and IFNγ signaling that promotes myocardial inflammation and show that previous exposure to CD40 agonists sensitizes the heart to secondary insults and accelerates left ventricular remodeling. Collectively, these findings highlight the potential for CD40 agonists to promote myocardial inflammation and potentiate heart failure pathogenesis.</p>","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 4","pages":"458-472"},"PeriodicalIF":9.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144057990","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":"Synthetic generation of cardiac tissue motion from surface electrocardiograms.","authors":"Aditya Radhakrishnan, Naveena Yanamala, Ankush Jamthikar, Yanting Wang, Sasha-Ann East, Yasmin Hamirani, Kameswari Maganti, Partho P Sengupta","doi":"10.1038/s44161-025-00629-x","DOIUrl":"https://doi.org/10.1038/s44161-025-00629-x","url":null,"abstract":"<p><p>Cardiac tissue motion is a sensitive biomarker for detecting early myocardial damage. Here, we show the similarity, interpretability and diagnostic accuracy of synthetic tissue Doppler imaging (TDI) waveforms generated from surface electrocardiograms (ECGs). Prospectively collected ECG and TDI data were cross-matched as 9,144 lateral and 8,722 septal TDI-ECG pairs (463 patients) for generating synthetic TDI across every 1% interval of the cardiac cycle. External validation using 816 lateral and 869 septal TDI-ECG pairs (314 patients) demonstrated strong correlation (repeated-measures r = 0.90, P < 0.0001), cosine similarity (0.89, P < 0.0001) and no differences during a randomized visual Turing test. Synthetic TDI correlated with clinical parameters (585 patients) and detected diastolic and systolic dysfunction with an area under the curve of 0.80 and 0.81, respectively. Furthermore, synthetic TDI systolic and early diastolic measurements generated from an external ECG dataset (233,647 patients) were associated with all-cause mortality during both sinus rhythm and atrial fibrillation, underscoring their potential for personalized cardiac care.</p>","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 4","pages":"445-457"},"PeriodicalIF":9.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144042670","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":"Engineered heart muscles in non-human primates sustain heart remuscularization","authors":"Elisa Martini","doi":"10.1038/s44161-025-00630-4","DOIUrl":"10.1038/s44161-025-00630-4","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 3","pages":"250-250"},"PeriodicalIF":9.4,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143627175","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":"Telemedicine improves the cardiovascular management of isolated patients","authors":"Andrea Tavosanis","doi":"10.1038/s44161-025-00627-z","DOIUrl":"10.1038/s44161-025-00627-z","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 3","pages":"249-249"},"PeriodicalIF":9.4,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143617228","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":"The journey of the cardiovascular polypill from its conception to the WHO List of Essential Medicines","authors":"Valentin Fuster,&nbsp;Gines Sanz,&nbsp;Jose M. Castellano","doi":"10.1038/s44161-025-00619-z","DOIUrl":"10.1038/s44161-025-00619-z","url":null,"abstract":"Cardiovascular disease (CVD) has achieved pandemic proportions and is currently the leading cause of death worldwide. Barriers to optimal secondary cardiovascular prevention include lack of access to chronic treatment as well as low adherence in those who receive these treatments. The polypill represents a simple, cost-effective, scalable strategy to improve access and adherence to medication and effectively bridge the current gap in secondary prevention of CVD. Here, we review the epidemiological need for such a strategy as well as the most notable clinical evidence reported in the past decade supporting the clinical use of the polypill. Furthermore, we discuss the barriers inherent to the acceptance and use of the polypill for secondary prevention of CVD compared to the uptake of other polypills for the treatment of communicable diseases where fixed-dose combinations have become accepted as the cornerstone of treatment for other global pandemics such as HIV. Fuster, Sanz &amp; Castellano review the need for a cardiovascular polypill, the evidence supporting its benefits and the various challenges still impeding its widespread implementation, suggesting potential solutions based on previous successful polypill strategies.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 3","pages":"259-265"},"PeriodicalIF":9.4,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143607441","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":"The cellular and molecular cardiac tissue responses in human inflammatory cardiomyopathies after SARS-CoV-2 infection and COVID-19 vaccination","authors":"Henrike Maatz,&nbsp;Eric L. Lindberg,&nbsp;Eleonora Adami,&nbsp;Natalia López-Anguita,&nbsp;Alvaro Perdomo-Sabogal,&nbsp;Lucía Cocera Ortega,&nbsp;Giannino Patone,&nbsp;Daniel Reichart,&nbsp;Anna Myronova,&nbsp;Sabine Schmidt,&nbsp;Ahmed Elsanhoury,&nbsp;Oliver Klein,&nbsp;Uwe Kühl,&nbsp;Emanuel Wyler,&nbsp;Markus Landthaler,&nbsp;Schayan Yousefian,&nbsp;Simon Haas,&nbsp;Florian Kurth,&nbsp;Sarah A. Teichmann,&nbsp;Gavin Y. Oudit,&nbsp;Hendrik Milting,&nbsp;Michela Noseda,&nbsp;Jonathan G. Seidman,&nbsp;Christine E. Seidman,&nbsp;Bettina Heidecker,&nbsp;Leif E. Sander,&nbsp;Birgit Sawitzki,&nbsp;Karin Klingel,&nbsp;Patrick Doeblin,&nbsp;Sebastian Kelle,&nbsp;Sophie Van Linthout,&nbsp;Norbert Hubner,&nbsp;Carsten Tschöpe","doi":"10.1038/s44161-025-00612-6","DOIUrl":"10.1038/s44161-025-00612-6","url":null,"abstract":"Myocarditis, characterized by inflammatory cell infiltration, can have multiple etiologies, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection or, rarely, mRNA-based coronavirus disease 2019 (COVID-19) vaccination. The underlying cellular and molecular mechanisms remain poorly understood. In this study, we performed single-nucleus RNA sequencing on left ventricular endomyocardial biopsies from patients with myocarditis unrelated to COVID-19 (Non-COVID-19), after SARS-CoV-2 infection (Post-COVID-19) and after COVID-19 vaccination (Post-Vaccination). We identified distinct cytokine expression patterns, with interferon-γ playing a key role in Post-COVID-19, and upregulated IL16 and IL18 expression serving as a hallmark of Post-Vaccination myocarditis. Although myeloid responses were similar across all groups, the Post-Vaccination group showed a higher proportion of CD4+ T cells, and the Post-COVID-19 group exhibited an expansion of cytotoxic CD8+ T and natural killer cells. Endothelial cells showed gene expression changes indicative of vascular barrier dysfunction in the Post-COVID-19 group and ongoing angiogenesis across all groups. These findings highlight shared and distinct mechanisms driving myocarditis in patients with and without a history of SARS-CoV-2 infection or vaccination. Maatz, Lindberg et al. identify molecular alterations and immune response changes in endomyocardial biopsies from patients with myocarditis after COVID-19 infection, after anti-COVID-19 vaccination or from non-COVID-related causes.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 3","pages":"330-345"},"PeriodicalIF":9.4,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s44161-025-00612-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143494999","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":"TRPM7 channel as a potential therapeutic target for AAA","authors":"Ryan Laloo,&nbsp;Marc Bailey","doi":"10.1038/s44161-024-00598-7","DOIUrl":"10.1038/s44161-024-00598-7","url":null,"abstract":"TRPM7 channel interference protects against abdominal aortic aneurysm (AAA) formation and progression in mice by regulating phenotypic switching of vascular smooth muscle cells, extracellular matrix degradation and vessel wall inflammation, all of which are hallmark features of abdominal aortic aneurysm pathogenesis.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 2","pages":"126-128"},"PeriodicalIF":9.4,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424380","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}