Cardiovascular Research最新文献

{"title":"Unravelling inflammation: the critical role of ETS2 in macrophage activation and chronic disease.","authors":"Soumaya Ben-Aicha,Gustavo Ramos","doi":"10.1093/cvr/cvaf072","DOIUrl":"https://doi.org/10.1093/cvr/cvaf072","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"33 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143871968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sleep protects the heart after myocardial infarction through a neuro-immune axis: time to implement healthy sleep for cardiovascular prevention?","authors":"Fabrizia Bonacina,Daniela Carnevale","doi":"10.1093/cvr/cvaf073","DOIUrl":"https://doi.org/10.1093/cvr/cvaf073","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"17 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143871967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Cellular mechanisms of oligoclonal vascular smooth muscle cell expansion in cardiovascular disease.","authors":"","doi":"10.1093/cvr/cvae251","DOIUrl":"10.1093/cvr/cvae251","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"367"},"PeriodicalIF":10.2,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12012440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardioprotection with nebivolol in patients undergoing anthracyclines: a randomized placebo-controlled trial.","authors":"Giulio Stefanini, Carmelo Carlo-Stella, Francesco Cannata, Mauro Chiarito, Stefano Figliozzi, Laura Novelli, Costanza Lisi, Sara Bombace, Federica Catapano, Eleonora Indolfi, Cristina Panico, Francesco Corrado, Giovanna Masci, Rita Mazza, Francesca Ricci, Lorenzo Monti, Giuseppe Ferrante, Bernhard Reimers, Armando Santoro, Marco Francone, Bruno R da Costa, Peter Jüni, Gianluigi Condorelli","doi":"10.1093/cvr/cvae266","DOIUrl":"10.1093/cvr/cvae266","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"227-229"},"PeriodicalIF":10.2,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12012441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143022164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Meis transcription factors regulate cardiac conduction system development and adult function.","authors":"Noelia Muñoz-Martín, Ana Simon-Chica, Covadonga Díaz-Díaz, Vanessa Cadenas, Susana Temiño, Isaac Esteban, Andreas Ludwig, Barbara Schormair, Juliane Winkelmann, Veronika Olejnickova, David Sedmera, David Filgueiras-Rama, Miguel Torres","doi":"10.1093/cvr/cvae258","DOIUrl":"10.1093/cvr/cvae258","url":null,"abstract":"<p><strong>Aims: </strong>The cardiac conduction system (CCS) is progressively specified during development by interactions among a discrete number of transcription factors (TFs) that ensure its proper patterning and the emergence of its functional properties. Meis genes encode homeodomain TFs with multiple roles in mammalian development. In humans, Meis genes associate with congenital cardiac malformations and alterations of cardiac electrical activity; however, the basis for these alterations has not been established. Here, we studied the role of Meis TFs in cardiomyocyte development and function during mouse development and adult life.</p><p><strong>Methods and results: </strong>We studied Meis1 and Meis2 conditional deletion mouse models that allowed cardiomyocyte-specific elimination of Meis function during development and inducible elimination of Meis function in cardiomyocytes of the adult CCS. We studied cardiac anatomy, contractility, and conduction. We report that Meis factors are global regulators of cardiac conduction, with a predominant role in the CCS. While constitutive Meis deletion in cardiomyocytes led to congenital malformations of the arterial pole and atria, as well as defects in ventricular conduction, Meis elimination in cardiomyocytes of the adult CCS produced sinus node dysfunction and delayed atrio-ventricular conduction. Molecular analyses unravelled Meis-controlled molecular pathways associated with these defects. Finally, we studied in transgenic mice the activity of a Meis1 human enhancer related to an single-nucleotide polymorphism (SNP) associated by Genome-wide association studies (GWAS) to PR (P and R waves of the electrocardiogram) elongation and found that the transgene drives expression in components of the atrio-ventricular conduction system.</p><p><strong>Conclusion: </strong>Our study identifies Meis TFs as essential regulators of the establishment of cardiac conduction function during development and its maintenance during adult life. In addition, we generated animal models and identified molecular alterations that will ease the study of Meis-associated conduction defects and congenital malformations in humans.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"311-323"},"PeriodicalIF":10.2,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12012448/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemokine receptor-directed imaging, prognostication, and treatment of abdominal aortic aneurysm: can we do it all with CXCR4?","authors":"Martin Andreas, Irene M Lang","doi":"10.1093/cvr/cvae259","DOIUrl":"10.1093/cvr/cvae259","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"222-223"},"PeriodicalIF":10.2,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Redirecting glucose into anabolic pathways participates in the protective effects of NRF2 activation in the heart under stress.","authors":"Thomas Eschenhagen","doi":"10.1093/cvr/cvaf003","DOIUrl":"10.1093/cvr/cvaf003","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"224-226"},"PeriodicalIF":10.2,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated proteomics identifies troponin I isoform switch as a regulator of a sarcomere-metabolism axis during cardiac regeneration","authors":"Timothy J Aballo, Jiyoung Bae, Wyatt G Paltzer, Emily A Chapman, Andrew J Perciaccante, Melissa R Pergande, Rebecca J Salamon, Dakota J Nuttall, Morgan W Mann, Ying Ge, Ahmed I Mahmoud","doi":"10.1093/cvr/cvaf069","DOIUrl":"https://doi.org/10.1093/cvr/cvaf069","url":null,"abstract":"Aims Adult mammalian cardiomyocytes have limited regenerative potential, and after myocardial infarction (MI), injured cardiac tissue is replaced with fibrotic scar. In contrast, the neonatal mouse heart possesses a regenerative capacity governed by cardiomyocyte proliferation; however, a metabolic switch from glycolysis to fatty acid oxidation during postnatal development results in loss of this regenerative capacity. Interestingly, a sarcomere isoform switch also takes place during postnatal development where slow skeletal troponin I (ssTnI) is replaced with cardiac troponin I (cTnI). It remains unclear whether there is an interplay between sarcomere isoform switching, cardiac metabolism, and regeneration. Methods and results In this study, we employ proteomics, metabolomics and lipidomics, transgenic mice, MI models, and histological analysis to delineate the molecular and sarcomeric transitions that occur during cardiac maturation and regeneration. First, we utilize integrated quantitative bottom-up and top-down proteomics to comprehensively define the proteomic and sarcomeric landscape during postnatal heart maturation. By employing a cardiomyocyte-specific ssTnI transgenic mouse model, we discovered that ssTnI overexpression increased cardiomyocyte proliferation and the cardiac regenerative capacity of the postnatal heart following MI compared to control mice by histological analysis. Our global proteomic analysis of ssTnI transgenic mice following MI reveals that ssTnI overexpression induces a significant shift in the cardiac proteomic landscape. Additionally, our lipidomic analysis demonstrated a significant upregulation of lipid species in the transgenic mice. This proteomic shift is characterized by an upregulation of key proteins involved in glycolytic metabolism. Conclusions Collectively, our data suggest that the postnatal TnI isoform switch may play a role in the metabolic shift from glycolysis to fatty acid oxidation during postnatal maturation. This underscores the significance of a sarcomere-metabolism axis during cardiomyocyte proliferation and heart regeneration.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"23 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143847137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhanced intracranial aneurysm development in a rat model of polycystic kidney disease","authors":"Anne F Cayron, Sandrine Morel, Maral Azam, Julien Haemmerli, Tomohiro Aoki, Philippe Bijlenga, Eric Allémann, Brenda R Kwak","doi":"10.1093/cvr/cvaf063","DOIUrl":"https://doi.org/10.1093/cvr/cvaf063","url":null,"abstract":"Aim Polycystic kidney disease (PKD) patients have a high intracranial aneurysms (IAs) incidence and risk of rupture. The mechanisms that make PKD patients more vulnerable to IA disease are still not completely understood. The PCK rat is a well-known PKD model and has been extensively used to study cyst development and kidney damage. Here, we used this rat model to study IA induction and vulnerability. Methods and results IAs were induced in wild-type (WT) and PCK rats and their incidence was followed. Variation in the anatomy of the circle of Willis was studied in PCK rats and PKD patients. Immunohistochemistry was performed in rat IAs and in human ruptured and unruptured IAs from patients enrolled in the @neurIST observational cohort. An increased frequency of fatal aortic dissection was unexpectedly observed in PCK rats, which was due to modifications in the elastic architecture of the aorta in combination with the induced hypertension. Interestingly, IAs developed faster in PCK rats compared to WT rats. Variations in the anatomy of the circle of Willis were identified in PCK rats and PKD patients, a risk factor that may (in part) explain the higher IA incidence found in these groups. At 2-weeks after induction, the endothelium of IAs from PCK rats showed a decrease in the tight junction proteins zonula occludens-1 and claudin-5. Furthermore, the type III collagen content was lower in IAs of PCK rats at 4-weeks post-surgery. The decrease in tight junction proteins was also observed in the endothelium of human ruptured IAs compared to unruptured IAs. Conclusions Our study showed that PCK rats are more sensitive to IA induction. Variations in the anatomy of the circle of Willis and impaired regulation of tight junction proteins might put PCK rats and PKD patients more at risk of developing vulnerable IAs.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"43 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143847175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"It's all c-Relative. A new perspective for a member of the NF-κB family.","authors":"Jonathan O'Connor-Miranda,Anthony Parent,Stephanie Lehoux","doi":"10.1093/cvr/cvaf053","DOIUrl":"https://doi.org/10.1093/cvr/cvaf053","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"17 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143846369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}