Cardiovascular Research最新文献

{"title":"Novel flow cytometry-based method for isolating and characterizing human coronary artery endothelial cells from catheter wires in coronary disease and microvascular dysfunction.","authors":"Philip Stapmanns,Youssef S Abdelwahed,Christopher Wolfram,Elisabeth Strässler,Arash Haghikia,Ulf Landmesser,David Manuel Leistner,Nicolle Kränkel,Teresa Gerhardt","doi":"10.1093/cvr/cvaf139","DOIUrl":"https://doi.org/10.1093/cvr/cvaf139","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"18 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144825092","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":"Indoxyl sulfate: fuelling cardiovascular inflammation and calcification.","authors":"Prabhash Kumar Jha,Masanori Aikawa,Elena Aikawa","doi":"10.1093/cvr/cvaf134","DOIUrl":"https://doi.org/10.1093/cvr/cvaf134","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"70 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144824937","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":"Phenotypic spectrum of cardiac conduction disturbance and cardiomyopathy linked to titin canonical splice-site variants.","authors":"Taisuke Ishikawa,Hiroki Kimoto,Akiko Seki,Manabu Shirai,Kenta Uto,Takeru Makiyama,Takeshi Kitai,Hiroyuki Mishima,Floriane Simonet,Estelle Baron,Pierre Lindenbaum,Florence Kyndt,Adeline Goudal,Norihide Fukushima,Tomoyuki Fujita,Kinta Hatakeyama,Nobuhisa Hagiwara,Koh-Ichiro Yoshiura,Richard Redon,Christian Dina,Xavier Estivill,Stephan Ossowski,Mathieu Courtheix,Vincent Probst,Julien Barc,Jean-Jacques Schott,Naomasa Makita","doi":"10.1093/cvr/cvaf135","DOIUrl":"https://doi.org/10.1093/cvr/cvaf135","url":null,"abstract":"AIMSTruncating variations in the titin gene (TTNtv) are the most common genetic cause of dilated cardiomyopathy (DCM) and have been implicated in various arrhythmic and heart failure phenotypes. Nonetheless, predicting the pathogenicity of a distinct subtype of TTNtv, canonical splice-site variations (TTNcsv), remains challenging. Furthermore, the precise transcriptional and phenotypic consequences associated with TTNcsv remain unclear. We evaluated the transcriptional profiles of TTN in vitro, focusing on TTNcsv found in patients with cardiac dysfunction, and compared them with their phenotypic manifestations.METHODS AND RESULTSGenome-wide linkage analysis, whole-exome sequencing and whole-genome sequencing were performed on a five-generation family with cardiac conduction disturbance (CCD). In addition, whole-genome sequencing was performed on 402 Japanese biobank patients with cardiomyopathy or unidentified cardiac dysfunction. Transcriptional profiles of TTNcsv were evaluated by RNA-Seq of induced pluripotent stem cell-derived cardiomyocytes and endomyocardial biopsy specimens, and by minigene assays. A rare segregating TTNcsv (c.49049-2A>C) was identified in the five-generation family with CCD. RNA-Seq and minigene assays revealed complex aberrant TTN splicing transcripts: predominant non-truncating transcripts caused by an 18-bp in-frame deletion (83-90%) and minor truncating transcripts (10-17%). Two additional TTNcsv were identified in biobank participants by whole-genome sequencing. A minigene assay of TTNcsv c.67348+1G>A, identified in a CCD patient with mild cardiac dysfunction, revealed predominant non-truncating transcripts (95%), caused by retention of a 90-bp in-frame intron, along with 5% truncating TTN transcripts, caused by a 50-bp frameshift deletion, mirroring the TTNcsv observed in the familial CCD. In contrast, the DCM-associated TTNcsv c.67637-2A>G generated 87% truncating TTN transcripts, attributed to frameshift intron retention and cryptic splicing.CONCLUSIONSThe clinical data from this family suggest a close association between TTNcsv and CCD, which may involve an increase in non-truncating transcripts. Further studies are required to determine their precise relationship and the underlying mechanisms.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"778 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144769609","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":"Bone morphogenetic protein 10 is increased in pre-capillary pulmonary hypertension patients.","authors":"Aida Llucià-Valldeperas, Jessie van Wezenbeek, Joanne A Groeneveldt, Rowan Smal, Gonzalo Sánchez-Duffhues, Clarissa Becher, Azar Kianzad, Samara M A Jansen, Jeroen N Wessels, M Louis Handoko, Lilian J Meijboom, J Tim Marcus, Petr Symersky, Hans W M Niessen, Anton Vonk-Noordegraaf, Harm Jan Bogaard, Marie José Goumans, Frances S de Man","doi":"10.1093/cvr/cvaf028","DOIUrl":"10.1093/cvr/cvaf028","url":null,"abstract":"<p><strong>Aims: </strong>Pre-capillary pulmonary hypertension (precPH) results in increased right atrial (RA) stretch and pressure. The right atrium is the major source of bone morphogenetic protein 10 (BMP10) in adults, primarily produced by RA cardiomyocytes. The aim of this study was to investigate BMP10 expression in the right heart and systemic circulation and to identify potential triggers for increased BMP10 secretion associated with precPH.</p><p><strong>Methods and results: </strong>We examined BMP10 mRNA and protein expressions in RA tissue. Circulating BMP10 plasma levels were determined using enzyme-linked immunosorbent assay. BMP10 transcriptional activity was studied using a BMP-responsive element luciferase assay. Correlation analyses were performed between circulating BMP10 and RA dilatation as well as right ventricular (RV) function. Finally, we determined the impact of pressure unloading on BMP10 activity in chronic thromboembolic pulmonary hypertension (CTEPH) patients before and after pulmonary endarterectomy (PEA). BMP10 mRNA's protein and activity were significantly increased in the precPH right atrium. While circulating BMP10 protein levels were elevated, no significant changes were observed in BMP10 transcriptional activity between precPH and controls. Interestingly, RA dilatation, increased RA pressure, high N-terminal pro b-type natriuretic peptide levels, and reduced RV ejection fraction were associated with high BMP10 activity. Finally, pressure unloading after PEA in a cohort of CTEPH patients resulted in reduced BMP10 activity.</p><p><strong>Conclusion: </strong>RA BMP10 expression and plasma levels are increased in precPH, likely triggered by excessive RA dilatation and pressure overload. Future studies are needed to determine whether increased BMP10 release is an adaptive mechanism or a potential therapeutic target.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"1254-1268"},"PeriodicalIF":13.3,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12310281/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482388","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":"Targeting autophagy to treat neointimal hyperplasia in vascular disease.","authors":"Runan Yan, Simon Tual-Chalot, Konstantinos Stellos","doi":"10.1093/cvr/cvaf104","DOIUrl":"10.1093/cvr/cvaf104","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"1149-1151"},"PeriodicalIF":13.3,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12310277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144511608","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":"Testosterone and atrial fibrillation: does the dose make the poison?","authors":"Fleur E Mason, Aiste Liutkute, Niels Voigt","doi":"10.1093/cvr/cvaf113","DOIUrl":"10.1093/cvr/cvaf113","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"1144-1145"},"PeriodicalIF":13.3,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144511609","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":"PRDM16, a new kid on the block in cardiovascular health and disease.","authors":"Jore Van Wauwe, Hannelore Kemps, Pieter Vrancaert, Alexia Mahy, Robin Schellingen, Mandy O J Grootaert, Manu Beerens, Aernout Luttun","doi":"10.1093/cvr/cvaf089","DOIUrl":"10.1093/cvr/cvaf089","url":null,"abstract":"<p><p>Transcriptional regulation is essential for the development, homeostasis, and function of all organisms. Transcription factors and epigenetic modifiers play an indispensable role by direct or indirect interaction with DNA or chromatin. Although the role of transcription factor PRDM16 in adipose, haematopoietic, skeletal, and neural cell lineage specification is well-documented, its function within the cardiovascular system has only recently gained significant attention. Similar as in adipose tissue, PRDM16 displays an asymmetric expression pattern within the cardiovascular system, where it is exclusively expressed by ventricular cardiomyocytes and endothelial and smooth muscle cells of arteries while being absent in their atrial and venous counterparts. Concordantly, an increasing number of clinical and preclinical studies have identified PRDM16 as an important multi-modal regulator of cardiovascular development and function. Moreover, aberrant PRDM16 expression has now been linked to (cardio)vascular diseases, including left ventricular non-compaction, migraine, and coronary artery disease. In this review, we give a synopsis of PRDM16's expression and function within (developing) cardiovascular tissues and provide insights into how impaired PRDM16 signalling contributes to cardiovascular disease.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"1156-1172"},"PeriodicalIF":13.3,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12310283/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144172729","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":"Obesity and heart failure: exploring the cardiometabolic axis.","authors":"Jennifer J Rayner, Ines Abdesselam, Jiliu Pan, Andrew J M Lewis, Oliver J Rider","doi":"10.1093/cvr/cvaf090","DOIUrl":"10.1093/cvr/cvaf090","url":null,"abstract":"<p><p>Obesity is one of the biggest risks to public health in both developed and developing countries, and yet incidence continues to skyrocket. Being the main risk factor for a large number of life-limiting conditions, obesity has the potential to cause enormous damage unless addressed urgently. Heart failure (HF) is the most common cardiovascular disease associated with obesity. The incidence of HF overall continues to rise and mortality rates remain high, despite the rapid and significant advances in pharmacotherapy that have recently transformed the landscape of HF treatment. Both obesity and heart failure are multisystem disorders that are closely interlinked. Obesity poses the body a number of challenges, ranging from haemodynamic, to neuroendocrine, to inflammatory, to intracellular physiology. This narrative review describes the pathophysiological 'vicious cycle' caused by the combination of obesity and HF. Management of obesity in established heart failure has for years been a controversial topic, and yet an increasing body of evidence suggests that there are numerous benefits to managing obesity and insulin resistance in heart failure. Here, we review the existing evidence base, as well as exciting new developments, suggesting that we may finally be on the brink of a revolution in managing obesity in heart failure.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"1173-1186"},"PeriodicalIF":13.3,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12310286/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207762","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":"Deciphering metabolic reprogramming in atherosclerosis through a multi-omics approach.","authors":"Pascal Azar, Marie-Luce Bochaton-Piallat","doi":"10.1093/cvr/cvaf114","DOIUrl":"10.1093/cvr/cvaf114","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"1138-1140"},"PeriodicalIF":13.3,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144511607","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":"Cardiac regeneration beyond stem cells: harnessing sarcomere dynamics and endogenous repair mechanisms.","authors":"Xiaoke Yin, Manuel Mayr","doi":"10.1093/cvr/cvaf103","DOIUrl":"10.1093/cvr/cvaf103","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"1146-1148"},"PeriodicalIF":13.3,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207761","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}