Cardiovascular Research最新文献

{"title":"Correction to: SerpinB1 targeting safeguards against pathological cardiac hypertrophy and remodelling by suppressing cardiomyocyte pyroptosis and inflammation initiation.","authors":"","doi":"10.1093/cvr/cvaf002","DOIUrl":"10.1093/cvr/cvaf002","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"522"},"PeriodicalIF":10.2,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945129","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":"A novel approach to modelling acute cardiac decompensation in rats.","authors":"Arne Thiele, Hendrik Bartolomaeus, Harithaa Anandakumar, Nadine Haase, Arnd Heuser, Dominik N Müller, Ralf Dechend, Nicola Wilck","doi":"10.1093/cvr/cvae268","DOIUrl":"10.1093/cvr/cvae268","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"379-381"},"PeriodicalIF":10.2,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930707","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":"International partnership to nurture future cardiovascular research leaders in Europe.","authors":"Metin Avkiran","doi":"10.1093/cvr/cvae176","DOIUrl":"10.1093/cvr/cvae176","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"369-370"},"PeriodicalIF":10.2,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104724","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":"Cardioprotective effects of a 'twincretin' drug tirzepatide in heart failure following myocardial infarction.","authors":"Rui Shang, Brian Rodrigues","doi":"10.1093/cvr/cvaf006","DOIUrl":"10.1093/cvr/cvaf006","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"371-373"},"PeriodicalIF":10.2,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12038244/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143188417","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":"Restoring balance with recombinant interleukin-37: hope for halting chronic inflammation in calcific aortic valve disease.","authors":"Nalin H Dayawansa, Sara Baratchi, Karlheinz Peter","doi":"10.1093/cvr/cvaf018","DOIUrl":"10.1093/cvr/cvaf018","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"376-378"},"PeriodicalIF":10.2,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143490901","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":"Stretch regulation of β2-Adrenoceptor signalling in cardiomyocytes requires caveolae.","authors":"Jiarong Fu, Catherine Mansfield, Ivan Diakonov, Aleksandra Judina, Matthew Delahaye, Navneet Bhogal, Jose L Sanchez-Alonso, Timothy Kamp, Julia Gorelik","doi":"10.1093/cvr/cvae265","DOIUrl":"10.1093/cvr/cvae265","url":null,"abstract":"<p><strong>Aims: </strong>Caveolin-3 is essential for the formation of caveolae in cardiomyocytes. Caveolar microdomains have been shown to regulate the distribution of signalling proteins such as beta-adrenoceptors (βAR) and may act as membrane reserves to protect the cell from damage during the mechanical stretch. Myocardial stretch occurs during haemodynamic overload and may be normal (e.g. exercise) or pathological (e.g. heart failure); therefore, it is important to understand the effect of stretch on signalling pathways associated with mechanosensitive structures, such as caveolae. In this study, we investigate the role of caveolae in regulating the effect of stretch on βAR-signalling.</p><p><strong>Methods and results: </strong>We used osmotic swelling of isolated rat ventricular cardiomyocytes as a method to stretch the cell membrane and investigate the effect of βAR stimulation on cyclic adenosine monophosphate (cAMP) activity and contractility. βAR response was measured using a Förster Resonance Energy Transfer reporter for the second messenger cAMP and using CytoCypher for the measurement of cell contractility. β1AR and β2AR blockers were used to selectively allow stimulation of β2AR and β1AR, respectively. We also investigated the effect of stretch on βAR response to isoprenaline stimulation in left ventricular trabeculae dissected from control and cardiac-specific caveolin-3 knock-out mice (Cav3KO). Stretching trabeculae produces increased baseline adenylyl cyclase activity and a higher level of cAMP and a greater β2AR-induced positive inotropy after stimulation of the β2AR but not β1AR, by isoprenaline. Similar findings were confirmed for isolated myocytes subjected to hypoosmotic conditions. In isolated cardiomyocytes, caveolae depletion using methyl-beta-cyclodextrin or Cav3KO abolished the increase in β2AR response induced by stretch.</p><p><strong>Conclusion: </strong>Our study reveals a stretch-regulation of the β2AR signalling pathway, which requires functional caveolae. This indicates caveolae are mechanosensitive membrane domains that undergo structural and functional changes in response to stretch, thus leading to mechanical regulation of caveolae-associated signalling pathways.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"440-453"},"PeriodicalIF":10.2,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12038227/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143405715","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":"Vasoconstriction-inhibiting factor: an endogenous inhibitor of vascular calcification as a calcimimetic of calcium-sensing receptor.","authors":"Sofía de la Puente-Secades, Dustin Mikolajetz, Nathalie Gayrard, Juliane Hermann, Vera Jankowski, Shruti Bhargava, Amina Meyer, Àngel Argilés, Turgay Saritas, Emiel P C van der Vorst, Zhuojun Wu, Heidi Noels, Martin Tepel, Khaleda Alghamdi, Donald Ward, Walter Zidek, Michael Wolf, Jürgen Floege, Leon Schurgers, Setareh Orth-Alampour, Joachim Jankowski","doi":"10.1093/cvr/cvaf016","DOIUrl":"10.1093/cvr/cvaf016","url":null,"abstract":"<p><strong>Aims: </strong>Patients with chronic kidney disease (CKD) show a high risk of cardiovascular diseases, predominantly caused by accelerated vascular calcification. Vascular calcification is a highly regulated process with no current treatment. The vasoconstriction-inhibiting factor (VIF) peptide was recently discovered with vasoregulatory properties, but no information regarding calcification has been described.</p><p><strong>Methods and results: </strong>In the present work, the inhibitory calcification effect of the VIF peptide was analysed in vitro in vascular smooth muscle cells (VSMCs), ex vivo in rat aortic rings, as well as in vivo in rats treated with vitamin D and nicotine (VDN). The VIF peptide inhibits vascular calcification by acting as a calcimimetic for the calcium-sensing receptor, increasing carboxylated matrix Gla protein production and blocking the activation of calcification pathways. The VIF peptide decreased calcium influx, the production of reactive oxygen species, and the activation of multiple kinases in VSMCs. Furthermore, calcium deposition in the aortas of patients with CKD negatively correlates with the VIF peptide concentration. Moreover, we show the cleavage of the VIF peptide from chromogranin-A by 'proprotein convertase subtilisin/kexin type 2' and 'carboxypeptidase E' enzymes. In addition, 'cathepsin K' degrades the VIF peptide. The active site of the native 35 amino acid-sequence long VIF peptide was identified with seven amino acids, constituting a promising drug candidate with promise for clinical translation.</p><p><strong>Conclusion: </strong>The elucidation of the underlying mechanism by which the VIF peptide inhibits vascular calcification, as well as the active sequence and the cleavage and degradation enzymes, forms the basis for developing preventive and therapeutic measures to counteract vascular calcification.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"507-521"},"PeriodicalIF":10.2,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12038241/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555991","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":"Optical coherence tomography assessment of the impact of colchicine on non-culprit coronary plaque composition after myocardial infarction.","authors":"Peter J Psaltis, Mau T Nguyen, Kuljit Singh, Ajay Sinhal, Dennis T L Wong, Richard Alcock, Sharmalar Rajendran, Rustem Dautov, Peter Barlis, Sanjay Patel, Thalia Salagaras, Jessica A Marathe, Christina A Bursill, Nicholas J Montarello, Stefan M Nidorf, Peter L Thompson, Julie Butters, Alana R Cuthbert, Lisa N Yelland, Juanita L Ottaway, Yu Kataoka, Giuseppe Di Giovanni, Stephen J Nicholls","doi":"10.1093/cvr/cvae191","DOIUrl":"10.1093/cvr/cvae191","url":null,"abstract":"<p><strong>Aims: </strong>Low-dose colchicine reduces the risk of cardiovascular events after myocardial infarction (MI). The purpose of this study was to assess the effect of colchicine post-MI on coronary plaque morphology in non-culprit segments by optical coherence tomography (OCT).</p><p><strong>Methods and results: </strong>COCOMO-ACS was a double-blind, placebo-controlled trial that randomized 64 patients (median age 61.5 years; 9.4% female) with acute non-ST-segment elevation MI to colchicine 0.5 mg daily or placebo for a median of 17.8 months in addition to guideline-recommended therapy. Participants underwent serial OCT imaging within a matched segment of non-culprit coronary artery that contained at least one lipid-rich plaque causing ≥20% stenosis. The primary outcome was the change in minimum fibrous cap thickness (FCT) in non-culprit segments from baseline to final visit. Of those randomized, 57 (29 placebo, 28 colchicine) had evaluable imaging at baseline and follow-up. Overall, colchicine had no effect on relative (placebo +48.0 ± 35.1% vs. colchicine +62.4 ± 38.1%, P = 0.18) or absolute changes in minimum FCT (+29.2 ± 20.9 µm vs. + 37.2 ± 21.3 µm, P = 0.18), or change in maximum lipid arc (-38.8 ± 32.2° vs. -54.8 ± 46.9°, P = 0.18) throughout the imaged non-culprit segment. However, in patients assigned colchicine, cap rupture was less frequent (placebo 27.6% vs. colchicine 3.6%, P = 0.03). In post hoc analysis of 43 participants who had been followed for at least 16 months, minimum FCT increased to a greater extent in the colchicine group (placebo +38.7 ± 25.4% vs. colchicine +64.7 ± 34.1%, P = 0.005).</p><p><strong>Conclusion: </strong>In this study, OCT failed to detect an effect of colchicine on the minimum FCT or maximum lipid arc of plaques in non-culprit segments post-MI. The post hoc observation that minimum FCT increased to a greater extent with colchicine after more prolonged treatment suggests that longer-term studies may be required to detect the effect of anti-inflammatory therapies on plaque morphology by OCT.</p><p><strong>Clinical trial number: </strong>Australian New Zealand Clinical Trials Registry Identifier, ACTRN12618000809235, registered on the 11 May 2018.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"468-478"},"PeriodicalIF":10.2,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072072","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":"Colchicine and stabilization of coronary artery plaques.","authors":"Valtteri Muroke, Jean-Claude Tardif","doi":"10.1093/cvr/cvaf019","DOIUrl":"10.1093/cvr/cvaf019","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"374-375"},"PeriodicalIF":10.2,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143405705","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":"Single cell RNA sequencing of haematopoietic cells in fresh and frozen human atheroma tissue.","authors":"Herra Ahmad, Jayakrishnan Gopakumar, Daniel C Nachun, Lisa Ma, Jessica D'Addabbo, Xianxi Huang, Tiffany Koyano, Jack Boyd, Yi-Ping Joseph Woo, Robyn Fong, Oliver Aalami, Patricia K Nguyen, Siddhartha Jaiswal","doi":"10.1093/cvr/cvaf014","DOIUrl":"10.1093/cvr/cvaf014","url":null,"abstract":"<p><strong>Aims: </strong>Single-cell RNA sequencing (scRNA-seq) is a powerful method for exploring the cellular heterogeneity within human atheroma but typically requires fresh tissue to preserve cell membrane integrity, limiting the feasibility of large-scale biobanking for later analysis. The aim of this study was to determine whether cryopreservation of fragile and necrotic atheroma tissue affects the viability and transcriptomic profiles of haematopoietic cells in subsequent scRNA-seq analysis, enabling the use of cryopreserved atheroma samples for future research.</p><p><strong>Methods and results: </strong>We performed scRNA-seq on five paired fresh and cryopreserved atheroma samples-three from coronary arteries and two from carotid arteries. Each sample was enzymatically digested, sorted for CD45+ haematopoietic cells, and processed using the 10× Genomics scRNA-seq workflow. Half of each sample was processed immediately, while the other half was cryopreserved in liquid nitrogen for an average of 5 weeks before thawing and processing. In carotid artery samples, we noted the absence of LYVE1+ macrophages, likely due to the loss of the adventitial layer during endarterectomy procedures. Our results indicated that cryopreservation modestly affected cellular integrity, leading to an increase in the relative abundance of mitochondrial RNA in frozen samples. Minimal differences were observed between fresh and cryopreserved samples in uniquely detected transcripts, cell clustering, or transcriptional profiles within haematopoietic populations.</p><p><strong>Conclusions: </strong>Our study demonstrates that cryopreserved human atheroma samples can be successfully profiled using scRNA-seq, with comparable transcriptomic data to that obtained from fresh samples. These findings suggest that cryopreservation is a viable method for biobanking atheroma tissues, facilitating large-scale studies without the need for immediate sample processing.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"396-404"},"PeriodicalIF":10.2,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12038232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143188419","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}