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Circulating GDF11 exacerbates myocardial injury in mice and associates with increased infarct size in humans Cardiovasc. Res. (IF 10.8) Pub Date : 2023-09-22 Simon Kraler, Carolina Balbi, Daria Vdovenko, Tetiana Lapikova-Bryhinska, Giovanni G Camici, Luca Liberale, Nicole Bonetti, Candela Diaz Canestro, Fabienne Burger, Aline Roth, Federico Carbone, Giuseppe Vassalli, François Mach, Shalender Bhasin, Florian A Wenzl, Olivier Muller, Lorenz Räber, Christian M Matter, Fabrizio Montecucco, Thomas F Lüscher, Alexander Akhmedov
Aims The heart rejuvenating effects of circulating growth differentiation factor 11 (GDF11), a TGF-β superfamily member that shares 90% homology with myostatin (MSTN), remains controversial. Here, we aimed to probe the role of GDF11 in acute myocardial infarction (MI), a frequent cause of heart failure and premature death during ageing. Methods and results In contrast to endogenous Mstn, myocardial
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Targeted activation of hERG channels rescues electrical instability induced by the hERG R56Q+/- Long QT Syndrome variant Cardiovasc. Res. (IF 10.8) Pub Date : 2023-09-20 R Venkateshappa, D V Hunter, P Muralidharan, R S Nagalingam, G Huen, S Faizi, S Luthra, E Lin, Y M Cheng, J Hughes, R Khelifi, P Dhunna, R Johal, V Sergeev, S Shafaattalab, L M Julian, D T Poburko, Z Laksman, G F Tibbits, T W Claydon
Aims Long QT Syndrome Type 2 (LQTS2) is associated with inherited variants in the cardiac hERG K+ channel. However, the pathogenicity of hERG channel gene variants is often uncertain. Using CRISPR-Cas9 gene-edited hiPSC-derived cardiomyocytes (hiPSC-CMs), we investigated the pathogenic mechanism underlying the LQTS-associated hERG R56Q variant, and its phenotypic rescue by the type 1 hERG activator
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Cardiomyocyte and endothelial cells play distinct roles in the tumor necrosis factor (TNF)-dependent atrial responses and increased atrial fibrillation vulnerability induced by endurance exercise training in mice Cardiovasc. Res. (IF 10.8) Pub Date : 2023-09-15 Robert Lakin, Nazari Polidovitch, Sibao Yang, Mihir Parikh, Xueyan Liu, Ryan Debi, Xiaodong Gao, Wenliang Chen, Camilo Guzman, Simona Yakobov, Farzad Izaddoustdar, Marianne Wauchop, Qian Lei, Weimin Xu, Sergei A Nedospasov, Vincent M Christoffels, Peter H Backx
Aims Endurance exercise is associated with an increased risk of atrial fibrillation (AF). We previously established that adverse atrial remodeling and AF susceptibility induced by intense exercise in mice requires the mechanosensitive and pro-inflammatory cytokine tumor necrosis factor (TNF). The cellular and mechanistic basis for these TNF-mediated effects is unknown. Methods and Results We studied
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Metabolic targeting of platelets to combat thrombosis: dawn of a new paradigm? Cardiovasc. Res. (IF 10.8) Pub Date : 2023-09-12 Gagan D Flora, Manasa K Nayak, Madankumar Ghatge, Anil K Chauhan
Current antithrombotic therapies used in clinical settings either target the coagulation pathways or platelet activation receptors (P2Y12 or GPIIb/IIIa), as well as the cyclooxygenase (COX) enzyme through aspirin. However, they are associated with bleeding risk and are not suitable for long-term use. Thus, novel strategies which provide broad protection against platelet activation with minimal bleeding
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Predictive metabolites for incident myocardial infarction: a two-step meta-analysis of individual patient data from six cohorts comprising 7,897 individuals from the the COnsortium of METabolomic Studies Cardiovasc. Res. (IF 10.8) Pub Date : 2023-09-12 Ana Nogal, Taryn Alkis, Yura Lee, Domagoj Kifer, Jie Hu, Rachel A Murphy, Zhe Huang, Rui Wang-Sattler, Gabi Kastenmüler, Birgit Linkohr, Clara Barrios, Marta Crespo, Christian Gieger, Annette Peters, Jackie Price, Kathryn M Rexrode, Bing Yu, Cristina Menni
Aims Myocardial infarction (MI) is a major cause of death and disability worldwide. Most metabolomics studies investigating metabolites predicting MI are limited by the participant number and/or the demographic diversity. We sought to identify biomarkers of incident MI in the Consortium of Metabolomics Studies (COMETS). Methods and Results We included 7,897 individuals aged on average 66 years from
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Atrial fibrillation-associated electrical remodelling in human induced pluripotent stem cell-derived atrial cardiomyocytes: a novel pathway for antiarrhythmic therapy development Cardiovasc. Res. (IF 10.8) Pub Date : 2023-09-05 Fitzwilliam Seibertz, Tony Rubio, Robin Springer, Fiona Popp, Melanie Ritter, Aiste Liutkute, Lena Bartelt, Lea Stelzer, Fereshteh Haghighi, Jan Pietras, Hendrik Windel, Núria Díaz i Pedrosa, Markus Rapedius, Yannic Döring, Richard Solano1, Robin Hindmarsh, Runzhu Shi, Malte Tiburcy, Tobias Brügmann, Ingo Kutschka, Katrin Streckfuss-Bömeke, George Kensah, Lukas Cyganek, Wolfram H Zimmermann, Niels
Background and Aims Atrial fibrillation (AF) is associated with tachycardia-induced cellular electrophysiology alterations which promote AF chronification and treatment resistance. Development of novel antiarrhythmic therapies is hampered by the absence of scalable experimental human models that reflect AF-associated electrical remodelling. Therefore, we aimed to assess if AF-associated remodelling
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Single-nuclear transcriptome profiling identifies persistent fibroblast activation in hypertrophic and failing human hearts of patients with longstanding disease Cardiovasc. Res. (IF 10.8) Pub Date : 2023-08-29 Badder Kattih, Felicitas Boeckling, Mariana Shumliakivska, Lukas Tombor, Tina Rasper, Katja Schmitz, Jedrzej Hoffmann, Luka Nicin, Wesley T Abplanalp, Daniel C Carstens, Mani Arsalan, Fabian Emrich, Tomas Holubec, Thomas Walther, Valentina O Puntmann, Eike Nagel, David John, Andreas M Zeiher, Stefanie Dimmeler
Aims Cardiac fibrosis drives the progression of heart failure in ischemic and hypertrophic cardiomyopathy. Therefore, the development of specific antifibrotic treatment regimens to counteract cardiac fibrosis is of high clinical relevance. Hence, this study examined the presence of persistent fibroblast activation during longstanding human heart disease at a single-cell resolution to identify putative
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PDE4D mediates impaired β-adrenergic receptor signaling in the sinoatrial node in mice with hypertensive heart disease Cardiovasc. Res. (IF 10.8) Pub Date : 2023-08-29 Tristan W Dorey, Megan D McRae, Darrell D Belke, Robert A Rose
Aims The sympathetic nervous system increases HR by activating β-adrenergic receptors (β-ARs) and increasing cAMP in sinoatrial node (SAN) myocytes while phosphodiesterases (PDEs) degrade cAMP. Chronotropic incompetence, the inability to regulate heart rate (HR) in response to sympathetic nervous system activation, is common in hypertensive heart disease; however, the basis for this is poorly understood
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Stroke risk management in carotid atherosclerotic disease: A Clinical Consensus Statement of the ESC Council on Stroke and the ESC Working Group on Aorta and Peripheral Vascular Diseases Cardiovasc. Res. (IF 10.8) Pub Date : 2023-08-23 Piotr Musialek, Leo H Bonati, Richard Bulbulia, Alison Halliday, Birgit Bock, Laura Capoccia, Hans-Henning Eckstein, Iris Q Grunwald, Peck Lin Lip, Andre Monteiro, Kosmas I Paraskevas, Anna Podlasek, Barbara Rantner, Kenneth Rosenfield, Adnan H Siddiqui, Henrik Sillesen, Isabelle Van Herzeele, Tomasz J Guzik, Lucia Mazzolai, Victor Aboyans, Gregory Y H Lip
Carotid atherosclerotic disease continues to be an important cause of stroke, often disabling or fatal. Such strokes could be largely prevented through optimal medical therapy and carotid revascularization. Advancements in discovery research and imaging along with evidence from recent pharmacology and interventional clinical trials and registries and the progress in acute stroke management have markedly
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Genetic inactivation of β-catenin is salubrious whereas its activation is deleterious in desmoplakin cardiomyopathy Cardiovasc. Res. (IF 10.8) Pub Date : 2023-08-23 Melis Olcum, Siyang Fan, Leila Rouhi, Sirisha Cheedipudi, Benjamin Cathcart, Hyun-Hwan Jeong, Zhongming Zhao, Priyatansh Gurha, Ali J Marian
Aim Mutations in the DSP gene encoding desmoplakin, a constituent of the desmosomes at the intercalated discs (IDs), cause a phenotype that spans arrhythmogenic cardiomyopathy (ACM) and dilated cardiomyopathy (DCM). It is typically characterized by biventricular enlargement and dysfunction, myocardial fibrosis, cell death, and arrhythmias. The canonical WNT (cWNT)/β-catenin pathway is implicated in
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Doxorubicin-induced cardiovascular toxicity: a longitudinal evaluation of functional and molecular markers Cardiovasc. Res. (IF 10.8) Pub Date : 2023-08-23 Matthias Bosman, Dustin Krüger, Charles Van Assche, Hanne Boen, Cédric Neutel, Kasper Favere, Constantijn Franssen, Wim Martinet, Lynn Roth, Guido De Meyer, Berta Cillero-Pastor, Leen Delrue, Ward Heggermont, Emeline Van Craenenbroeck, Pieter-Jan Guns
Aims Apart from cardiotoxicity, the chemotherapeutic doxorubicin (DOX) induces vascular toxicity, represented by arterial stiffness and endothelial dysfunction. Both parameters are of interest for cardiovascular risk stratification as they are independent predictors of future cardiovascular events in the general population. However, the time course of DOX-induced cardiovascular toxicity remains unclear
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Inhibition of galectin-3 post-infarction impedes progressive fibrosis by regulating inflammatory profibrotic cascades Cardiovasc. Res. (IF 10.8) Pub Date : 2023-08-21 Xiaoyin Wang, Meenakshi Gaur, Khalid Mounzih, Hilda J Rodriguez, Huiliang Qiu, Ming Chen, Liqiu Yan, Brian A Cooper, Shilpa Narayan, Ronak Derakhshandeh, Poonam Rao, Daniel D Han, Pooneh Nabavizadeh, Matthew L Springer, Constance M John
Aims Acute myocardial infarction (MI) causes inflammation, collagen deposition, and reparative fibrosis in response to myocyte death and, subsequently, a pathological myocardial remodelling process characterized by excessive interstitial fibrosis, driving heart failure (HF). Nonetheless, how or when to limit excessive fibrosis for therapeutic purposes remains uncertain. Galectin-3, a major mediator
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C5a-C5aR1 induces endoplasmic reticulum stress to accelerate vascular calcification via PERK-eIF2α-ATF4-CREB3L1 pathway Cardiovasc. Res. (IF 10.8) Pub Date : 2023-08-21 Aiting Liu, Zhenwei Chen, Xiaoxue Li, Chen Xie, Yanlian Chen, Xiaoyan Su, Ying Chen, Mengbi Zhang, Jie Chen, Tiecheng Yang, Jiangang Shen, Hui Huang
Aims Vascular calcification (VC) predicts the morbidity and mortality in cardiovascular diseases. Vascular smooth muscle cells (VSMCs) osteogenic transdifferentiation is the crucial pathological basis for VC. To date, the molecular pathogenesis is still largely unclear. Notably, C5a-C5aR1 contributes to the development of cardiovascular diseases, and it’s closely related to physiological bone mineralization
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Targeting endothelial VCAM-1 in atherosclerosis: drug discovery and development of VCAM-1-directed novel therapeutics Cardiovasc. Res. (IF 10.8) Pub Date : 2023-08-18 Jess R Pickett, Yuao Wu, Lucia F Zacchi, Hang T Ta
Vascular cell adhesion molecule-1 (VCAM-1) has been well established as a critical contributor to atherosclerosis and consequently, as an attractive therapeutic target for anti-atherosclerotic drug candidates. Many publications have demonstrated that disrupting VCAM-1 function blocks monocyte infiltration into the subendothelial space, which effectively prevents macrophage maturation and foam cell
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Activation of endothelial TRPM2 exacerbates blood-brain barrier degradation in ischemic stroke Cardiovasc. Res. (IF 10.8) Pub Date : 2023-08-18 Pengyu Zong, Jianlin Feng, Cindy X Li, Evan R Jellison, Zhichao Yue, Barbara Miller, Lixia Yue
Aims Damage of the blood-brain barrier (BBB) is a hallmark of brain injury during the early stages of ischemic stroke. The subsequent endothelial hyperpermeability drives the initial pathological changes and aggravates neuronal death. Transient receptor potential melastatin 2 (TRPM2) is a Ca2+-permeable nonselective cation channel activated by oxidative stress. However, whether TRPM2 is involved in
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Sex-biased TGFβ signaling in pulmonary arterial hypertension Cardiovasc. Res. (IF 10.8) Pub Date : 2023-08-18 Marius Wits, Clarissa Becher, Frances de Man, Gonzalo Sanchez-Duffhues, Marie-José Goumans
Pulmonary arterial hypertension (PAH) is a rare cardiovascular disorder leading to pulmonary hypertension and, often fatal, right heart failure. Sex-differences in PAH are evident, which primarily presents with a female predominance and increased male severity. Disturbed transduction of the transforming growth factor-β (TGFβ) signaling family and gene mutations in the Bone morphogenetic protein receptor
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Mitochondrial pannexin1 controls cardiac sensitivity to ischaemia/reperfusion injury Cardiovasc. Res. (IF 10.8) Pub Date : 2023-08-09 Olga M Rusiecka, Filippo Molica, Morten S Nielsen, Axel Tollance, Sandrine Morel, Maud Frieden, Marc Chanson, Kerstin Boengler, Brenda R Kwak
Aims No effective therapy is available in clinics to protect the heart from ischaemia/reperfusion (I/R) injury. Endothelial cells are activated after I/R, which may drive the inflammatory response by releasing ATP through pannexin1 (Panx1) channels. Here, we investigated the role of Panx1 in cardiac I/R. Methods and results Panx1 was found in cardiac endothelial cells, neutrophils, and cardiomyocytes
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p55γ degrades RIP3 via MG53 to suppress ischemia-induced myocardial necroptosis and mediates cardioprotection of preconditioning Cardiovasc. Res. (IF 10.8) Pub Date : 2023-08-01 Zhenyan Li, Rilei Dai, Min Chen, Lixuan Huang, Kun Zhu, Mingyang Li, Wenting Zhu, Yang Li, Ning Xie, Jingchen Li, Li Wang, Feng Lan, Chun-Mei Cao
Aims Regulated necrosis (necroptosis) and apoptosis are important biological features of myocardial infarction, ischemia-reperfusion (I/R) injury, and heart failure. However, the molecular mechanisms underlying myocardial necroptosis remain elusive. Ischemic preconditioning (IPC) is the most powerful intrinsic cardioprotection against myocardial I/R injury. In this study, we aimed to determine whether
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FAM210A regulates mitochondrial translation and maintains cardiac mitochondrial homeostasis Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-31 Jiangbin Wu, Kadiam C Venkata Subbaiah, Omar Hedaya, Si Chen, Joshua Munger, Wai Hong Wilson Tang, Chen Yan, Peng Yao
Aims Mitochondria play a vital role in cellular metabolism and energetics and support normal cardiac function. Disrupted mitochondrial function and homeostasis cause a variety of heart diseases. Fam210a (family with sequence similarity 210 member A), a novel mitochondrial gene, is identified as a hub gene in mouse cardiac remodeling by multi-omics studies. Human FAM210A mutations are associated with
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Immediate and sustained increases in the activity of vagal preganglionic neurons during exercise and after exercise training Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-30 Alla Korsak, Daniel O Kellett, Qadeer Aziz, Cali Anderson, Alicia D’Souza, Andrew Tinker, Gareth L Ackland, Alexander V Gourine
Background The brain controls the heart by dynamic recruitment and withdrawal of cardiac parasympathetic (vagal) and sympathetic activity. Autonomic control is essential for the development of cardiovascular responses during exercise, however, the patterns of changes in the activity of the two autonomic limbs, and their functional interactions in orchestrating physiological responses during exercise
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LncRNA-encoded peptides: unveiling their significance in cardiovascular physiology and pathology - current research insights Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-30 Li Zhang, Mi Tang, Haoyang Diao, Liling Xiong, Xiao Yang, Shasha Xing
Long non-coding RNAs (lncRNAs), which are RNA transcripts exceeding 200 nucleotides, were believed to lack any protein-coding capacity. But advancements in -omics technology have revealed that some lncRNAs have small open reading frames (sORFs) that can be translated by ribosomes to encode peptides, some of which have important biological functions. These encoded peptides subserve important biological
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Donor circadian clock influences the long-term survival of heart transplantation by immunoregulation Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-30 Wai Yen Yim, Tixiusi Xiong, Bingchuan Geng, Li Xu, Yu Feng, Jiangyang Chi, Ruikang Guo, Chenghao Li, Yuqi Chen, Jiawei Shi, Yixuan Wang, Nianguo Dong
Aims Circadian clocks play important role in immunoregulation. We aimed to investigate cardiac circadian clock specific pathways and compare cardiac grafts procured at different timing on survival after transplantation to explore novel criteria for donor selection. Methods and Results In primate heart, Phase Set Enrichment Analysis (PSEA) showed rhythmic transcripts were enriched in antigen processing
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SGLT2 inhibitor canagliflozin alleviates vascular calcification through suppression of NLRP3 inflammasome Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-28 An Chen, Zirong Lan, Li Li, Luting Xie, Xiaoyu Liu, Xiulin Yang, Siyi Wang, Qingchun Liang, Qianqian Dong, Liyun Feng, Yining Li, Yuanzhi Ye, Mingwei Fu, Lihe Lu, Jianyun Yan
Aims Vascular calcification is prevalent in pathological processes such as diabetes, chronic kidney disease (CKD) and atherosclerosis, but effective therapies are still lacking by far. Canagliflozin (CANA), an SGLT2 inhibitor, has been approved for the treatment of type 2 diabetes mellitus and exhibits beneficial effects against cardiovascular disease. However, the effect of CANA on vascular calcification
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Integrative human atrial modeling unravels interactive PKA and CaMKII signaling as key determinant of atrial arrhythmogenesis Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-28 Haibo Ni, Stefano Morotti, Xianwei Zhang, Dobromir Dobrev, Eleonora Grandi
Atrial fibrillation (AF), the most prevalent clinical arrhythmia, is associated with atrial remodeling manifesting as acute and chronic alterations in expression, function, and regulation of atrial electrophysiological and Ca2+-handling processes. These AF-induced modifications crosstalk and propagate across spatial scales creating a complex pathophysiological network, which renders AF resistant to
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Aortic valve calcification is promoted by interleukin-8 and restricted through antagonizing CXCR2 Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-28 Kawthar Dhayni, Yuthiline Chabry, Lucie Hénaut, Carine Avondo, Cedric Boudot, Hakim Ouled-Haddou, Edith Bigot-Corbel, Gilles Touati, Thierry Caus, Hind Messaoudi, Jérémy Bellien, Christophe Tribouilloy, David Messika-Zeitoun, Kazem Zibara, Saïd Kamel, Youssef Bennis
Aims Inflammatory cytokines play a critical role in the progression of calcific aortic valve disease (CAVD), for which there is currently no pharmacological treatment. The aim of this study was to test the hypothesis that interleukin-8 (IL-8), known to be involved in arterial calcification, also promotes aortic valve calcification (AVC) and to evaluate whether pharmacologically blocking the IL-8 receptor
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Genetic variation in SLC5A2 mimicking SGLT2-inhibition and risk of cardiovascular disease and all-cause mortality: reduced risk not explained by lower plasma glucose Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-28 Louise E Bechmann, Frida Emanuelsson, Børge G Nordestgaard, Marianne Benn
Aims Treatment with sodium-glucose co-transporter 2(SGLT2)-inhibitors reduces risk of cardiovascular disease and mortality, but the mechanism is unclear. We hypothesized that a functional genetic variant in SLC5A2, known to be associated with familial renal glucosuria, would mimic pharmacological SGLT2-inhibition, and thus provide an opportunity to examine potential mediators of the effects on lower
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E-cigarettes and arrhythmogenesis: a comprehensive review of preclinical studies and their clinical implications Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-27 Carson A Jones, Michael J Wallace, Priya Bandaru, Emerson D Woodbury, Peter J Mohler, Loren E Wold
Electronic cigarette use has grown exponentially in recent years, and while their popularity has increased, the long-term effects on the heart are yet to be fully studied and understood. Originally designed as devices to assist with those trying to quit traditional combustible cigarette use, their popularity has attracted use by teens and adolescents who traditionally have not smoked combustible cigarettes
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Epigenetic regulation of vascular smooth muscle cell phenotypic switch and neointimal formation by PRMT5 Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-24 Ni Zhu, Zhi-Fu Guo, Kyosuke Kazama, Bing Yi, Nopprarat Tongmuang, Huijun Yao, Ruifeng Yang, Chen Zhang, Yongwen Qin, Lin Han, Jianxin Sun
Aims Phenotypic transition of vascular smooth muscle cells (VSMCs) from a contractile to a synthetic state is involved in the development of cardiovascular diseases, including atherosclerosis, hypertension, and post-angioplasty restenosis. Arginine methylation catalyzed by protein arginine methyltransferases (PRMTs) has been implicated in multiple cellular processes, however, its role in VSMC biology
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Pathophysiology of the right ventricle in health and disease: an update Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-18 Khodr Tello, Robert Naeije, Frances de Man, Marco Guazzi
The contribution of the right ventricle (RV) to cardiac output is negligible in normal resting conditions when pressures in the pulmonary circulation are low. However, the RV becomes relevant in healthy subjects during exercise, and definitely so in patients with increased pulmonary artery pressures both at rest and during exercise. The adaptation of RV function to loading rests basically on an increased
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RNA interference or small molecule inhibition of Runx1 in the border zone prevents cardiac contractile dysfunction following myocardial infarction Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-07 Tamara P Martin, Eilidh A MacDonald, Ashley Bradley, Holly Watson, Priyanka Saxena, Eva A Rog-Zielinska, Anmar Raheem, Simon Fisher, Ali Ali Mohamed Elbassioni, Ohood Almuzaini, Catriona Booth, Morna Campbell, Alex Riddell, Pawel Herzyk, Karen Blyth, Colin Nixon, Lorena Zentilin, Colin Berry, Thomas Braun, Mauro Giacca, Martin W McBride, Stuart A Nicklin, Ewan R Cameron, Christopher M Loughrey
Background Myocardial infarction is a major cause of death worldwide. Effective treatments are required to improve recovery of cardiac function following myocardial infarction, with the aim of improving patient outcomes and preventing progression to heart failure. The perfused but hypocontractile region bordering an infarct is functionally distinct from the remote surviving myocardium and is a determinant
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Has genetic disposition implications for treatment decisions in atrial fibrillation? Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-05 Felix Bourier,Heribert Schunkert
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Chronic SIRT1 supplementation in diabetic mice improves endothelial function by suppressing oxidative stress Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-03 Kangmin Yang, Srividya Velagapudi, Alexander Akhmedov, Simon Kraler, Tetiana Lapikova-Bryhinska, Martin O Schmiady, Xiaoping Wu, Leiluo Geng, Giovanni G Camici, Aimin Xu, Thomas F Lüscher
Aims Enhancing SIRT1 activity exerts beneficial cardiovascular effects. In diabetes, plasma SIRT1 levels are reduced. We aimed to investigate the therapeutic potential of chronic recombinant murine SIRT1 (rmSIRT1) supplementation in diabetic mice (db/db) to alleviate endothelial and vascular dysfunction. Methods and Results Left-internal mammary arteries from patients undergoing coronary artery bypass
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Tissue specific differences in the assembly of mitochondrial complex I is revealed by a novel ENU mutation in ECSIT Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-03 Thomas Nicol, Sara Falcone, Andrew Blease, Pratik Vikhe, Gabriele Civiletto, Saleh Salman Omairi, Carlo Viscomi, Ketan Patel, Paul K Potter
Aims Mitochondrial complex I assembly is a multi-step process which necessitates the involvement of a variety of assembly factors and chaperones to ensure the final active enzyme is correctly assembled. The role of the assembly factor ECSIT was studied across various murine tissues to determine its role in this process and how this varied between tissues of varying energetic demands. We hypothesised
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Smoke on the blood stream: Novel insights in cigarette smoke-induced atherosclerosis and plaque erosion. Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-01 Henning Morawietz
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BMAL1 regulates cell cycle progression and angiogenesis of endothelial cells. Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-01 Inna Rabinovich-Nikitin,Lorrie A Kirshenbaum
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Cardiac lipid metabolism, mitochondrial function and heart failure Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-01 Lorenzo Da Dalt, Ainara G Cabodevilla, Ira J Goldberg, Giuseppe Danilo Norata
A fine balance between uptake, storage and the use of high energy fuels, like lipids, is crucial in the homeostasis of different metabolic tissues. Nowhere is this balance more important and more precarious than in the heart. This highly energy demanding muscle normally oxidizes almost all the available substrates to generate energy, with fatty acids being the preferred source under physiological conditions
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Lipocalin 10 is essential for protection against inflammation-triggered vascular leakage by activating LRP2-Ssh1 signaling pathway Cardiovasc. Res. (IF 10.8) Pub Date : 2023-06-30 Hongyan Zhao, Peng Wang, Xiaohong Wang, Wa Du, Hui-Hui Yang, Yueying Liu, Shu-Nan Cui, Wei Huang, Tianqing Peng, Jing Chen, Chen Gao, Yigang Wang, Sakthivel Sadayappan, Chengen Ma, Yanbo Fan, Chunting Wang, Guo-Chang Fan
Aims Systemic inflammation occurs commonly during many human disease settings and increases vascular permeability, leading to organ failure and lethal outcomes. Lipocalin 10 (Lcn10), a poorly characterized member of the lipocalin family, is remarkably altered in the cardiovascular system of human patients with inflammatory conditions. Nonetheless, whether Lcn10 regulates inflammation-induced endothelial
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ITGBL1 mediates fibroblast–cardiomyocyte crosstalk to promote cardiac fibrosis and hypertrophy Cardiovasc. Res. (IF 10.8) Pub Date : 2023-06-30 XiaoQiang Chen, XinTao Li, XiaoYu Wu, Yu Ding, Ya Li, GenQing Zhou, Yong Wei, SongWen Chen, XiaoFeng Lu, Juan Xu, ShaoWen Liu, Jun Li, LiDong Cai
Aims Crosstalk between fibroblasts and cardiomyocytes plays a critical role in cardiac remodeling during heart failure (HF); however, the underlying molecular mechanisms remain obscure. Recently, a secretory protein, Integrin beta-like 1 (ITGBL1) was revealed to have detrimental effects on several diseases, such as tumors, pulmonary fibrosis, and hepatic fibrosis; whereas the effect of ITGBL1 on heart
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Single-cell profiling reveals age-associated immunity in atherosclerosis Cardiovasc. Res. (IF 10.8) Pub Date : 2023-06-30 Virginia Smit, Jill de Mol, Frank H Schaftenaar, Marie A C Depuydt, Rimke J Postel, Diede Smeets, Fenne W M Verheijen, Laurens Bogers, Janine van Duijn, Robin A F Verwilligen, Hendrika W Grievink, Mireia N A Bernabé Kleijn, Eva van Ingen, Maaike J M de Jong, Lauren Goncalves, Judith A H M Peeters, Harm J Smeets, Anouk Wezel, Julia K Polansky, Menno P J de Winther, Christoph J Binder, Dimitrios Tsiantoulas
Aims Aging is a dominant driver of atherosclerosis and induces a series of immunological alterations, called immunosenescence. Given the demographic shift towards elderly, elucidating the unknown impact of aging on the immunological landscape in atherosclerosis is highly relevant. While the young Western diet-fed Ldlr-deficient (Ldlr-/-) mouse is a widely used model to study atherosclerosis, it does
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Non-alcoholic fatty liver disease: pathophysiological concepts and treatment options Cardiovasc. Res. (IF 10.8) Pub Date : 2023-06-26 Christoph Grander, Felix Grabherr, Herbert Tilg
The prevalence of non-alcoholic fatty liver disease (NAFLD) is continually increasing due to the global obesity epidemic. NAFLD comprises a systemic metabolic disease accompanied frequently by insulin resistance and hepatic and systemic inflammation. Whereas simple hepatic steatosis is the most common disease manifestation, a more progressive disease course characterized by liver fibrosis and inflammation
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Cardiorenal interactions in heart failure – insights from recent therapeutic advances Cardiovasc. Res. (IF 10.8) Pub Date : 2023-06-26 Kevin Damman, Jeffrey Testani
Heart failure is a syndrome that may develop when cardiovascular disease progresses or is insufficiently treated and associated with a poor quality of life, high mortality rates and increased health care expenditures. Prevention and treatment of heart failure is therefore of utmost importance. New therapies in patients with cardiovascular disease have recently been shown to be effective in the prevention
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Preemptive iron supplementation prevents myocardial iron deficiency and attenuates adverse remodelling after myocardial infarction. Cardiovasc. Res. (IF 10.8) Pub Date : 2023-06-14 Bomee Chung,Yong Wang,Marleen Thiel,Fatemeh Rostami,Anika Rogoll,Valentin G Hirsch,Zulaikha Malik,Anne Bührke,Christian Bär,Michael Klintschar,Jan D Schmitto,Carla Vogt,Christopher Werlein,Danny Jonigk,Johann Bauersachs,Kai C Wollert,Tibor Kempf
AIMS Heart failure (HF) after myocardial infarction (MI) is a major cause of morbidity and mortality. We sought to investigate the functional importance of cardiac iron status after MI and the potential of preemptive iron supplementation in preventing cardiac iron deficiency (ID) and attenuating left ventricular (LV) remodelling. METHODS AND RESULTS MI was induced in C57BL/6J male mice by left anterior
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Immune profiling of murine cardiac leukocytes identifies Trem2 as a novel mediator of hypertensive heart failure Cardiovasc. Res. (IF 10.8) Pub Date : 2023-06-14 C Duncan Smart, Daniel J Fehrenbach, Jean W Wassenaar, Vineet Agrawal, Niki L Fortune, Debra D Dixon, Matthew A Cottam, Alyssa H Hasty, Anna R Hemnes, Amanda C Doran, Deepak K Gupta, Meena S Madhur
Heart failure with preserved ejection fraction (HFpEF) is characterized by diastolic dysfunction, microvascular dysfunction, and myocardial fibrosis with recent evidence implicating the immune system in orchestrating cardiac remodeling. Here, we show the mouse model of deoxycorticosterone acetate (DOCA)-salt hypertension induces key elements of HFpEF, including diastolic dysfunction, exercise intolerance
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Thrombin activated Interleukin-1α drives atherogenesis, but also promotes VSMC proliferation and collagen production Cardiovasc. Res. (IF 10.8) Pub Date : 2023-06-13 Burzynski C Laura, Maria A Morales-Maldonado, Amanda Rodgers, Lauren A Kitt, Melanie Humphry, Nichola Figg, Martin R Bennett, Murray C H Clarke
Aims Atherosclerosis is driven by multiple processes across multiple body systems. For example, the innate immune system drives both atherogenesis and plaque rupture via inflammation, while coronary artery-occluding thrombi formed by the coagulation system cause myocardial infarction and death. However, the interplay between these systems during atherogenesis is understudied. We recently showed that
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Endothelial CCRL2 induced by disturbed flow promotes atherosclerosis via chemerin-dependent β2 integrin activation in monocytes Cardiovasc. Res. (IF 10.8) Pub Date : 2023-06-09 Chaojun Tang, Guona Chen, Fan Wu, Yiren Cao, Fei Yang, Tao You, Chu Liu, Menglu Li, Shuhong Hu, Lijie Ren, Qiongyu Lu, Wei Deng, Ying Xu, Guixue Wang, Hanjoong Jo, Yonghong Zhang, Yi Wu, Brian A Zabel, Li Zhu
Aims Chemoattractants and their cognate receptors are essential for leukocyte recruitment during atherogenesis, and atherosclerotic plaques preferentially occur at predilection sites of the arterial wall with disturbed flow (d-flow). In profiling the endothelial expression of atypical chemoattractant receptors (ACKRs), we found that Ackr5 (CCRL2) was upregulated in an endothelial subpopulation by atherosclerotic
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Cardiac-specific BACH1 ablation attenuates pathological cardiac hypertrophy by inhibiting the Ang II type 1 receptor expression and the Ca2+/CaMKII pathway Cardiovasc. Res. (IF 10.8) Pub Date : 2023-06-09 Xiangxiang Wei, Jiayu Jin, Jian Wu, Yunquan He, Jieyu Guo, Zhaohua Yang, Liang Chen, Kui Hu, Liliang Li, Mengping Jia, Qinhan Li, Xiaoyu Lv, Fei Ge, Siyu Ma, Huijie Wu, Xiuling Zhi, Xinhong Wang, Lindi Jiang, Elena Osto, Jianyi Zhang, Dan Meng
Aims BACH1 is upregulated in hypertrophic hearts, but its function in cardiac hypertrophy remains largely unknown. This research investigates the function and mechanisms of BACH1 in the regulation of cardiac hypertrophy. Methods and results Male cardiac-specific BACH1 knockout mice or cardiac-specific BACH1 transgenic (BACH1-Tg) mice and their respective wild-type littermates developed cardiac hypertrophy
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Vascular Smooth Muscle Cells Specific Deletion of Angiopoietin-Like Protein 8 Prevents AngII-Promoted Hypertension and Cardiovascular Hypertrophy Cardiovasc. Res. (IF 10.8) Pub Date : 2023-06-08 Xiaolu Jiao, Huahui Yu, Zhiyong Du, Linyi Li, Chaowei Hu, Yunhui Du, Jing Zhang, Xiaoping Zhang, Qianwen Lv, Fan Li, Qiuju Sun, Yu Wang, Yanwen Qin
Aims Angiopoietin-like protein 8 (ANGPTL8) plays important roles in lipid metabolism, glucose metabolism, inflammation, and cell proliferation and migration. Clinical studies have indicated that circulating ANGPTL8 concentrations are increased in patients with hypertension and positively associated with blood pressure. ANGPTL8 deficiency ameliorates blood pressure in mice treated with chronic intermittent
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Modulation of lncRNA links endothelial glycocalyx to vascular dysfunction of tyrosine kinase inhibitor. Cardiovasc. Res. (IF 10.8) Pub Date : 2023-06-03 Sarath Babu Nukala, Jordan Jousma, Gege Yan, Zhenbo Han, Youjeong Kwon, Yoonje Cho, Chuyu Liu, Keith Gagnon, Sandra Pinho, Jalees Rehman, Ning-Yi Shao, Sang-Bing Ong, Won Hee Lee, Sang-Ging Ong
Aims Novel cancer therapies leading to increased survivorship of cancer patients have been negated by a concomitant rise in cancer therapies-related cardiovascular toxicities. Sunitinib, a first line multi receptor tyrosine kinase inhibitor (TKI), has been reported to cause vascular dysfunction although the initiating mechanisms contributing to this side effect remain unknown. Long non-coding RNAs
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Association of genetic risk and outcomes in patients with atrial fibrillation: interactions with early rhythm control in the EAST-AFNET4 trial Cardiovasc. Res. (IF 10.8) Pub Date : 2023-06-02 Shinwan Kany, Christoph Al-Taie, Carolina Roselli, James P Pirruccello, Katrin Borof, Carla Reinbold, Anna Suling, Linda Krause, Bruno Reissmann, Renate B Schnabel, Tanja Zeller, Antonia Zapf, Karl Wegscheider, Larissa Fabritz, Patrick T Ellinor, Paulus Kirchhof
Aims The randomized Early Treatment of Atrial Fibrillation for Stroke Prevention Trial found that early rhythm control reduces cardiovascular events in patients with recently diagnosed atrial fibrillation (AF) compared with usual care. How genetic predisposition to AF and stroke interacts with early rhythm-control therapy is not known. Methods and results Array genotyping and imputation for common
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NLRP3 inflammasome and interleukin-1 contributions to COVID-19-associated coagulopathy and immunothrombosis. Cardiovasc. Res. (IF 10.8) Pub Date : 2023-05-30 Nicola Potere,Evan Garrad,Yogendra Kanthi,Marcello Di Nisio,Gilles Kaplanski,Aldo Bonaventura,Jean Marie Connors,Raffaele De Caterina,Antonio Abbate
Immunothrombosis - immune-mediated activation of coagulation - is protective against pathogens, but excessive immunothrombosis can result in pathological thrombosis and multiorgan damage, as in severe Coronavirus Disease 2019 (COVID-19). The NACHT-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome produces major proinflammatory cytokines of the interleukin (IL)-1 family, IL-1β and IL-18
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Cardiovascular complications in chronic kidney disease - A review from the European Renal and Cardiovascular Medicine Working Group (EURECA-m) of the European Renal Association (ERA). Cardiovasc. Res. (IF 10.8) Pub Date : 2023-05-30 Carmine Zoccali,Francesca Mallamaci,Marcin Adamczak,Rodrigo Bueno de Oliveira,Ziad A Massy,Pantelis Sarafidis,Rajiv Agarwal,Patrick B Mark,Peter Kotanko,Charles J Ferro,Christoph Wanner,Michel Burnier,Raymond Vanholder,Andrzej Wiecek
Chronic kidney disease (CKD) is classified into 5 stages with kidney failure being the most severe stage (stage G5). CKD conveys a high risk for coronary artery disease, heart failure, arrhythmias, and sudden cardiac death. Cardiovascular complications are the most common causes of death in patients with kidney failure (stage G5) who are maintained on regular dialysis treatment. Because of the high
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Macrophage angiotensin-converting enzyme (ACE) reduces atherosclerosis by increasing PPARα and fundamentally changing lipid metabolism Cardiovasc. Res. (IF 10.8) Pub Date : 2023-05-25 DuoYao Cao, Zakir Khan, Xiaomo Li, Suguru Saito, Ellen A Bernstein, Aaron R Victor, Faizan Ahmed, Aoi O Hoshi, Luciana C Veiras, Tomohiro Shibata, Mingtian Che, Lei Cai, Ryan E Temel, Jorge F Giani, Daniel J Luthringer, Ajit S Divakaruni, Derick Okwan-Duodu, Kenneth E Bernstein
Aims The metabolic failure of macrophages to adequately process lipid is central to the etiology of atherosclerosis. Here, we examine the role of macrophage angiotensin converting enzyme (ACE) in a mouse model of PCSK9 induced atherosclerosis. Methods and results Atherosclerosis in mice was induced with AAV-PCSK9 and a high fat diet. Animals with increased macrophage ACE (ACE 10/10 mice) have a marked
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Breaking the macrophage code in atherosclerosis. Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-06 Claudia Monaco,Lea Dib
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Salty secrets of the brain: the link between stress, salt, and hypertension. Cardiovasc. Res. (IF 10.8) Pub Date : 2023-07-06 Agnieszka H Ludwig-Słomczyńska,Tomasz J Guzik
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Professor Ryszard Jerzy Gryglewski: pioneer of pharmacology of vascular endothelium. Cardiovasc. Res. (IF 10.8) Pub Date : 2023-05-22 Stefan Chlopicki,Rafal Olszanecki,Rod J Flower
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Inhibition of the extracellular enzyme ADAMTS4 prevents cardiac fibrosis and dysfunction Cardiovasc. Res. (IF 10.8) Pub Date : 2023-05-22 Maria Vistnes, Pugazendhi Murugan Erusappan, Athiramol Sasi, Einar Sjaastad Nordén, Kaja Bergo, Andreas Romaine, Ida Gjervold Lunde, Lili Zhang, Maria Belland Olsen, Jonas Øgaard, Cathrine Rein Carlson, Christian Hjorth Wang, Jon Riise, Christen P Dahl, Arnt Eltvedt Fiane, IdaMarie Hauge-Iversen, Emil Espe, Arne Olav Melleby, Theis Tønnessen, Jan Magnus Aronsen, Ivar Sjaastad, Geir Christensen
Aims Heart failure is a condition with high mortality rates, and there is a lack of therapies that directly target maladaptive changes in the extracellular matrix (ECM), such as fibrosis. We investigated whether the ECM enzyme known as A disintegrin and metalloprotease with thrombospondin motif (ADAMTS) 4 might serve as a therapeutic target in treatment of heart failure and cardiac fibrosis. Methods
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PRMT5-mediated arginine methylation stabilizes KLF4 to accelerate neointimal formation Cardiovasc. Res. (IF 10.8) Pub Date : 2023-05-18 He Liu, Xiaoliang Dong, Kunpeng Jia, Baohui Yuan, Zhengnan Ren, Xiaohua Pan, Jianjin Wu, Jiahong Li, Jingwen Zhou, Ru-Xing Wang, Lefeng Qu, Jia Sun, Li-Long Pan
Aims Accumulating evidence supports an indispensable role of protein arginine methyltransferase 5 (PRMT5) in the pathological progression of several human cancers. As an important enzyme regulating protein methylation, how PRMT5 participates in vascular remodeling remains unknown. To investigate the role and underlying mechanism of PRMT5 in neointimal formation and to evaluate its potential as an effective
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Transforming growth factor-β2 is associated with atherosclerotic plaque stability and lower risk for cardiovascular events Cardiovasc. Res. (IF 10.8) Pub Date : 2023-05-18 Andreas Edsfeldt, Pratibha Singh, Frank Matthes, Christoffer Tengryd, Michele Cavalera, Eva Bengtsson, Pontus Dunér, Petr Volkov, Glykeria Karadimou, Anton Gisterå, Marju Orho-Melander, Jan Nilsson, Jiangming Sun, Isabel Gonçalves
Aims Transforming growth factor-beta (TGF-β) exists in three isoforms TGF-β1, -β2 and -β3. TGF-β1 has been suggested to be important for maintaining plaque stability, yet the role of TGF-β2 and -β3 in atherosclerosis remains to be investigated. Objective This study explores the association of these three isoforms of TGF-β with plaque stability in the human atherosclerotic disease. Methods and Results