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Emerging opportunities to target inflammation: myocardial infarction and type 2 diabetes Cardiovasc. Res. (IF 10.2) Pub Date : 2024-07-19 Tafadzwa T J Kufazvinei, Jason Chai, Katherine A Boden, Keith M Channon, Robin P Choudhury
After myocardial infarction (MI), patients with type 2 diabetes have an increased rate of adverse outcomes, compared to patients without. Diabetes confers a 1.5–2-fold increase in early mortality and, importantly, this discrepancy has been consistent over recent decades, despite advances in treatment and overall survival. Certain assumptions have emerged to explain this increased risk, such as differences
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CircARCN1 aggravates atherosclerosis by regulating HuR-mediated USP31 mRNA in macrophages Cardiovasc. Res. (IF 10.2) Pub Date : 2024-07-18 Zhicheng Pan, Jialan Lv, Liding Zhao, Kaidi Xing, Runze Ye, Yuesheng Zhang, Siyuan Chen, Peng Yang, Hailong Yu, Yangkai Lin, Ruobing Li, Dongfei Wang, Juan Fang, Yang Dong, Jianpeng Sheng, Xiaolin Wang, Ge Shan, Shan Zhang, Hongqiang Cheng, Qingbo Xu, Xiaogang Guo
Aims Circular RNAs (circRNAs) are considered important regulators of biological processes, but their impact on atherosclerosis development, a key factor in coronary artery disease (CAD), has not been fully elucidated. We aimed to investigate their potential use in patients with CAD and the pathogenesis of atherosclerosis. Methods and Results Patients with stable angina (SA) or acute coronary syndrome
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Extra-domain A containing fibronectin in pulmonary hypertension and treatment effects of a function-blocking antibody Cardiovasc. Res. (IF 10.2) Pub Date : 2024-07-18 Isabell Singerer, Laura Tempel, Katja Gruen, Judith Heiß, Clara Gutte, Mattia Matasci, Andrea Schrepper, Reinhard Bauer, Alexander Berndt, Christian Jung, P Christian Schulze, Dario Neri, Marcus Franz
Aims Pulmonary vascular and right ventricular remodelling processes are important for development and progression of pulmonary hypertension (PH). The current study analyzed the functional role of the extra domain A containing fibronectin (ED-A+ Fn) for the development of PH by comparing ED-A+ Fn knockout (KO) and wild-type (WT) mice as well as the effects of an antibody-based therapeutical approach
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Beneficial normalization of cardiac repolarization by carnitine in transgenic SQT1 rabbit models Cardiovasc. Res. (IF 10.2) Pub Date : 2024-07-16 Ilona Bodi, Lea Mettke, Konstantin Michaelides, Tibor Hornyik, Stefan Meier, Saranda Nimani, Stefanie Perez-Feliz, Ibrahim el-Battrawy, Heiko Bugger, Manfred Zehender, Michael Brunner, Jordi Heijman, Katja E Odening
Aims Short-QT-syndrome type 1 (SQT1) is a genetic channelopathy caused by gain-of-function variants in HERG underlying the rapid delayed-rectifier K+ current (IKr), leading to QT-shortening, ventricular arrhythmias, and sudden cardiac death. Data on efficient pharmaco-therapy for SQT1 are scarce. In patients with primary carnitine-deficiency, acquired-SQTS has been observed and rescued by carnitine-supplementation
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Genetic deletion or pharmacologic inhibition of HDAC6 protects the heart against ischemia/reperfusion injury by limiting TNFα-induced mitochondrial injury in experimental diabetes Cardiovasc. Res. (IF 10.2) Pub Date : 2024-07-13 Shelley L Baumgardt, Juan Fang, Xuebin Fu, Yanan Liu, Zhengyuan Xia, Ming Zhao, Ling Chen, Rachana Mishra, Muthukumar Gunasekaran, Progyaparamita Saha, Joseph M Forbess, Zeljko J Bosnjak, Amadou KS Camara, Judy R Kersten, Edward B Thorp, Sunjay Kaushal, Zhi-Dong Ge
Aims The histone deacetylase 6 (HDAC6) inhibitor, tubastatin A, reduces myocardial ischemia/reperfusion injury (MIRI) in type 1 diabetic rats. It remains unclear whether HDAC6 regulates MIRI in type 2 diabetic animals. Diabetes augments activity of HDAC6 and generation of tumor necrosis factor α (TNFα) and impairs mitochondrial complex I (mCI). Here we examined how HDAC6 regulates TNFα production,
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Advances in nucleic acid-targeted therapies for cardiovascular disease prevention Cardiovasc. Res. (IF 10.2) Pub Date : 2024-07-06 Umidakhon Makhmudova, Elisabeth Steinhagen-Thiessen, Massimo Volpe, Ulf Landmesser
Nucleic acid-based therapies are being rapidly developed for prevention and management of cardiovascular diseases (CVD). Remarkable advancements have been achieved in the delivery, safety, and effectiveness of these therapeutics in the past decade. These therapies can also modulate therapeutic targets that cannot be sufficiently addressed using traditional drugs or antibodies. Among the nucleic acid-targeted
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Forward programming of hiPSCs via the transcription factor ETV2: rapid, reproducible, and cost-effective generation of highly enriched, functional endothelial cells Cardiovasc. Res. (IF 10.2) Pub Date : 2024-06-25 Sarah Rieck, Kritika Sharma, Carlotta Altringer, Michael Hesse, Christos Triantafyllou, Yanhui Zhang, Volker Busskamp, Bernd K Fleischmann
Aims Endothelial cell (EC) dysfunction plays a key role in the initiation and progression of cardiovascular disease. However, studying these disorders in ECs from patients is challenging, hence the use of human induced pluripotent stem cells (hiPSCs) and their in vitro differentiation into ECs represents a very promising approach. Still, the generation of hiPSC-derived ECs (hECs) remains demanding
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Intraplatelet miRNA-126 regulates thrombosis and its reduction contributes to platelet inhibition Cardiovasc. Res. (IF 10.2) Pub Date : 2024-06-20 Lu-Jun Zhang, Yang-Xi Hu, Rong-Zhong Huang, Yan-Yan Xu, Shao-Hua Dong, Fang-Hao Guo, Jun-Jun Guo, Jing-Jing Qiu, Zi-Yun Cao, Li-Jiang Wei, Jia-Hao Mao, Ankang Lyu, Jun-Ling Liu, Xian-Xian Zhao, Zhi-Fu Guo, Qing Jing
Aims MicroRNA-126 (miR-126), one of the most abundant microRNAs in platelets, is involved in the regulation of platelet activity and the circulating miR-126 is reduced during antiplatelet therapy. However, whether intraplatelet miR-126 plays a role in thrombosis and platelet inhibition remains unclear. Methods and results Here, using tissue-specific knockout mice, we reported that the deficiency of
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Novel formylpeptide receptor 1/2 agonist limits hypertension-induced cardiovascular damage Cardiovasc. Res. (IF 10.2) Pub Date : 2024-06-16 Jaideep Singh, Kristy L Jackson, Haoyun Fang, Audrey Gumanti, Bethany Claridge, Feng Shii Tang, Helen Kiriazis, Ekaterina Salimova, Alex M Parker, Cameron Nowell, Owen L Woodman, David W Greening, Rebecca H Ritchie, Geoffrey A Head, Cheng Xue Qin
Aims Formylpeptide receptors (FPRs) play a critical role in the regulation of inflammation, an important driver of hypertension-induced end-organ damage. We have previously reported that the biased FPR small-molecule agonist, compound17b (Cmpd17b), is cardioprotective against acute, severe inflammatory insults. Here, we reveal the first compelling evidence of the therapeutic potential of this novel
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SCUBE2 regulates adherens junction dynamics and vascular barrier function during inflammation Cardiovasc. Res. (IF 10.2) Pub Date : 2024-06-14 Yuh-Charn Lin, Ya-Jen Chang, Shiang-Shin Gau, Chun-Min Lo, Ruey-Bing Yang
Aims SCUBE2 (Signal peptide-CUB-epidermal growth factor-like domain-containing protein 2) is a secreted or membrane-bound protein originally identified from endothelial cells (ECs). Our previous work showed that SCUBE2 forms a complex with E-cadherin and stabilizes epithelial adherens junctions (AJs) to promote epithelial phenotypes. However, it remains unclear whether SCUBE2 also interacts with vascular
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Loss of Cavin-2 destabilizes PTEN and enhances Akt signaling pathway in cardiomyocytes Cardiovasc. Res. (IF 10.2) Pub Date : 2024-06-11 Naoki Maruyama, Takehiro Ogata, Takeru Kasahara, Tetsuro Hamaoka, Yusuke Higuchi, Yumika Tsuji, Shinya Tomita, Akira Sakamoto, Naohiko Nakanishi, Satoaki Matoba
Aims Specific cavins and caveolins, known as caveolae-related proteins, have been implicated in cardiac hypertrophy and myocardial injury. Cavin-2 forms complexes with other caveolae-related proteins, but the role of Cavin-2 in cardiomyocytes (CMs) is poorly understood. Here, we investigated an unknown function of Cavin-2 in CMs. Methods and results Under cardiac stress-free conditions, systemic Cavin-2
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Increased bone morphogenetic protein 10 in precapillary pulmonary hypertension patients Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 A Llucia-Valldeperas, J Van Wezenbeek, J A Groeneveldt, R Smal, G Sanchez-Duffhues, C Becher, M L Handoko, L Meijboom, J T Marcus, P Symersky, H W M Niessen, A Vonk-Noordegraaf, H J Bogaard, M J Goumans, F S De Man
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Netherlands Organization for Scientific Research: NWO-VICI num. 918.16.610 and NWO-VIDI num. 917.18.338. Dutch Heart Foundation Dekker senior post-doc grant num. 2018T059 and the Netherlands CardioVascular Research Initiative: CVON-2017-10 DOLPHIN-GENESIS and CVON-2018-29 PHAEDRA-IMPACT
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Modulation of mitochondrial dynamism in kupffer cells impacts systemic metabolism Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 F Fantini, L Da Dalt, A Moregola, G B Vingiani, M Svecla, O Terenghi, J Nour, R Bellini, F Bonacina, G D Norata
Funding Acknowledgements Type of funding sources: Public Institution(s). Main funding source(s): University of Milan Background Kupffer Cells (KC) are hepatic resident macrophages that are essential for liver physiology and contribute to the development of Non-Alcoholic Fatty Liver Disease (NAFLD). The liver of patients with NAFLD shows different expression of some key regulators of inner mitochondrial
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Whole-blood transcriptome unveils altered immune response in acute myocardial infarction patients with aortic valve sclerosis Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 P Poggio, L Piacentini, V A Myasoedova, M Chiesa, C Vavassori, D Moschetta, V Valerio, G Giovanetti, I Massaiu, N Cosentino, G Marenzi, G I Colombo
Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Fondazione Umberto Veronesi (Research Grant 2011-12 to GIC) Fondazione Gigi e Pupa Ferrari ONLUS (FPF-14 to PP) Background Aortic valve sclerosis (AVSc) presents similar pathogenetic mechanisms to coronary artery disease (CAD) and is associated with short- and long-term mortality in CAD patients. Evidence of AVSc-specific
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Ketone-based metabolism and signalling in heart failure with preserved ejection fraction (HFpEF) Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 R Wang, F Capone, F Capone, L Luo, L L, D Keller, D Keller, S Jung, S Jung, F Pauline, F Pauline, P Mertins, P Mertins, C Sotomayor-Flores, C Sotomayor-Flores, D Bode, D Bode, N Grunert, N Grunert, G Schiattarella, G Schiattarella
Funding Acknowledgements Type of funding sources: Public grant(s) – EU funding. Main funding source(s): DZHK Deutsche Forschungsgemeinschaft (DFG-SFB_1470_A02) Cardiac metabolic remodelling in heart failure with preserved ejection fraction (HFpEF) underlies the pathogenesis of this syndrome. Yet, our understanding of metabolic alterations occurring in HFpEF hearts is still limited. Ketone bodies (KBs)
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Impaired cardiac mitochondrial bioenergetics contribute to loss of cardiac function, in a porcine multiple risk factor model Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 L M Zandbergen, C G M Van Dijk, R W A Van Drie, B Shashikadze, T Frohlich, P A C Specht, C Cheng, R C I Wust, N J H Raat, M C Verhaar, D J Duncker, D Merkus
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Dutch CardioVascular Alliance (an initiative with support of the Dutch Heart Foundation) Grant 2020B008 RECONNEXT, and the German Center for Cardiovascular Research (DZHK; 81Z0600207) Background Heart failure with preserved ejection fraction lacks targeted therapies, due to insufficient
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The role of serotonin receptor 7 signalling in macrophages for the inflammatory response after myocardial infarction Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 F S Bahr, F E Mueller, N Weber, W Aguapong, S Neumueller, N Benen, M Ricke-Hoch, E Ponimaskin
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Deutsche Forschungsgemeinschaft (DFG) Background The hormone and neurotransmitter serotonin regulates multiple processes, including immune responses and inflammatory signalling. After a cardiac injury, such as myocardial infarction (MI), a precise regulation of the local inflammation is
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EZH2 inhibition reduces macrophage inflammatory responses in atherosclerosis Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 R W M Kempkes, L C M Rief, C P A A Roomen, G R Griffith, W G Vos, L A Bosmans, M J J Gijbels, M A Hoeksema, K H M Prange, M P J De Winther, A E Neele
Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Dutch Heart Foundation (Hartstichting) Aim Epigenetic processes are essential modulators of macrophage inflammatory responses. We postulate that interference in the epigenetic machinery of macrophages might offer novel approaches to combat atherosclerosis. Here, we investigate the repressive histone modification H3K27Me3
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Poor in vivo transduction of myocardium by lentiviral vectors is likely caused by a post-entry block of transduction Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 R Visser, A M D Vegh, V M Portero, J Wang, T Jonker, M M Ramirez, L Fokkert, M Klerk, A Boender, K Neef, H A M Geerts, A A F De Vries, V Christoffels, M J Goumans, G J J Boink
Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Stichting LSH-TKI Introduction In cardiac gene therapy, two prototypic viral vectors are typically considered for long-term transgene expression, i.e. lentivirus (LV) and adeno-associated virus (AAV) vectors. Compared to AAV vectors, LV vectors have the advantages of a larger insert capacity and the ability to confer
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Nuclear eNOS interacts with and S-nitrosates ADAR1 to modulate endothelial gene expression Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 X Zhou, S Guenther, K Kuenne, I Wittig, I Fleming, M Siragusa
Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Collaborative Research Centre (CRC 1366); Chinese Scholarship Council (CSC) Introduction and Aim Nitric oxide (NO) generated by the endothelial NO synthase (eNOS) regulates vascular tone and endothelial homeostasis to counteract vascular inflammation. The effects of NO are attributable to its interaction with heme-containing
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The calcium-sensing-receptor (CaSR) in adipocytes contributes to sex-differences in the susceptibility to high fat diet induced obesity and atherosclerosis Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 S L Maas, S Adam, R Huchzermeier, K Abschlag, M Hohl, D Santovito, J Jankowski, E A L Biessen, E P C Van Der Vorst
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): IZKF Female mice are more resistant to the obesogenic effects of a high-fat diet (HFD), compared to male mice. Although the underlying mechanisms are poorly understood, sex hormones seem to play an important role. Interestingly, the activity of the estrogen receptor-α (ERα) is affected
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Incomplete microvascular reperfusion in a swine model of recanalized acute ischemic stroke Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 M Wang, A Taha, J D Raben, R Noort, M Stam, D J Duncker, D W J Dippel, J Bobi, H M M Beusekom
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): CONTRAST CONSORTIUM (CVON, Dutch Heart Foundation) Background Incomplete microvascular reperfusion (IMR) could be a detrimental factor impairing regained functionality in stroke patients despite early recanalization. However, the presence of this phenomenon remains to be ascertained. Gyrencephalic
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Atheroprotective WSS effects on human aortic endothelial cells in a new generation bioreactor Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 L Spartano, E Pederzani, F Roda, E Riva, G B Fiore, M Soncini, C Foglieni
Funding Acknowledgements None. Background Luminal arterial endothelial cells are mainly aligned along the blood flow direction, whereas the in vitro endothelial cells (EC) showed heterogeneous distribution. In atherosclerosis the altered blood flow, acting on mechano-transduction, contributes to endothelial dysfunction and barrier disorganization. A low wall shear stress (WSS) has a pro-atherosclerotic
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OPA1 affects lipid metabolism and atherosclerosis progression Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 L Da Dalt, A Moregola, M Svecla, S Pedretti, F Fantini, E Donetti, N Mitro, L Scorrano, G D Norata
Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): European Atherosclerosis Society Introduction Mitochondria are involved in cellular metabolism, energy generation, calcium homeostasis, sterol and bile acids (BAs) production. Mitochondria continuously undergo biogenesis, fusion, fission and mitophagy, maintaining a continuous balance between all forms. Purpose On
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Proteomic profiling reveals higher presence of glycolytic enzymes in vulnerable atherosclerotic lesions Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 K C A Palm, K Theofilatos, S Van Der Laan, E Diez Benavente, G J De Borst, D P V De Kleijn, J Wotja, M Mayr, H Den Ruijter, M Mokry, G Pasterkamp
Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Leducq PlaqOmics Background Our definition of vulnerable plaques is predominantly driven by histological analysis. The molecular mechanisms behind the vulnerable histological characteristics are not fully understood. Here we use mass spectrometry-based proteomics data, to identify molecular mechanisms linked to vulnerable
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The impact of SLCO1B1 single nucleotide polymorphism and non-genetic factors on statin-induced myopathy Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 T H Alaryan, L Youssef
Funding Acknowledgements None. Background Statins, also known as HMG CoA Reductase Inhibitors, are a class of drugs considered the drug of choice for treating hypercholesterolemia. Statins are well tolerated; however, they may cause severe myopathy in 20% to 30% of patients, due to the individual variation regarding its efficacy and related adverse effects. Of these, comes the Single Nucleotide Polymorphism
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MicroRNA-31-5p is upregulated during neointima formation and influences human coronary artery smooth muscle cell functions by regulating PIAS3 and DKK1 Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 S Guerlach, K Kalies, J Koester, S Boettcher, F Daniel, L Hehl, K Knoepp, D Sedding, J M Daniel
Funding Acknowledgements None. Background and purpose MicroRNAs (miRs) have emerged as potential therapeutic targets in cardiovascular disease, given their ability to modulate multiple signaling pathways and cellular processes. Neointima formation as an angioplasty-related complication remains a major issue calling for innovative therapeutic options and is predominantly mediated by phenotypic and functional
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2-Aminoethoxydiphenyl borate prolongs atrial and shortens ventricular action potential duration through modulation of ion channels in the sarcolemma Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 M Rivaud, F M Bosada, S C M Van Amersfoort, C A Schumacher, R F Al Shama, J R De Groot, A O Verkerk, R F Coronel, M W Veldkamp
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): PPP allowance, Health holland ZonmW Background 2-Aminoethoxydiphenyl Borate (2-APB) has been shown to prevent atrial fibrillation in animal models, supposedly through its inhibitory action on the intracellular IP3 receptor and subsequent calcium regulation. However, 2-APB may modulate other
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A novel DSP zebrafish model reveals training- and drug-induced modulation of arrhythmogenic cardiomyopathy phenotypes Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 R Celeghin, G Risato, G Beffagna, M Cason, M Bueno Marinas, M Della Barbera, N Facchinello, R Branas Casas, S Rizzo, L Dalla Valle, F Argenton, G Thiene, N Tiso, K Pilichou, C Basso
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Associazione Italiana per la Ricerca sul Cancro [AIRC grant IG-2017-19928], Italian Ministry of University and Research [grant PRIN 20173ZWACS] Introduction Arrhythmogenic cardiomyopathy (AC) is an inherited disorder characterized by progressive loss of the ventricular myocardium causing
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Red blood cell-derived extracellular vesicles from type 2 diabetes patients induce endothelial dysfunction through a mechanism involving arginase 1 Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 A Collado, R Humoud, E Kontidou, M Eldh, J Yang, T Jiao, E Domingo, A Mahdi, S Gabrielsson, P Eriksson, Z Zhou, J Pernow
Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Foundation for Geriatric Diseases Karolinska Institutet (2023-01860). Swedish Heart and Lung Foundation (20220210) Background The mechanisms driving the development of cardiovascular injury in type 2 diabetes (T2D) remain incompletely understood. We have recently demonstrated that red blood cells (RBCs) from patients
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Therapeutic inhibition of biomechanically-activated YAP-TAZ signaling prevents vein graft atherosclerosis Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 T Sluiter, G Garoffolo, T Yokoyama, P H A Quax, M Pesce, M R De Vries
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Rembrandt Institute for Cardiovascular Sciences Background Venous bypass grafts may have limited patency due to excessive intimal hyperplasia and accelerated atherosclerosis. YAP-TAZ signaling regulates cellular responses to biomechanical cues, such as disturbed flow or vessel distention
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The smooth-walled human RVOT contains trabeculations that cause conduction delay Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 B Jensen, F M Bosada, M Blok, K T Scholman, I R Efimov, B J Boukens
Funding Acknowledgements None. Background The right ventricular outflow tract (RVOT) is the outlet from the right ventricle and is the initiating substrate of life-threatening arrhythmias. While the luminal wall of the RVOT is often assumed to be without the complex trabecular meshwork that characterizes the right ventricular free wall, the anatomy of the RVOT is an understudied subject. Aim to investigate
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Aging related changes in cardiovascular system in healthy female population: photoplethysmography method and DFA analysis Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 B Djuric, K Zikic, N Milosevic, Z Nestorovic, D Zikic
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Ministry of Science Technological Development and Innovation Background The cardiovascular system undergoes dynamic changes during the biological aging in humans, leading to chronic cardiovascular and cerebrovascular diseases. Purpose Developing the novel method for non-invasive monitoring
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Exploring the mechanisms of metabolic adaptations to cardiotoxic doxorubicin Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 G Guerra, M Russo, R Priolo, C Riganti, S Reano, N Filigheddu, E Hirsch, A Ghigo
Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Leducq Foundation Background Doxorubicin (DOX) is an anthracycline chemotherapeutic agent whose clinical application is hindered by the emergence of early and late cardiotoxic effects. Recent findings demonstrated that DOX damages cardiac mitochondria, with subsequent metabolic perturbation and energetic imbalance
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Cardiomyocyte-stromal cell interplay modulates the pathogenesis of arrhythmogenic cardiomyopathy Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 A S Maione, L Iengo, L Sala, I Massaiu, M Chiesa, S Ghilardi, C Florindi, F Lodola, A Zaza, C Tondo, M Schiavone, C Banfi, G Pompilio, P Poggio, E Sommariva
Funding Acknowledgements Type of funding sources: Public grant(s) – EU funding. Main funding source(s): Transnational Research Projects on Cardiovascular Diseases Background Arrhythmogenic Cardiomyopathy (ACM) is an inherited heart disorder characterized by a high incidence of sudden death at young age. Mutations linked to ACM occur primarily in desmosomal genes (e.g. PKP2) [1]. Different cell types
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Postnatal overfeeding in mice induces early lipidic changes in heart tissue and impacts cardiomyocyte proliferation Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 M Josse, E Rigal, N Rosenblatt, F Rochais, J P Pais De Barros, L Rochette, C Vergely
Funding Acknowledgements Type of funding sources: Public Institution(s). Main funding source(s): French Federation of Cardiology Foundation of France Background Shortly after birth, cardiomyocytes lose their ability to proliferate to switch towards a hypertrophic growth and this ability is known to be influenced by nutritional factors. Postnatal overfeeding (PNOF) induced by litter size reduction in
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MicroRNA-127-3p regulates inflammatory response in injury-induced vascular remodeling and cellular senescence in vascular smooth muscle cells through mTor Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 F Daniel, K Kalies, L Hehl, S Guerlach, J M Koester, S Boettcher, K Knoepp, J Dutzmann, D Sedding
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Martin-Luther-Universität Halle-Wittenberg Background and Purpose The accumulation of senescent cells in the vasculature contributes to impaired vascular function over the lifetime. Micro RNAs (miRs) are promising therapeutic targets due to their cell-specific functions. Targeting miR-127-3p
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Mechanical load regulates the proliferation of multiple cell types in the heart Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 G Ciucci, A Colliva, S Vodret, B Texler, B Cardini, R Oberhuber, R Vuerich, E Zago, M Maglione, G Sinagra, M Giacca, T Eschenhagen, P Golino, F Loffredo, S Zacchigna
Funding Acknowledgements None. Introduction The adult mammalian heart has a poor regenerative and angiogenic potential. At the same time, both primary cardiac tumors and cardiac metastases are extremely rare. This suggests that shared mechanisms may halt the proliferation of cardiac (both cardiomyocyte and endothelial) and cancer cells. Among the mechanisms that have been claimed to be responsible
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The effects of HIV-1-proteins and antiretroviral therapy on aortic endothelial cells (AECs). A mechanistic in vitro approach Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 A Genis, C Marincowitz, H Strijdom
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): National Research Foundation Introduction Endothelial dysfunction (ED) is an early precursor of cardiovascular disease characterized by decreased nitric oxide (NO) and increased oxidative stress, creating a pro-inflammatory environment. Increased ED and cardiovascular risk have been observed
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Acquired control over proliferation and differentiation of ventricular cardiomyocytes to break down the mechanisms of cardiac repair Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 A Ramkisoensing, J Zhang, D A Pijnappels, A A F De Vries
Funding Acknowledgements None. Loss of myocardial tissue remains a leading cause of morbidity and mortality by causing heart rhythm disturbances and heart failure. The (pre-)clinical effects of inducing cardiac regeneration by cardiac cell therapy have been disappointing. In order to find new curative options for these disabling cardiac diseases a shift of focus towards steering the heart to regenerate
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Deeper insights into heart failure with preserved ejection fraction through rna-sequencing of circulating endothelial cells - advanced protocol establishment enables complete transcriptome analysis Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 L Wurmbrand, K Kalies, K Knoepp, J Dutzmann, D Sedding
Funding Acknowledgements None. Heart failure with preserved ejection fraction (HFpEF) continues to pose a significant challenge with a bleak prognosis and a rising incidence, particularly among the aging population in Western countries. An in-depth comprehension of cellular-level pathogenesis, with a specific emphasis on the pivotal role of cellular senescence in endothelial dysfunction, is imperative
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SGK1 inhibition normalizes action potential duration in transgenic LQT2 rabbits but not in LQT1, suggesting a novel gene-specific therapeutic approach in long QT syndrome Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 M Barbieri, J Lourdaour, N Alerni, L Giammarino, S Nimani, L Matas, A Horvath, K E Odening
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): SNSF (Swiss National Science Fundation) Background Increasing evidence suggests that secondary remodeling in Na+ and Ca2+ homeostasis may further enhance the propensity to develop arrhythmias in K-channelopathies LQT1 and LQT2 syndrome. In this context, the Serum and Glucocorticoid regulated
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Modelling chemotherapy-induced cardiotoxicity with live myocardial slices: from bedside to bench and back again Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 V Sampaio-Pinto, I R Kelters, J S A Van Der Geest, P P Zwetsloot, A J Teske, T P De Boer, N P Van Der Kaaij, J P G Sluijter, L W Van Laake
Funding Acknowledgements Type of funding sources: Public Institution(s). Main funding source(s): Netherlands Heart Institute & Dutch Heart Foundation (Dekker Senior Clinical Scientist 2019) Introduction Cancer therapy related cardiac dysfunction (CTRCD) is a common side-effect of many oncological regimens. The prevention, diagnosis and treatment of CTRCD requires a well-orchestrated management by a
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Dissecting signal transduction pathways that regulate cardiomyocyte proliferation Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 R Artioli, R Cannilla, M Dal Ferro, L Zentilin, M Giacca, C Collesi
Funding Acknowledgements None. Introduction During cardiac development, the Notch, Hippo, and Wnt/β-catenin signalling pathways play a crucial role in the tuning of cardiomyocyte proliferation. The individual engagement of each of these pathways during the early postnatal life, however, is still unclear. Purpose We wanted to develop a method to visualize over time, both in vitro and in vivo, the topography
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Arrhythmogenic cardiomyopathy related phenotypes are detected and pharmacologically modulated in Galectin-3 zebrafish models Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 G Risato, R Celeghin, G Beffagna, M Cason, M Bueno Marinas, M Della Barbera, N Facchinello, R Branas Casas, S Rizzo, F Argenton, G Thiene, N Tiso, K Pilichou, C Basso
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Italian Ministry of University and Research Introduction Arrhythmogenic Cardiomyopathy (AC) is a rare inherited cardiac disorder characterized by fibro-fatty replacement and progressive loss of the ventricular myocardium, causing life-threatening arrhythmias, syncope and sudden cardiac
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Macrophage transcriptome changes in response to cardiac injuries are determined by the type of lesion rather than their ontogenetic nature Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 T Vico, G Witte, M Taglinger, V K Haacke, B Dufner, S Perez Feliz, C Koentges, T S Dederichs, A Von Ehr, S Preissl, D Westermann, I Hilgendorf
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): CRC1425 - DFG Introduction Resident macrophages account for 5% of the cells in the healthy heart. In response to cardiac injury, monocytes infiltrate and differentiate into recruited macrophages complementing the original resident macrophage population, and together orchestrate cardiac
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Sirt1 in focus: unveiling molecular insights and therapeutic prospects in calcific aortic stenosis with sglt2i inhibitors Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 V Valerio, I Massaiu, M Franchi, A Bonomi, G Pellegrini, D Moschetta, F Trombara, V Rusconi, F Bertolini, V A Myasoedova, G Marenzi, G Corrao, S Genovese, P Poggio
Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Fondazione Gigi & Pupa Ferrari ONLUS Background Calcific aortic stenosis (AS) affects 3% of older adults and lacks medical treatment. The well-known deacetylase Sirtuin1 (SIRT1) could be involved in many pathways linked to AS progression. Sodium-glucose co-transporter 2 inhibitors (SGLT2i), a class of antihyperglycemic
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Bradycardia in a long QT type 2 family: coinciding KCNH2 and HCN4 variants Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 J S Copier, K Andrzejczyk, A S Amin, S N Van Der Crabben, L Beekman, C R Bezzina, A O Verkerk, E M Lodder
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): the Dutch Research Council: NWO Talent Scheme Background A large multigenerational family harboring a pathogenic KCNH2 variant (L69P) was identified. This gene encodes the hERG channel, responsible for the cardiac rapid delayed rectifier K+ current (IKr). Pathogenic variants in KCNH2 can
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Novel method for induction of myocardial infarction in rats by ultrasound guided electrocoagulation of the left anterior descending artery Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 M Nordfalk, S S Groenager, M Flethoej, I Hunter, R S Ripa, A Kjaer, P J Pedersen
Funding Acknowledgements Type of funding sources: Private company. Main funding source(s): Minerva Imaging Background Murine models of acute myocardial infarction (MI) are commonly established through ligation of the left anterior descending artery (LAD). Despite inherent procedural challenges, including high mortality rates, limited improvements of the induction procedure have been made. Ultrasound-guided
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Identifying novel small molecule integrin agonists to mimic the favourable effects of the RGD domain of IGFBP-1 to treat cardiometabolic disease Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 E R Rolfe, L E De Faveri, M J Mcphillie, P J Meakin, K J Simmons, S B Wheatcroft
Funding Acknowledgements Type of funding sources: Other. Main funding source(s): British Heart Foundation (BHF) 4-Year PhD Programme Background Insulin-like growth factor binding protein (IGFBP)-1 has previously been shown to be associated with reduced type 2 diabetes (T2D) progression and preferable cardiovascular profiles in patients. Our laboratory previously demonstrated that IGFBP-1 is an insulin
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Phosphoinositide 3-Kinase C2alpha controls cardiac contractility through regulation of beta2-adrenergic receptor recycling Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 S Cnudde, T Brand, J Fender, L Prever, A Murabito, M Russo, F Gulluni, K Lorenz, E Hirsch, A Ghigo
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Doctoral fellowship Introduction Phosphoinositide 3-kinase C2α (PI3KC2α) is a ubiquitously expressed class II PI3K isoform, which has been previously shown to be involved in the control of vesicular trafficking. However, its role in the myocardium has not been investigated. The primary
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Exploring translational approaches for fully biological cardiac rhythm restoration through ion channel gene therapy Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 T De Coster, B Ordog, A A F De Vries, A V Panfilov, D A Pijnappels
Funding Acknowledgements Type of funding sources: Public grant(s) – EU funding. Main funding source(s): European Research Council (Starting grant 716509) to D.A. Pijnappels Background Recently it was demonstrated how the heart itself could be enabled to quickly restore its rhythm by realizing a biologically-integrated cardiac defibrillator (BioICD) through modification and subsequent expression of
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Transcriptional regulation of hexokinase 2 by BRD4 drives perivascular adipose tissue meta-inflammation in cardiometabolic disease Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 A Mengozzi, S Costantino, A Mongelli, E Duranti, S A Mohammed, E Gorica, M Telesca, S Armenia, F Cappelli, C M Matter, S Taddei, S Masi, F Ruschitzka, A Virdis, F Paneni
Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Holcim Stiftung SwissLife Stiftung Background/Introduction BRD4 is an epigenetic reader that modulates inflammatory transcriptional programmes implicated in cancer. The therapeutic potential of BRD4 modulation in cardiometabolic disorders remains elusive. Purpose We investigate BRD4-related transcriptional programmes
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Erythrocyte aggregability, and fibrinogen during atrial fibrillation Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 M Gotsadze, T Kandashvili, N Momtselidze, M Mantskava
Funding Acknowledgements Type of funding sources: Public Institution(s). Main funding source(s): Academician N. Kipshidze University Clinic - Republican Hospital; IVANE BERITASHVILI CENTER OF EXPERIMENTAL BIOMEDICINE, Department of rheology and diagnostic analytical services. Introduction Despite all biomedical efforts, the prevalence of atrial fibrillation and its associated morbidity and mortality
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Cardiomyocyte Notch1 signaling is essential for protection of the maternal heart from peripartum stress Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 M Ricke-Hoch, B Stapel, S Pietzsch, S Erschow, M Scherr, J Viereck, T Thum, J Bauersachs, D Hilfiker-Kleiner
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Deutsche Forschungsgemeinschaft Background Peripartum cardiomyopathy (PPCM) is a life-threatening disease in women without known cardiovascular disease and is characterized by a sudden onset of heart failure (HF) before, under or after delivery. Previous studies suggest impaired endothelial
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Endothelial cells in chronic thromboembolic pulmonary hypertension exhibit cytoskeletal alteration Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 M Peracaula, A Martinez-Blanco, N Gavara, M Gratacos, V I Peinado, I Blanco, J A Barbera, O Tura-Ceide
Funding Acknowledgements Type of funding sources: Public grant(s) – EU funding. Main funding source(s): Health Research Fund (Fondo de Investigación Sanitaria [FIS]) from the Instituto de Salud Carlos III Introduction Endothelial dysfunction (ED) is pivotal in Chronic Thromboembolic Pulmonary Hypertension (CTEPH) due to structural and functional alterations in endothelial. Previous studies have shown
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Mitochondrial players as novel therapeutic options in arrhythmogenic cardiomyopathy Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 C Volani, A Medici, R Philippe, A Lavdas, I Della Corte, M Lang, L S Frommelt, M Blumer, E Sommariva, G Pompilio, J Troppmair, A Rossini
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Joint Project Südtirol- FWF (grant number 23623; Italy-Austria) and the Department of Innovation, Research and University of the Autonomous Province of Bolzano-South Tyrol (Italy) Background Mitochondria are dynamic organelles that sense and respond to environmental, nutritional, and pathological
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Exploring PD-1+ and tissue resident memory T cells in atherosclerotic diseases Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 K Van Dijk, A De Jong, P H A Quax, M R De Vries
Funding Acknowledgements Type of funding sources: Other. Main funding source(s): Health Holland Visual Sonics Background Checkpoint inhibitor therapy (ICI), a potent oncologic treatment, has been associated with an enhanced risk for atherosclerotic cardiovascular events and increased plaque progression. Among the key players affected by ICI are tissue resident memory T cells (Trm), a subset residing
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Pirfenidone treatment reduces cardiac allograft vasculopathy in a mouse model Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 C Graebner, M Scheunchen, F Theil, A Kuckhahn, N Vogg, A Gessner, N Fritz, M Ramsperger-Gleixner, O Dewald, C Heim
Funding Acknowledgements Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): ISHLT research grant Objectives Chronic rejection in the form of cardiac allograft vasculopathy after heart transplantation remains without effective treatment. Main characteristics of cardiac allograft vasculopathy are immigration of leukocytes and proliferation of smooth muscle cells - collectively
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The novel bispecific anti-NLRP3 inflammasome antibody InflamAb inhibits atherosclerosis in apolipoprotein E-deficient mice Cardiovasc. Res. (IF 10.2) Pub Date : 2024-05-29 L Delfos, M A C Depuydt, M N A Bernabe Kleijn, A C Foks, J Kuiper, M Chemaly, A Peace, V Mcgilligan, I Bot
Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Dutch Heart Foundation Background/Introduction Atherosclerosis is the underlying pathology of many cardiovascular diseases and is characterized by chronic inflammation in the larger arteries. Activation of the NLRP3 inflammasome is one of the drivers of inflammation during atherosclerosis. Purpose Therefore, we aimed