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Cardiovascular Research

Juhana Frösen, Anne Joutel
Cerebrovascular diseases that cause ischemic or hemorrhagic stroke with subsequent loss of life or functional capacity due to damage of the brain tissue are among the leading causes of human suffering and economic burden inflicted by diseases in the developed world. Diseases affecting intracranial vessels are significant contributors to ischemic and hemorrhagic strokes. Brain arteriovenous malformations (bAVM), which are a collection of abnormal blood vessels connecting arteries to veins, are the most common cause of intracranial hemorrhage in children and young adults...
January 16, 2018: Cardiovascular Research
Marialuisa Perrotta, Andrea Lori, Lorenzo Carnevale, Stefania Fardella, Giuseppe Cifelli, Roberta Iacobucci, Francesco Mastroiacovo, Daniele Iodice, Fabio Pallante, Marianna Storto, Giuseppe Lembo, Daniela Carnevale
Aims: Chronic increase of mineralocorticoids obtained by administration of Deoxycorticosterone acetate (DOCA) results in salt dependent hypertension in animals. Despite the lack of a generalized sympathoexcitation, DOCA-salt hypertension has been also associated to overdrive of peripheral nervous system in organs typically targeted by blood pressure (BP), as kidneys and vasculature. Aim of this study was to explore whether DOCA-salt recruits immune system by overactivating sympathetic nervous system in lymphoid organs and whether this is relevant for hypertension...
January 8, 2018: Cardiovascular Research
Henning Morawietz
No abstract text is available yet for this article.
January 8, 2018: Cardiovascular Research
Celine E M Souihol, Martin C Harmsen, Paul C Evans, Guido Krenning
Atherosclerosis is an inflammatory disease resulting in the hardening and thickening of the wall of arteries and the formation of plaques, which comprise of immune cells, mesenchymal cells, lipids and extracellular matrix (ECM). The source of mesenchymal cells in the atherosclerotic plaques have been under scrutiny for years. Current endothelial-lineage tracing studies indicate that the endothelium is a source for plaque-associated mesenchymal cells. Endothelial cells can acquire a mesenchymal phenotype through endothelial-mesenchymal transition (EndMT), wherein the expression of endothelial markers and functions is lost and the expression of mesenchymal cell marker and functions acquired...
January 4, 2018: Cardiovascular Research
Nicholas J Leeper, Lars Maegdefessel
The vascular smooth muscle cell (SMC) is one of the most plastic cells in the body. Understanding how non-coding RNAs regulate SMC cell-fate decision making in the vasculature has significantly enhanced our understanding of disease development, and opened up exciting new avenues for potential therapeutic applications. Recent studies on SMC physiology have in addition challenged our traditional view on their role and contribution to vascular disease, mainly in the setting of atherosclerosis as well as aneurysm disease, and restenosis after angioplasties...
December 29, 2017: Cardiovascular Research
Jacob F Bentzon, Mark W Majesky
No abstract text is available yet for this article.
December 23, 2017: Cardiovascular Research
Tobias Bruegmann, Thomas Beiert, Christoph C Vogt, Jan W Schrickel, Philipp Sasse
Aims: The primary goal in the treatment of symptomatic atrial fibrillation (AF) is to restore sinus rhythm by cardioversion. Electrical shocks are highly effective, but have to be applied under analgo-sedation and can further harm the heart. In order to develop a novel pain-free and less harmful approach, we explored herein the optogenetic cardioversion by light-induced depolarization. Methods and Results: Hearts from mice expressing Channelrhodopsin-2 (ChR2) and the AF-promoting loss-of-function Connexin 40 Ala96Ser mutation were explanted and perfused with low K+ Tyrode's solution and an atrial KATP-channel activator...
December 23, 2017: Cardiovascular Research
Pascal Kusters, Esther Lutgens, Tom T P Seijkens
In the past decades, the inflammatory nature of atherosclerosis has been well recognized and despite the development of therapeutic strategies targeted at its classical risk factors such as dyslipidemia and hypertension, atherosclerosis remains a major cause of morbidity and mortality. Additional strategies targeting the chronic inflammatory pathways underlying the development of atherosclerosis are therefore required. Interactions between different immune cells result in the secretion of inflammatory mediators, such as cytokines and chemokines, and fuel atherogenesis...
December 22, 2017: Cardiovascular Research
Ying Liu, Vincent Hs Chen, Weinian Shou
No abstract text is available yet for this article.
December 21, 2017: Cardiovascular Research
Steven E Lipshultz, Eugene H Herman
No abstract text is available yet for this article.
December 19, 2017: Cardiovascular Research
Allen Kelly, Simona Salerno, Adam Connolly, Martin Bishop, Flavien Charpentier, Tomas Stølen, Godfrey L Smith
AIMS: Loss-of-function of the cardiac sodium channel NaV1.5 is a common feature of Brugada syndrome. Arrhythmias arise preferentially from the right ventricle (RV) despite equivalent NaV1.5 downregulation in the left ventricle (LV). The reasons for increased RV sensitivity to NaV1.5 loss-of-function mutations remains unclear. Because ventricular electrical activation occurs predominantly in the transmural axis, we compare RV and LV transmural electrophysiology to determine the underlying cause of the asymmetrical conduction abnormalities in Scn5a haploinsufficient mice (Scn5a+/-)...
December 18, 2017: Cardiovascular Research
Fang Yuan, John R Woollard, Kyra L Jordan, Amir Lerman, Lilach O Lerman, Alfonso Eirin
The mechanisms responsible for cardiac damage in the early stages of metabolic syndrome (MetS) remain unknown. Mitochondria are intimately associated with cellular myofibrils, with the cytoskeleton functioning as a linkage coordinator, and closely associated to the calcium release sites of the sarcoplasmic reticulum (SR). Objective: We hypothesized that early MetS is characterized by mitochondria-related myocardial damage, associated with altered cytoskeletal-mitochondria-SR interaction. Methods and Results: Domestic pigs were studied after 16 weeks of diet-induced MetS, MetS treated for the last 4 weeks with the mitochondrial-targeted peptide elamipretide (ELAM, 0...
December 18, 2017: Cardiovascular Research
Tomasz J Guzik
No abstract text is available yet for this article.
December 15, 2017: Cardiovascular Research
Veronica Larcher, Paolo Kunderfranco, Marco Vacchiano, Pierluigi Carullo, Marco Erreni, Irene Salamon, Federico Simone Colombo, Enrico Lugli, Marta Mazzola, Achille Anselmo, Gianluigi Condorelli
Aims: The aim of our study was to set up a simple and reliable isolation method of living ventricular cardiomyocytes (vCMs) for molecular and biological studies. Methods: A standard technique for the retrograde perfusion of an enzymatic solution was used to isolate cardiac cells from adult mouse heart. Fluorescence-activated cell sorting (FACS) on adult murine cardiac ventricle cells was performed, comparing the intrinsic autofluorescence in the FITC channel and the forward scatter (FSC) parameter in order to isolate highly fluorescent cells...
December 13, 2017: Cardiovascular Research
Sandra Crnko, Isabelle Ernens, Linda W van Laake
No abstract text is available yet for this article.
December 11, 2017: Cardiovascular Research
Kiterie M E Faller, Dorothee Atzler, Debra J McAndrew, Sevasti Zervou, Hannah J Whittington, Jillian N Simon, Dunja Aksentijevic, Michiel Ten Hove, Chi-Un Choe, Dirk Isbrandt, Barbara Casadei, Jurgen E Schneider, Stefan Neubauer, Craig A Lygate
Aims: Creatine buffers cellular ATP via the creatine kinase reaction. Creatine levels are reduced in heart failure, but their contribution to pathophysiology is unclear. Arginine:glycine amidinotransferase (AGAT) in the kidney catalyses both the first step in creatine biosynthesis as well as homoarginine synthesis. AGAT-/- mice fed a creatine-free diet have a whole body creatine-deficiency. We hypothesised that AGAT-/- mice would develop cardiac dysfunction and rescue by dietary creatine would imply causality...
December 11, 2017: Cardiovascular Research
(no author information available yet)
No abstract text is available yet for this article.
December 9, 2017: Cardiovascular Research
Santa Mundi, Marika Massaro, Egeria Scoditti, Maria Annunziata Carluccio, Victor W M van Hinsbergh, M Luisa Iruela-Arispe, Raffaele De Caterina
Early atherosclerosis features functional and structural changes in the endothelial barrier function that affect the traffic of molecules and solutes between the vessel lumen and the vascular wall. Such changes are mechanistically related to the development of atherosclerosis.Proatherogenic stimuli and cardiovascular risk factors, such as dyslipidemias, diabetes, obesity, and smoking, all increase endothelial permeability sharing a common signalling denominator: an imbalance in the production/disposal of reactive oxygen species (ROS), broadly termed oxidative stress...
December 8, 2017: Cardiovascular Research
Karl Herbert, Clett Erridge
Systemic inflammation, induced by disease or experimental intervention, is well established to result in elevated levels of circulating triglycerides, and reduced levels of high-density lipoprotein-cholesterol (HDL-C), in most mammalian species. However, the relationship between inflammation and low-density lipoprotein-cholesterol (LDL-C) concentrations is less clear. Most reports indicate that systemic inflammation, as observed during sepsis or following high dose experimental endotoxaemia, lowers total and LDL-C in man...
November 30, 2017: Cardiovascular Research
Cheng Zhang, Dan Chen, Eithne Margaret Maguire, Shiping He, Jiangyong Chen, Weiwei An, Mei Yang, Tayyab Adeel Afzal, Le Anh Luong, Li Zhang, Han Lei, Qingchen Wu, Qingzhong Xiao
Objective: To investigate the role of chromobox protein homolog 3 (Cbx3) in vascular smooth muscle cell (VSMC) proliferation, migration and neointima formation following vascular injury. Methods and Results: Overexpression of Cbx3 led to a significant increase in VSMC contractile gene expression and VSMC apoptosis, as well as a dramatic decrease in collagen gene expression, VSMC proliferation and migration. Meanwhile the opposite was observed following inhibition of endogenous Cbx3...
November 30, 2017: Cardiovascular Research
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