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Cardiovascular Research

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https://www.readbyqxmd.com/read/28096168/sk-channel-enhancers-attenuate-ca2-dependent-arrhythmia-in-hypertrophic-hearts-by-regulating-mito-ros-dependent-oxidation-and-activity-of-ryr
#1
Tae Yun Kim, Radmila Terentyeva, Karim H F Roder, Weiyan Li, Man Liu, Ian Greener, Shanna Hamilton, Iuliia Polina, Kevin R Murphy, Richard T Clements, Samuel C Dudley, Gideon Koren, Bum-Rak Choi, Dmitry Terentyev
AIM: s: Plasmamembrane small conductance Ca<su2+p>-activated K<su+ p > (SK) channels were implicated in ventricular arrhythmias in infarcted and failing hearts. Recently, SK channels were detected in the mitochondria inner membrane (mSK), and their activation protected from acute ischemia-reperfusion injury by reducing intracellular levels of reactive oxygen species (ROS). We hypothesized that mSK play an important role in regulating mitochondrial function in chronic cardiac diseases...
January 17, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28088753/mitochondrial-redox-plays-a-critical-role-in-the-paradoxical-effects-of-napdh-oxidase-derived-ros-on-coronary-endothelium
#2
Ehtesham Shafique, Anali Torina, Karla Reichert, Bonnie Colantuono, Nasifa Nur, Khawaja Zeeshan, Vani Ravichandran, Yuhong Liu, Jun Feng, Khawaja Zeeshan, Laura E Benjamin, Kaikobad Irani, Elizabeth O Harrington, Frank W Sellke, Md Ruhul Abid
AIMS: There are conflicting reports on the role of reactive oxygen species (ROS) i.e. beneficial vs. harmful, in vascular endothelium. Here, we aim to examine whether duration of exposure to ROS and/or subcellular ROS levels are responsible for the apparently paradoxical effects of oxidants on endothelium. METHODS AND RESULTS: We have recently generated binary (Tet-ON/OFF) conditional transgenic mice (Tet-Nox2:VE-Cad-tTA) that can induce 1.8 ± 0.42-fold increase in NADPH oxidase (NOX)-derived ROS specifically in vascular endothelium upon withdrawal of tetracycline from the drinking water...
January 14, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28087645/corrigendum
#3
(no author information available yet)
No abstract text is available yet for this article.
January 12, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28082452/sphingosine-1-phosphate-signalling-a-key-player-in-the-pathogenesis-of-angiotensin-ii-induced-hypertension
#4
Anja Meissner, Francesc Miro, Francesc Jiménez-Altayó, Andrés Jurado, Elisabet Vila, Anna M Planas
AIMS: Hypertension is a complex condition involving functional and structural alterations of the microvasculature and an activation of the immune system. T-lymphocytes play a crucial role during the development of hypertension in experimental models, yet the underlying mechanisms remain elusive. Lymphocyte egress from lymph nodes is controlled by sphingosine-1-phosphate (S1P), a natural lipid mediator regulating immune cell and vascular function in health and disease. We therefore investigated the involvement of S1P signalling in the pathogenesis of hypertension...
January 12, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28082451/the-neuronal-transcription-factor-npas4-is-a-strong-inducer-of-sprouting-angiogenesis-and-tip-cell-formation
#5
Jennifer S Esser, Anne Charlet, Mei Schmidt, Sophia Heck, Anita Allen, Achim Lother, Daniel Epting, Cam Patterson, Christoph Bode, Martin Moser
RATIONALE: Regarding branching morphogenesis, neurogenesis and angiogenesis share common principle mechanisms and make use of the same molecules. Therefore, the investigation of neuronal molecules involved in vascular morphogenesis provides new possibilities for pro-angiogenic approaches in cardiovascular diseases. OBJECTIVE: In this study we investigated the role of the neuronal transcription factor NPAS4 in angiogenesis. METHODS AND RESULTS: Here, we demonstrate that the neuronal transcription factor NPAS4 is expressed in endothelial cells of different origin using reverse transcription PCR and western blot analysis...
January 12, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28082450/a-landscape-of-circular-rna-expression-in-the-human-heart
#6
Wilson L W Tan, Benson T S Lim, Chukwuemeka G O Anene-Nzelu, Matthew Ackers-Johnson, Albert Dashi, Kelvin See, Zenia Tiang, Dominic Paul Lee, W W Chua, Tuan D A Luu, Peter Y Q Li, Arthur Mark Richards, Roger S Y Foo
BACKGROUND: Circular RNA (circRNA) is a newly validated class of single-stranded RNA, ubiquitously expressed in mammalian tissues and possessing key functions including acting as microRNA sponges and as transcriptional regulators by binding to RNA-binding proteins. While independent studies confirm the expression of circRNA in various tissue types, a detailed annotation and analysis of genome-wide circRNA expression in the heart is still lacking. METHODS AND RESULTS: We performed deep RNA-sequencing on ribosomal-depleted RNA isolated from 14 human hearts, 25 mouse hearts and across a 28-day differentiation time-course of human embryonic stem cell-derived cardiomyocytes (hESC-CM)...
January 12, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28082449/a-novel-protective-role-for-activating-transcription-factor-3-in-the-cardiac-response-to-metabolic-stress
#7
EDITORIAL
Alessandra Ghigo, Giacomo Frati, Sebastiano Sciarretta
No abstract text is available yet for this article.
January 12, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28077437/sensitized-signalling-between-l-type-ca2-channels-and-ryanodine-receptors-in-the-absence-or-inhibition-of-fkbp12-6-in-cardiomyocytes
#8
Yan-Ting Zhao, Yun-Bo Guo, Lei Gu, Xue-Xin Fan, Hua-Qian Yang, Zheng Chen, Peng Zhou, Qi Yuan, Guang-Ju Ji, Shi-Qiang Wang
AIMS: The heart contraction is controlled by the Ca(2+)-induced Ca(2+ )release (CICR) between L-type Ca(2+ )channels and ryanodine receptors (RyRs). The FK506-binding protein FKBP12.6 binds to RyR subunits, but its role in stabilizing RyR function has been debated for long. Recent reports of high-resolution RyR structure show that the HD2 domain that binds to the SPRY2 domain of neighbouring subunit in FKBP-bound RyR1 is detached and invisible in FKBP-null RyR2. The present study was to test the consequence of FKBP12...
January 10, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28073833/exosomal-mir-142-3p-is-increased-during-cardiac-allograft-rejection-and-augments-vascular-permeability-through-down-regulation-of-endothelial-rab11fip2-expression
#9
Ihdina Sukma Dewi, Selvi Celik, Anna Karlsson, Zsuzsanna Hollander, Karen Lam, Janet-Wilson McManus, Scott Tebbutt, Raymond Ng, Paul Keown, Robert McMaster, Bruce McManus, Jenny Öhman, Olof Gidlöf
AIMS: Exosome-mediated microRNA transfer is a recently discovered mode of cell-to-cell communication, in which microRNAs act as paracrine molecules, exerting their regulatory effects in recipient cells. T cells and endothelial cells are two main players in the mechanism of acute cellular cardiac rejection. The aim of this study was to investigate the role of exosomal microRNAs in the crosstalk between T cells and endothelial cells and its implications for the molecular mechanisms that drive acute cellular rejection in heart transplantation...
January 10, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28073832/reperfusion-therapy-with-recombinant-human-relaxin-2-serelaxin-attenuates-myocardial-infarct-size-and-nlrp3-inflammasome-following-ischemia-reperfusion-injury-via-enos-dependent-mechanism
#10
Juan Valle Raleigh, Adolfo G Mauro, Teja Devarakonda, Carlo Marchetti, Jun He, Erica Kim, Scott Filippone, Anindita Das, Stefano Toldo, Antonio Abbate, Fadi N Salloum
AIMS: The preconditioning-like infarct-sparing and anti-inflammatory effects of the peptide hormone relaxin following ischemic injury have been studied in the heart. Whether reperfusion therapy with recombinant human relaxin-2, serelaxin, reduces myocardial infarct size and attenuates the subsequent NLRP3 inflammasome activation leading to further loss of functional myocardium following ischemia/reperfusion (I/R) injury is unknown. METHODS AND RESULTS: After baseline echocardiography, adult male wild-type C57BL or eNOS knockout mice underwent myocardial infarction (MI) by coronary artery ligation for 30 min followed by 24 h reperfusion...
January 10, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28069669/refining-the-molecular-organization-of-the-cardiac-intercalated-disc
#11
REVIEW
Sarah H Vermij, Hugues Abriel, Toon A B van Veen
This review presents an extensively integrated model of the cardiac intercalated disc (ID), a highly orchestrated structure that connects adjacent cardiomyocytes. Classically, three main structures are distinguished: gap junctions (GJs) metabolically and electrically connect cytoplasm of adjacent cardiomyocytes; adherens junctions (AJs) connect the actin cytoskeleton of adjacent cells; and desmosomes function as cell anchors and connect intermediate filaments. Furthermore, ion channels reside in the ID. Mutations in ID proteins have been associated with cardiac arrhythmias such as Brugada syndrome and arrhythmogenic cardiomyopathy...
January 8, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28025386/tweak-up-regulates-endothelin-1-system-in-mouse-and-human-endothelial-cells
#12
Patricia Martínez-Miguel, Diana Medrano-Andrés, Mercedes Griera-Merino, Alberto Ortiz, Manuel Rodríguez-Puyol, Diego Rodríguez-Puyol, Susana López-Ongil
: TNF-like weak inducer of apoptosis (TWEAK) is a member of TNF superfamily; it has different biological functions such as inflammation, angiogenesis, proliferation and apoptosis. TWEAK and Fn14 are expressed in different cell types, including endothelial and smooth muscle cells. Despite their presence in endothelial cells, the effect of TWEAK on endothelial function is incompletely defined. AIM: To analyze the ability of TWEAK to modify the endothelin system, particularly ET-1 and ECE-1, studying the intracellular mechanisms implied...
December 25, 2016: Cardiovascular Research
https://www.readbyqxmd.com/read/28003271/a-new-side-to-an-old-coin-dynamin-related-protein-1-with-benefits-in-the-heart
#13
EDITORIAL
Klitos Konstantinidis
No abstract text is available yet for this article.
December 21, 2016: Cardiovascular Research
https://www.readbyqxmd.com/read/28003270/akap-mediated-signaling-the-importance-of-being-in-the-right-place-at-the-right-time
#14
Cinzia Perrino, Bruno Trimarco
No abstract text is available yet for this article.
December 21, 2016: Cardiovascular Research
https://www.readbyqxmd.com/read/28003269/srf-myocardin-a-novel-molecular-axis-regulating-vascular-smooth-muscle-cell-stiffening-in-hypertension
#15
Patrick Lacolley, Zhenlin Li, Pascal Challande, Véronique Regnault
No abstract text is available yet for this article.
December 21, 2016: Cardiovascular Research
https://www.readbyqxmd.com/read/27856612/corrigendum
#16
(no author information available yet)
No abstract text is available yet for this article.
November 17, 2016: Cardiovascular Research
https://www.readbyqxmd.com/read/27856611/loss-of-akap150-promotes-pathological-remodelling-and-heart-failure-propensity-by-disrupting-calcium-cycling-and-contractile-reserve
#17
Lei Li, Jing Li, Benjamin M Drum, Yi Chen, Haifeng Yin, Xiaoyun Guo, Stephen W Luckey, Merle L Gilbert, G Stanley McKnight, John D Scott, L Fernando Santana, Qinghang Liu
AIMS: Impaired Ca(2 + )cycling and myocyte contractility are a hallmark of heart failure triggered by pathological stress such as hemodynamic overload. The A-Kinase anchoring protein AKAP150 has been shown to coordinate key aspects of adrenergic regulation of Ca(2+ )cycling and excitation-contraction in cardiomyocytes. However, the role of the AKAP150 signalling complexes in the pathogenesis of heart failure has not been investigated. METHODS AND RESULTS: Here we examined how AKAP150 signalling complexes impact Ca(2+ )cycling, myocyte contractility, and heart failure susceptibility following pathological stress...
November 17, 2016: Cardiovascular Research
https://www.readbyqxmd.com/read/27856610/corrigendum
#18
(no author information available yet)
No abstract text is available yet for this article.
November 17, 2016: Cardiovascular Research
https://www.readbyqxmd.com/read/28028070/ticagrelor-but-not-clopidogrel-reduces-arterial-thrombosis-via-endothelial-tissue-factor-suppression
#19
Martin F Reiner, Alexander Akhmedov, Simona Stivala, Stephan Keller, Daniel S Gaul, Nicole R Bonetti, Gianluigi Savarese, Martina Glanzmann, Cuicui Zhu, Wolfram Ruf, Zhihong Yang, Christian M Matter, Thomas F Lüscher, Giovanni G Camici, Juerg H Beer
AIMS: The P2Y12 antagonist ticagrelor reduces mortality in patients with acute coronary syndrome (ACS), compared with clopidogrel, and the mechanisms underlying this effect are not clearly understood. Arterial thrombosis is the key event in ACS; however, direct vascular effects of either ticagrelor or clopidogrel with focus on arterial thrombosis and its key trigger tissue factor have not been previously investigated. METHODS AND RESULTS: Human aortic endothelial cells were treated with ticagrelor or clopidogrel active metabolite (CAM) and stimulated with tumour necrosis factor-alpha (TNF-α); effects on procoagulant tissue factor (TF) expression and activity, its counter-player TF pathway inhibitor (TFPI) and the underlying mechanisms were determined...
November 15, 2016: Cardiovascular Research
https://www.readbyqxmd.com/read/28082453/atf3-expression-in-cardiomyocytes-preserves-homeostasis-in-the-heart-and-controls-peripheral-glucose-tolerance
#20
Roy Kalfon, Lilach Koren, Sharon Aviram, Ortal Schwartz, Tsonwin Hai, Ami Aronheim
AIMS: Obesity and type 2 diabetes (T2D) trigger a harmful stress-induced cardiac remodeling process known as cardiomyopathy. These diseases represent a serious and widespread health problem in the Western world; however the underlying molecular basis is not clear. ATF3 is an 'immediate early' gene whose expression is highly and transiently induced in response to multiple stressors such as metabolic, oxidative, endoplasmic reticulum and inflammation, stressors that are involved in T2D cardiomyopathy...
November 7, 2016: Cardiovascular Research
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