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Circulation Research

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https://www.readbyqxmd.com/read/29764841/genetic-targeting-of-organ-specific-blood-vessels
#1
Wenjuan Pu, Lingjuan He, Ximeng Han, Xueying Tian, Yan Li, Hui Zhang, Qiaozhen Liu, Xiuzhen Huang, Libo Zhang, Qing-Dong Wang, Zhenyang Yu, Xiao Yang, Nicola Smart, Bin Zhou
<u>Rationale:</u> Organs of the body require vascular networks to supply oxygen and nutrients and maintain physiological function. The blood vessels of different organs are structurally and functionally heterogeneous in nature. To more precisely dissect their distinct in vivo function in individual organs, without potential interference from off-site targets, it is necessary to genetically target them in an organ-specific manner. <u>Objective:</u> To generate a genetic system that targets vascular endothelial cells in an organ- or tissue- specific manner and to exemplify the potential application of intersectional genetics for precise, target-specific gene manipulation in vivo...
May 15, 2018: Circulation Research
https://www.readbyqxmd.com/read/29760016/diabetes-induced-cardiomyocyte-passive-stiffening-is-caused-by-impaired-insulin-dependent-titin-modification-and-can-be-modulated-by-neuregulin-1
#2
Anna-Eliane Hopf, Christian Andresen, Sebastian Kötter, Malgorzata Isic, Kamila Ulrich, Senem Sahin, Sabine Bongardt, Wilhelm Roell, Felicitas Drove, Nina Scheerer, Leni Vandekerckhove, Gilles W De Keulenaer, Nazha Hamdani, Wolfgang A Linke, Martina Krüger
<u>Rationale:</u> Increased titin-dependent cardiomyocyte tension is a hallmark of heart failure with preserved ejection fraction (HFpEF) associated with type-2 diabetes mellitus (T2DM). However, the insulin-related signaling pathways that modify titin-based cardiomyocyte tension, thereby contributing to modulation of diastolic function, are largely unknown. <u>Objective:</u> We aimed to determine how impaired insulin signaling affects titin expression and phosphorylation and thus increases passive cardiomyocyte tension, and whether metformin or neuregulin-1 can correct disturbed titin modifications and increased titin-based stiffness...
May 14, 2018: Circulation Research
https://www.readbyqxmd.com/read/29728415/crispr-mediated-gene-editing-to-assess-the-roles-of-tet2-and-dnmt3a-in-clonal-hematopoiesis-and-cardiovascular-disease
#3
Soichi Sano, Kousei Ohshima, Ying Wang, Yasufumi Katanasaka, Miho Sano, Kenneth Walsh
<u>Rationale:</u> Clonal hematopoiesis has been associated with increased mortality and cardiovascular disease (CVD). This condition can arise from somatic mutations in pre-leukemic driver genes within hematopoietic stem/progenitor cells (HSPC). Approximately 40 candidate driver genes have been identified, but mutations in only one of these genes, Ten-Eleven Translocation-2 (TET2), has been shown to casually contribute to CVD in murine models. <u>Objective:</u> To develop a facile system to evaluate the disease characteristics of different clonal hematopoiesis driver genes using lentivirus vector and CRISPR/Cas9 methodology...
May 4, 2018: Circulation Research
https://www.readbyqxmd.com/read/29720384/plasma-biomarkers-of-inflammation-and-angiogenesis-predict-cerebral-cavernous-malformation-symptomatic-hemorrhage-or-lesional-growth
#4
Romuald Girard, Hussein A Zeineddine, Janne Koskimaki, Maged D Fam, Ying Cao, Changbin Shi, Thomas J Moore, Rhonda Lightle, Agnieszka Stadnik, Kiranj K Chaudager, Sean P Polster, Robert Shenkar, Ryan C Duggan, David Leclerc, Kevin J Whitehead, Dean Li, Issam A Awad
<u>Rationale:</u> The clinical course of cerebral cavernous malformations (CCMs) is highly unpredictable, with few cross-sectional studies correlating pro-inflammatory genotypes and plasma biomarkers with prior disease severity. <u>Objective:</u> We hypothesize that a panel of 24 candidate plasma biomarkers, with a reported role in the physiopathology of CCMs, may predict subsequent clinically relevant disease activity. <u>Methods and Results:</u> Plasma biomarkers were assessed in non-fasting peripheral venous blood collected from consecutive CCM subjects followed for one year after initial sample collection...
May 2, 2018: Circulation Research
https://www.readbyqxmd.com/read/29703749/rationale-and-design-of-the-concert-hf-combination-of-mesenchymal-and-c-kit-cardiac-stem-cells-as-regenerative-therapy-for-heart-failure-trial
#5
Roberto Bolli, Joshua M Hare, Keith L March, Carl J Pepine, James T Willerson, Emerson C Perin, Phillip C Yang, Timothy D Henry, Jay H Traverse, Raul D Mitrani, Aisha Khan, Ivonne H Schulman, Doris A Taylor, Darcy L DiFede, João A Lima, Atul R Chugh, John Loughran, Rachel W Vojvodic, Shelly L Sayre, Judy Bettencourt, Michelle Cohen, Lem Moyé, Ray F Ebert, Robert D Simari
<u>Rationale:</u> Autologous bone marrow (BM) mesenchymal stem cells (MSCs) and c-kit+ cardiac progenitor cells (CPCs) are two promising cell types being evaluated for patients with heart failure (HF) secondary to ischemic cardiomyopathy. No information is available in humans regarding the relative efficacy of MSCs and CPCs and whether their combination is more efficacious than either cell type alone. <u>Objective:</u> CONCERT-HF (Combination Of meseNchymal and c-kit+ Cardiac stEm cells as Regenerative Therapy for Heart Failure) is a Phase II trial aimed at elucidating these issues by assessing the feasibility, safety, and efficacy of transendocardial administration of autologous MSCs and CPCs, alone and in combination, in patients with HF caused by chronic ischemic cardiomyopathy (coronary artery disease and old myocardial infarction)...
April 27, 2018: Circulation Research
https://www.readbyqxmd.com/read/29691232/topological-arrangement-of-cardiac-fibroblasts-regulates-cellular-plasticity
#6
Jingyi Yu, Marcus M Seldin, Kai Fu, Shen Li, Larry Lam, Ping Wang, Yijie Wang, Dian Huang, Thang L Nguyen, Bowen Wei, Rajan P Kulkarni, Dino Di Carlo, Michael Teitell, Matteo Pellegrini, Aldons J Lusis, Arjun Deb
<u>Rationale:</u> Cardiac fibroblasts do not form a syncytium but reside in the interstitium between myocytes. This topological relationship between fibroblasts and myocytes is maintained throughout post-natal life until acute myocardial injury occurs, when fibroblasts are recruited to, proliferate and aggregate in the region of myocyte necrosis. The accumulation or aggregation of fibroblasts in the area of injury thus represents a unique event in the life cycle of the fibroblast but little is known about how changes in the topological arrangement of fibroblasts following cardiac injury affect fibroblast function...
April 24, 2018: Circulation Research
https://www.readbyqxmd.com/read/29669713/heme-oxygenase-1-in-macrophages-drives-septic-cardiac-dysfunction-via-suppressing-lysosomal-degradation-of-inducible-nitric-oxide-synthase
#7
Liangliang Jia, Yaping Wang, Yidong Wang, Yuankun Ma, Jian Shen, Zurong Fu, Yue Wu, Sheng'an Su, Yuhao Zhang, Zhejun Cai, Jian'an Wang, Meixiang Xiang
<u>Rationale:</u> To date, our understanding of the role of heme oxygenase-1 (HO-1) in inflammatory diseases has mostly been limited to its catalytic function and the potential for its heme-related catabolic products to suppress inflammation and oxidative stress. Whether and how HO-1 in macrophages plays a role in the development of septic cardiac dysfunction has never been explored. <u>Objective:</u> Here, we investigated the role of macrophage-derived HO-1 in septic cardiac dysfunction...
April 18, 2018: Circulation Research
https://www.readbyqxmd.com/read/29669712/er-chaperone-grp78-protects-heart-from-ischemia-reperfusion-injury-through-akt-activation
#8
Xukun Bi, Guangyu Zhang, Xiaoding Wang, Chau Yt Nguyen, Herman I May, Xiaoting Li, Ali Al-Hashimi, Richard C Austin, Thomas G Gillette, Guo Sheng Fu, Zhao V Wang, Joseph A Hill
<u>Rationale:</u> Restoration of coronary artery blood flow is the most effective means of ameliorating myocardial damage triggered by ischemic heart disease. However, coronary reperfusion elicits an increment of additional injury to the myocardium. Accumulating evidence indicates that the unfolded protein response (UPR) in cardiomyocytes is activated by ischemia/reperfusion (I/R) injury. Xbp1s, the most highly conserved branch of the UPR, is protective in response to cardiac I/R injury. GRP78, a master regulator of the UPR and an Xbp1s target, is up-regulated after I/R...
April 18, 2018: Circulation Research
https://www.readbyqxmd.com/read/29636378/cardiac-c-kit-biology-revealed-by-inducible-transgenesis
#9
Natalie A Gude, Fareheh Firouzi, Kathleen M Broughton, Kelli Ilves, Kristine P Nguyen, Christina R Payne, Veronica Sacchi, Megan M Monsanto, Alexandria R Casillas, Farid G Khalafalla, Bingyan J Wang, David Ebeid, Roberto Alvarez, Walter P Dembitsky, Barbara A Bailey, Jop H van Berlo, Mark A Sussman
<u>Rationale:</u> Biological significance of c-Kit as a cardiac stem cell marker and role(s) of c-Kit+ cells in myocardial development or response to pathologic injury remain unresolved due to varied and discrepant findings. Alternative experimental models are required to contextualize and reconcile discordant published observations of cardiac c-Kit myocardial biology and provide meaningful insights regarding clinical relevance of c-Kit signaling for translational cell therapy. <u>Objective:</u> Demonstration of c-Kit myocardial biology through combined studies of both human and murine cardiac cells...
April 10, 2018: Circulation Research
https://www.readbyqxmd.com/read/29618597/regulation-of-vascular-calcification-by-growth-hormone-releasing-hormone-and-its-agonists
#10
Jian Shen, Ning Zhang, Yi-Nuo Lin, PingPing Xiang, Xian-Bao Liu, Peng-Fei Shan, Xin-Yang Hu, Wei Zhu, Yao-Liang Tang, Keith A Webster, Ren-Zhi Cai, Andrew Schally, Jian'an Wang, Hong Yu
<u>Rationale:</u> Vascular calcification (VC) is a marker of the severity of atherosclerotic disease. Hormones play important roles in regulating calcification; estrogen and parathyroid hormones exert opposing effects, the former alleviating VC and the latter exacerbating it. So far no treatment strategies have been developed to regulate clinical VC. <u>Objective:</u> To investigate the effect of growth hormone-releasing hormone (GHRH) and its agonist (GHRH-A) on the blocking of VC in a mouse model...
April 4, 2018: Circulation Research
https://www.readbyqxmd.com/read/29618596/alternative-splicing-of-foxp3-controls-regulatory-t-cell-effector-functions-and-is-associated-with-human-atherosclerotic-plaque-stability
#11
Anne-Laure Joly, Christina Seitz, Sang Liu, Nikolai V Kouznetsov, Karl Gertow, Lisa S Westerberg, Gabrielle Paulsson-Berne, Göran K Hansson, John Andersson
<u>Rationale:</u> Regulatory T (Treg) cells suppress immune responses and have been shown to attenuate atherosclerosis. The Treg cell lineage specification factor FOXP3 is essential for Treg cells' ability to uphold immunological tolerance. In humans, FOXP3 exists in several different isoforms, however, their specific role is poorly understood. <u>Objective:</u> To define the regulation and functions of the two major FOXP3 isoforms, FOXP3fl and FOXP3Δ2, as well as to establish whether their expression is associated with ischemic atherosclerotic disease...
April 4, 2018: Circulation Research
https://www.readbyqxmd.com/read/29592957/intra-cardiac-release-of-extracellular-vesicles-shapes-inflammation-following-myocardial-infarction
#12
Xavier Loyer, Ivana Zlatanova, Cécile Devue, Min Yin, Kiave-Yune Howangyin, Phatchanat Klaihmon, Coralie L Guerin, Marouane Kheloufi, José Vilar, Konstantinos Zannis, Bernd K Fleischmann, Do Won Hwang, Jongmin Park, Hakho Lee, Philippe Menasche, Jean-Sébastien Silvestre, Chantal M Boulanger
<u>Rationale:</u> A rapid and massive influx of inflammatory cells occurs into ischemic area following myocardial infarction, resulting in local release of cytokines and growth factors. Yet, the mechanisms regulating their production are not fully explored. The release of extracellular vesicles (EV) in the interstitial space curbs important biological functions, including inflammation, and influences the development of cardiovascular diseases. So far, there is no evidence for in situ release of cardiac EVs following myocardial infarction...
March 28, 2018: Circulation Research
https://www.readbyqxmd.com/read/29572206/roles-of-pad4-and-netosis-in-experimental-atherosclerosis-and-arterial-injury-implications-for-superficial-erosion
#13
Grégory Franck, Thomas L Mawson, Eduardo J Folco, Roberto Molinaro, Victoria Ruvkun, Daniel Engelbertsen, Xin Liu, Yevgenia Tesmenitsky, Eugenia Shvartz, Galina K Sukhova, Jean-Baptiste Michel, Antonino Nicoletti, Andrew H Lichtman, Denisa D Wagner, Kevin J Croce, Peter Libby
<u>Rationale:</u> Neutrophils likely contribute to the thrombotic complications of human atheromata. In particular, neutrophil extracellular traps (NETs) could exacerbate local inflammation and amplify and propagate arterial intimal injury and thrombosis. Peptidyl arginine deiminase 4 (PAD4) participates in NET formation, but understanding of this enzyme's role in atherothrombosis remains scant. <u>Objective:</u> This study tested the hypothesis that PAD4 and NETs influence experimental atherogenesis and in processes implicated in superficial erosion, a form of plaque complication we previously associated with NETs...
March 23, 2018: Circulation Research
https://www.readbyqxmd.com/read/29563102/protein-s-nitrosylation-controls-glycogen-synthase-kinase-3%C3%AE-function-independent-of-its-phosphorylation-state
#14
Shengbing Wang, Vidya Venkatraman, Erin L Crowgey, Ting Liu, Zongming Fu, Ronald J Holewinski, Mark J J Ranek, David A Kass, Brian O'Rourke, Jennifer E Van Eyk
<u>Rationale:</u> Glycogen synthase kinase 3β (GSK3β) is a multifunctional and constitutively active kinase known to regulate a myriad of cellular processes. The primary mechanism to regulate its function is through phosphorylation-dependent inhibition at serine-9 residue. Emerging evidence indicates that there may be alternative mechanisms that control GSK3β for certain functions. <u>Objective:</u> Here we sought to understand the role of protein S-nitrosylation (SNO) on the function of GSK3β...
March 21, 2018: Circulation Research
https://www.readbyqxmd.com/read/29545368/commd-family-regulates-plasma-ldl-levels-and-attenuates-atherosclerosis-through-stabilizing-the-ccc-complex-in-endosomal-ldlr-trafficking
#15
Alina Fedoseienko, Melinde Wijers, Justina C Wolters, Daphne Dekker, Marieke Smit, Nicolette Huijkman, Niels Kloosterhuis, Helene Klug, Aloys Schepers, Ko Willems van Dijk, Johannes H Levels, Daniel D Billadeau, Marten H Hofker, Jan van Deursen, Marit Westerterp, Ezra Burstein, Jan Albert Kuivenhoven, Bart van de Sluis
<u>Rationale:</u> <u>CO</u>pper <u>M</u>etabolism <u>M</u>URR1 Domain-containing (COMMD) proteins are a part of the COMMD-CCDC22-CCDC93 (CCC) complexes facilitating endosomal trafficking of cell surface receptors. Hepatic COMMD1 inactivation decreases CCDC22 and CCDC93 protein levels, impairs the recycling of the low-density lipoprotein receptor (LDLR), and increases plasma LDL cholesterol levels in mice. However, whether any of the other COMMD members function similarly as COMMD1, and whether perturbation in the CCC complex promotes atherogenesis remain unclear...
March 15, 2018: Circulation Research
https://www.readbyqxmd.com/read/29545367/a-dominant-role-for-regulatory-t-cells-in-protecting-females-against-pulmonary-hypertension
#16
Rasa Tamosiuniene, Olga Manouvakhova, Paul Mesange, Toshie Saito, Jin Qian, Mrinmoy Sanyal, Yu-Chun Lin, Linh P Nguyen, Amir Luria, Allen B Tu, Joshua M Sante, Marlene Rabinovitch, Desmond J Fitzgerald, Brian B Graham, Aida Habtezion, Norbert F Voelkel, Laure Aurelian, Mark R Nicolls
<u>Rationale:</u> Pulmonary arterial hypertension (PH) is a life-threatening condition associated with immune dysregulation and abnormal regulatory T cell (Treg) activity, but it is currently unknown whether and how abnormal Treg function differentially affects males and females. <u>Objective:</u> To evaluate whether and how Treg-deficiency differentially affects male and female rats in experimental PH. <u>Methods and Results:</u> Male and female athymic rnu/rnu rats, lacking Tregs, were treated with the vascular endothelial growth factor receptor-2 (VEGFR2) inhibitor SU5416 or chronic hypoxia and evaluated for PH; some animals underwent Treg immune reconstitution (IR) before SU5416 administration...
March 15, 2018: Circulation Research
https://www.readbyqxmd.com/read/29545366/atlas-of-the-immune-cell-repertoire-in-mouse-atherosclerosis-defined-by-single-cell-rna-sequencing-and-mass-cytometry
#17
Holger Winkels, Erik Ehinger, Melanie Vassallo, Konrad Buscher, Huy Dinh, Kouji Kobiyama, Anouk Hamers, Clément Cochain, Ehsan Vafadarnejad, Antoine-Emmanuel Saliba, Alma Zernecke, Akula Pramod, Amlan Ghosh, Nathaly Anto Michel, Natalie Hoppe, Ingo Hilgendorf, Andreas Zirlik, Catherine Hedrick, Klaus Ley, Dennis Wolf
<u>Rationale:</u> Atherosclerosis is a chronic inflammatory disease that is driven by the interplay of pro- and anti-inflammatory leukocytes in the aorta. Yet, the phenotypic and transcriptional diversity of aortic leukocytes is only poorly understood. <u>Objective:</u> We characterized leukocytes from healthy and atherosclerotic mouse aortas in-depth by single cell RNA-sequencing (scRNAseq) and mass cytometry (CyTOF) to define an atlas of the immune cell landscape in atherosclerosis...
March 15, 2018: Circulation Research
https://www.readbyqxmd.com/read/29545365/single-cell-rna-seq-reveals-the-transcriptional-landscape-and-heterogeneity-of-aortic-macrophages-in-murine-atherosclerosis
#18
Clément Cochain, Ehsan Vafadarnejad, Panagiota Arampatzi, Pelisek Jaroslav, Holger Winkels, Klaus Ley, Dennis Wolf, Antoine-Emmanuel Saliba, Alma Zernecke
<u>Rationale:</u> It is assumed that atherosclerotic arteries contain several macrophage subsets endowed with specific functions. The precise identity of these subsets is poorly characterized as they ha ve been defined by the expression of a restricted number of markers. <u>Objective:</u> We have applied single-cell RNA-seq as an unbiased profiling strategy to interrogate and classify aortic macrophage heterogeneity at the single-cell level in atherosclerosis. <u>Methods and Results:</u> We performed single-cell RNA sequencing of total aortic CD45+ cells extracted from the non-diseased (chow fed) and atherosclerotic (11 weeks of high fat diet) aorta of Ldlr-/- mice...
March 15, 2018: Circulation Research
https://www.readbyqxmd.com/read/29535164/glycosylation-profile-of-immunoglobulin-g-is-cross-sectionally-associated-with-cardiovascular-disease-risk-score-and-subclinical-atherosclerosis-in-two-independent-cohorts
#19
Cristina Menni, Ivan Gudelj, Erin MacDonald-Dunlop, Massimo Mangino, Jonas Zierer, Erim Bešić, Peter Joshi, Irena Trbojević-Akmačić, Phil J Chowienczyk, Timothy D Spector, James F Wilson, Gordan Lauc, Ana M Valdes
<u>Rationale:</u> One measure of protein glycosylation (GlycA) has been reported to predict higher cardiovascular risk by reflecting inflammatory pathways <u>Objective:</u> To assess the role of a comprehensive panel of immunoglobulin (IgG) glycosylation traits on traditional risk factors for cardiovascular disease and on presence of subclinical atherosclerosis in addition to GlycA. <u>Methods and Results:</u> We measured 76 IgG glycosylation traits in 2970 women (age range 40-79 years) from the TwinsUK cohort and correlated it to their estimated 10-year atherosclerotic cardiovascular disease (ASCVD) risk score and their carotid and femoral plaque measured by ultrasound imaging...
March 13, 2018: Circulation Research
https://www.readbyqxmd.com/read/29514831/cardiac-kir2-1-and-na-v-1-5-channels-traffic-together-to-the-sarcolemma-to-control-excitability
#20
Daniela Ponce-Balbuena, Guadalupe Guerrero-Serna, Carmen R Valdivia, Ricardo Caballero, F J Díez-Guerra, Eric N Jiménez-Vázquez, Rafael J Ramirez, Andre Monteiro da Rocha, Todd J Herron, Katherine F Campbell, B C Willis, Francisco J Alvarado, Manuel Zarzoso, Kuljeet Kaur, Marta Pérez-Hernández, Marcos Matamoros, Héctor H Valdivia, Eva Delpón, José Jalife
<u>Rationale:</u> In cardiomyocytes, NaV 1.5 and Kir2.1 channels interact dynamically as part of membrane bound macromolecular complexes. <u>Objective:</u> To test whether NaV 1.5 and Kir2.1 preassemble during early forward trafficking and travel together to common membrane microdomains. <u>Methods and Results:</u> In patch-clamp experiments, co-expression of trafficking deficient mutants Kir2.1Δ314-315 or Kir2.1R44A/R46A with wildtype (WT) NaV 1.5WT in heterologous cells reduced INa , compared to NaV 1...
March 7, 2018: Circulation Research
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