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Circulation Research

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https://www.readbyqxmd.com/read/28729354/continuous-flow-lvad-support-causes-a-distinct-form-of-intestinal-angiodysplasia
#1
Jooeun Kang, Samson Hennessy-Strahs, Pawel Kwiatkowski, Christian Bermudez, Michael A Acker, Pavan Atluri, Patrick McConnell, Carlo R Bartoli
Rationale: The objective of this autopsy study was to determine whether abnormal gastrointestinal vascularity develops during continuous-flow LVAD support. Objective: Left ventricular assist device (LVAD) support causes pathologic degradation of von Willebrand factor (vWF) and bleeding from gastrointestinal angiodysplasia at an alarming rate. It has been speculated that LVAD support, itself may cause angiodysplasia. The relationship to abnormal vWF metabolism is unknown. We tested the hypothesis that abnormal gastrointestinal vascularity develops during continuous-flow LVAD support...
July 20, 2017: Circulation Research
https://www.readbyqxmd.com/read/28729353/recommendation-on-design-execution-and-reporting-of-animal-atherosclerosis-studies-a-scientific-statement-from-the-american-heart-association
#2
REVIEW
Alan Daugherty, Alan R Tall, Mat J A P Daemen, Erling Falk, Edward A Fisher, Guillermo García-Cardeña, Aldons J Lusis, A Phillip Owens, Michael E Rosenfeld, Renu Virmani
Animal studies are a foundation for defining mechanisms of atherosclerosis and potential targets of drugs to prevent lesion development or reverse the disease. In the current literature, it is common to see contradictions of outcomes in animal studies from different research groups, leading to the paucity of extrapolations of experimental findings into understanding the human disease. The purpose of this statement is to provide guidelines for development and execution of experimental design and interpretation in animal studies...
July 20, 2017: Circulation Research
https://www.readbyqxmd.com/read/28724746/therapeutic-targeting-tumor-progression-locus-2-tpl2-activating-transcription-factor-4-atf4-chemokine-stromal-cell-derived-factor-%C3%AE-sdf1%C3%AE-axis-suppresses-diabetic-retinopathy
#3
De-Wei Lai, Keng-Hung Lin, Wayne Huey-Herng Sheu, Maw-Rong Lee, Chung-Yu Chen, Wen-Jane Lee, Yi-Wen Hung, Chin-Chang Shen, Tsung-Ju Chung, Shing-Hwa Liu, Meei-Ling Sheu
Rationale: Diabetic retinopathy is characterized by vasopermeability, vascular leakage, inflammation, blood-retinal barrier breakdown, capillary degeneration and neovascularization. However, the mechanisms underlying the association between diabetes and progression retinopathy remain unclear. Objective: Tumor progression locus 2 (TPL2), a serine-threonine protein kinase, exerts a pathological effect on vascular angiogenesis. This study investigated the role of N(ε)-(carboxymethyl)lysine (CML), a major advanced glycation end products, and the involved TPL2-related molecular signals in diabetic retinopathy using models of in vitro and in vivo and human samples...
July 19, 2017: Circulation Research
https://www.readbyqxmd.com/read/28724745/seq-identifies-circulating-mir-125a-5p-mir-125b-5p-and-mir-143-3p-as-potential-biomarkers-for-acute-ischemic-stroke
#4
Steffen Tiedt, Matthias Prestel, Rainer Malik, Nicola Schieferdecker, Marco Düring, Veronika Kautzky, Ivelina Stoycheva, Julia Böck, Bernd H Northoff, Matthias Klein, Franziska Dorn, Knut Krohn, Daniel Teupser, Arthur Liesz, Nikolaus Plesnila, Lesca M Holdt, Martin Dichgans
Rationale: Currently, there are no blood-based biomarkers with clinical utility for acute ischemic stroke (IS). microRNAs (miRNAs) show promise as disease markers due to their cell-type specific expression patterns and stability in peripheral blood. Objective: To identify circulating miRNAs associated with acute IS, determine their temporal course up to 90 days post-stroke, and explore their utility as an early diagnostic marker. Methods and Results: We used RNA sequencing to study expression changes of circulating miRNAs in a discovery sample of 20 IS patients and 20 matched healthy control subjects (HCs)...
July 19, 2017: Circulation Research
https://www.readbyqxmd.com/read/28701309/arhgap18-protects-against-thoracic-aortic-aneurysm-formation-by-mitigating-the-synthetic-and-pro-inflammatory-smooth-muscle-cell-phenotype
#5
Renjing Liu, Lisa Lo, Angelina J Lay, Yang Zhao, Ka Ka Ting, Elizabeth N Robertson, Andrew G Sherrah, Sorour R Jarrah, Haibo Li, Zhaoxiong Zhou, Brett D Hambly, David R Richmond, Richmond W Jeremy, Paul G Bannon, Matthew A Vadas, Jennifer Gamble
Rationale: Thoracic aortic aneurysm (TAA) is a potentially lethal condition which can affect individuals of all ages. TAA may be complicated by the sudden onset of life threatening dissection or rupture. The underlying mechanisms leading to TAA formation, particularly in the non-syndromal idiopathic group of patients, are not well understood. Thus, identification of new genes and targets that are involved in TAA pathogenesis are required to help prevent and/or reverse the disease phenotype. Objective: Here we explore the role of ARHGAP18, a novel Rho GAP expressed by smooth muscle cells (SMC), in the pathogenesis of TAA...
July 12, 2017: Circulation Research
https://www.readbyqxmd.com/read/28698179/a-novel-regulatory-mechanism-of-smooth-muscle-%C3%AE-actin-expression-by-nrg-1-circacta2-mir-548f-5p-axis
#6
Yan Sun, Zhan Yang, Bin Zheng, Xin-Hua Zhang, Man-Li Zhang, Xue-Shan Zhao, Hong-Ye Zhao, Toru Suzuki, Jin-Kun Wen
Rationale: Neuregulin-1 (NRG-1) includes an extracellular EGF-like domain and an intracellular domain (NRG-1-ICD). In response to transforming growth factor (TGF)-β1,its cleavage by proteolytic enzymes releases a bioactive fragment, which suppresses the vascular smooth muscle cell (VSMC) proliferation by activating ErbB receptor. However, NRG-1-ICD function in VSMCs remains unknown. Objective: Here, we characterize the function of NRG-1-ICD and underlying mechanisms in VSMCs. Methods and Results: Immunofluorescence staining, Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) showed that NRG-1 was expressed in rat, mouse and human VSMCs and was upregulated and cleaved in response to TGF-β1...
July 11, 2017: Circulation Research
https://www.readbyqxmd.com/read/28696252/thermoneutrality-but-not-ucp1-deficiency-suppresses-monocyte-mobilization-into-blood
#7
Jesse W Williams, Andrew F Elvington, Stoyan Ivanov, Skyler Kessler, Hannah Luehmann, Osamu Baba, Brian T Saunders, Ki-Wook Kim, Michael W Johnson, Clarissa S Craft, Jae-Hoon Choi, Mary G Sorci-Thomas, Bernd H Zinselmeyer, Jonathan R Brestoff, Yongjian Liu, Gwendalyn J Randolph
Rationale: Ambient temperature is a risk factor for cardiovascular disease. Cold weather increases cardiovascular events, but paradoxically, cold exposure is metabolically protective due to UCP1-dependent thermogenesis. Objective: We sought to determine the differential effects of ambient environmental temperature challenge and UCP1 activation in relation to cardiovascular disease progression. Methods and Results: Using mouse models of atherosclerosis housed at three different ambient temperatures, we observed that cold temperature enhanced while thermoneutral housing temperature inhibited atherosclerotic plaque growth, as did deficiency in UCP1...
July 10, 2017: Circulation Research
https://www.readbyqxmd.com/read/28696251/endothelin-1-stimulates-vasoconstriction-through-rab11a-serine-177-phosphorylation
#8
Xue Zhai, Marie D Leo, Jonathan H Jaggar
Rationale: Large-conductance calcium (Ca(2+))-activated potassium channels (BK) are composed of pore-forming BKα and auxiliary β1 subunits in arterial smooth muscle cells (myocytes). Vasoconstrictors, including endothelin-1 (ET-1), inhibit myocyte BK channels, leading to contraction, but mechanisms involved are unclear. Recent evidence indicates that BKα is primarily plasma membrane-localized, whereas the cellular location of β1 can be rapidly altered by Rab11A-positive recycling endosomes. Whether vasoconstrictors regulate the multi-subunit composition of surface BK channels to stimulate contraction is unclear...
July 10, 2017: Circulation Research
https://www.readbyqxmd.com/read/28684631/peer-review-practices-for-evaluating-biomedical-research-grants-a-scientific-statement-from-the-american-heart-association
#9
REVIEW
Lucy Liaw, Jane E Freedman, Lance B Becker, Nehal N Mehta, Laura Liscum
The biomedical research enterprise depends on the fair and objective peer review of research grants, leading to the distribution of resources through efficient and robust competitive methods. In the United States, federal funding agencies and foundations collectively distribute billions of dollars annually to support biomedical research. For the American Heart Association, a Peer Review Subcommittee is charged with establishing the highest standards for peer review. This scientific statement reviews the current literature on peer review practices, describes the current American Heart Association peer review process and those of other agencies, analyzes the strengths and weaknesses of American Heart Association peer review practices, and recommends best practices for the future...
July 6, 2017: Circulation Research
https://www.readbyqxmd.com/read/28684630/sirt3-impairment-and-sod2-hyperacetylation-in-vascular-oxidative-stress-and-hypertension
#10
Anna E Dikalova, Hana A Itani, Rafal R Nazarewicz, William G McMaster, Charles R Flynn, Roman V Uzhachenko, Joshua P Fessel, Jorge L Gamboa, David G Harrison, Sergey I Dikalov
Rationale: Clinical studies have shown that Sirt3 expression declines by 40% by age 65 paralleling the increased incidence of hypertension and metabolic conditions further inactivate Sirt3 due to increased NADH and acetyl-CoA levels. Sirt3 impairment reduces the activity of a key mitochondrial antioxidant enzyme, superoxide dismutase 2 (SOD2), due to hyperacetylation. Objective: In this study we examined if loss of Sirt3 activity increases vascular oxidative stress due to SOD2 hyperacetylation and promotes endothelial dysfunction and hypertension...
July 6, 2017: Circulation Research
https://www.readbyqxmd.com/read/28684629/genetic-deletion-of-nadph-oxidase-1-rescues-microvascular-function-in-mice-with-metabolic-disease
#11
Jennifer A Thompson, Sebastian Larion, James D Mintz, Eric J Belin de Chantemele, David J Fulton, David W Stepp
Rationale: Early vascular changes in metabolic disease that precipitate the development of cardiovascular complications are largely driven by reactive oxygen species (ROS) accumulation, yet the extent to which excess ROS derive from specific Nox isoforms remains ill-defined. Objective: Identify the role of Nox1 in the development of microvascular dysfunction in metabolic disease. Methods and Results: Four genotypes were generated by breeding Nox1 knock-out (KO) mice with db/db mice: lean (HdbWnox1); lean Nox1 KO (HdbKnox1); obese (KdbWnox1); obese KK (KdbKnox1)...
July 6, 2017: Circulation Research
https://www.readbyqxmd.com/read/28674041/transient-notch-activation-induces-long-term-gene-expression-changes-leading-to-sick-sinus-syndrome-in-mice
#12
Yun Qiao, Catherine Lipovsky, Stephanie Hicks, Somya Bhatnagar, Gang Li, Aditi Khandekar, Robert Guzy, Kel Vin Woo, Colin G Nichols, Igor R Efimov, Stacey Rentschler
Rationale: Notch signaling programs cardiac conduction during development, and in the adult ventricle, injury-induced Notch reactivation initiates global transcriptional and epigenetic changes. Objective: To determine whether Notch reactivation may stably alter atrial ion channel gene expression and arrhythmia inducibility. Methods and Results: To model an injury response and determine the effects of Notch signaling on atrial electrophysiology, we transiently activate Notch signaling within adult myocardium using a doxycycline-inducible genetic system (iNICD)...
July 3, 2017: Circulation Research
https://www.readbyqxmd.com/read/28663367/genome-wide-temporal-profiling-of-transcriptome-and-open-chromatin-of-early-cardiomyocyte-differentiation-derived-from-hipscs-and-hescs
#13
Qing Liu, Chao Jiang, Jin Xu, Mingtao Zhao, Kevin Van Bortle, Xun Cheng, Guangwen Wang, Howard Y Chang, Joseph C Wu, Michael P Snyder
Rationale: Recent advances have improved our ability to generate cardiomyocytes from human induced pluripotent stem cells (hiPSCs) and human embryonic stem cells (hESCs). However, our understanding of the transcriptional regulatory networks underlying early stages (i.e. from mesoderm to cardiac mesoderm) of cardiomyocyte differentiation remains limited. Objective: To characterize transcriptome and chromatin accessibility during early cardiomyocyte differentiation from hiPSCs and hESCs. Methods and Results: We profiled the temporal changes in transcriptome and chromatin accessibility at genome-wide levels during cardiomyocyte differentiation derived from two hiPSC lines and two hESC lines at four stages: pluripotent stem cells, mesoderm, cardiac mesoderm, and differentiated cardiomyocytes...
June 29, 2017: Circulation Research
https://www.readbyqxmd.com/read/28655832/an-unbiased-high-throughput-screen-to-identify-novel-effectors-that-impact-on-cardiomyocyte-aggregate-levels
#14
Patrick M McLendon, Gregory Davis, James Gulick, Sonia R Singh, Na Xu, Nathan Salomonis, Jeffery D Molkentin, Jeffrey Robbins
Rationale: Post-mitotic cells such as cardiomyocytes appear to be particularly susceptible to proteotoxic stimuli, and large, proteinaceous deposits are characteristic of the Desmin Related Cardiomyopathies and crystallin cardiomyopathic diseases. Increased activity of protein clearance pathways in the cardiomyocyte such as proteasomal degradation and autophagy have proven to be beneficial in maintaining cellular and cardiac function in the face of multiple proteotoxic insults, holding open the possibility of targeting these processes for the development of effective therapeutics...
June 27, 2017: Circulation Research
https://www.readbyqxmd.com/read/28652256/fundamental-cardiovascular-research-returns-on-societal-investment-a-scientific-statement-from-the-american-heart-association
#15
REVIEW
Joseph A Hill, Reza Ardehali, Kimberli Taylor Clarke, Gregory J Del Zoppo, Lee L Eckhardt, Kathy K Griendling, Peter Libby, Dan M Roden, Hesham A Sadek, Christine E Seidman, Douglas E Vaughan
Recent decades have witnessed robust successes in conquering the acutely lethal manifestations of heart and vascular diseases. Many patients who previously would have died now survive. Lifesaving successes like these provide a tremendous and easily recognized benefit to individuals and society. Although cardiovascular mortality has declined, the devastating impact of chronic heart disease and comorbidities on quality of life and healthcare resources continues unabated. Future strides, extending those made in recent decades, will require continued research into mechanisms underlying disease prevention, pathogenesis, progression, and therapeutic intervention...
June 26, 2017: Circulation Research
https://www.readbyqxmd.com/read/28642329/experimental-and-computational-insight-into-human-mesenchymal-stem-cell-paracrine-signaling-and-heterocellular-coupling-effects-on-cardiac-contractility-and-arrhythmogenicity
#16
Joshua Mayourian, Timothy J Cashman, Delaine K Ceholski, Bryce V Johnson, David Sachs, Deepak A Kaji, Susmita Sahoo, Joshua M Hare, Roger J Hajjar, Eric A Sobie, Kevin D Costa
Rationale: Myocardial delivery of human mesenchymal stem cells (hMSCs) is an emerging therapy for treating the failing heart. However, the relative effects of hMSC-mediated heterocellular coupling (HC) and paracrine signaling (PS) on human cardiac contractility and arrhythmogenicity remain unresolved. Objective: To better understand hMSC PS and HC effects on human cardiac contractility and arrhythmogenicity by integrating experimental and computational approaches. Methods and Results: : Extending our previous hMSC-cardiomyocyte HC computational model, we incorporated experimentally calibrated hMSC PS effects on cardiomyocyte L-type calcium channel/SERCA activity and cardiac tissue fibrosis...
June 22, 2017: Circulation Research
https://www.readbyqxmd.com/read/28637784/tnfr2-stimulation-promotes-mitochondrial-fusion-via-stat3-and-nf-kb-dependent-activation-of-opa1-expression
#17
Jinliang Nan, Hengxun Hu, Yong Sun, Lianlian Zhu, Yingchao Wang, Zhiwei Zhong, Jing Zhao, Na Zhang, Ya Wang, Yaping Wang, Jian Ye, Ling Zhang, Xinyang Hu, Wei Zhu, Jian'an Wang
Rationale: Mitochondria are important cellular organelles and play essential roles in maintaining cell structure and function. Emerging evidence indicates that in addition to having pro-inflammatory and pro-apoptotic effects, tumor necrosis factor α (TNFα) can, under certain circumstances, promote improvements in mitochondrial integrity and function, phenomena that can be ascribed to the existence of TNFα receptor 2 (TNFR2). Objective: The present study aimed to investigate whether and how TNFR2 activation mediates the effects of TNFα on mitochondria...
June 21, 2017: Circulation Research
https://www.readbyqxmd.com/read/28637783/paradoxical-suppression-of-atherosclerosis-in-the-absence-of-microrna-146a
#18
Henry S Cheng, Rickvinder Besla, Angela Li, Zhiqi Chen, Eric A Shikatani, Maliheh Nazari-Jahantigh, Adel Hammoutène, My-Anh Nguyen, Michele Geoffrion, Lei Cai, Nadiya Khyzha, Tong Li, Sonya A MacParland, Mansoor Husain, Myron I Cybulsky, Chantal M Boulanger, Ryan E Temel, Andreas Schober, Katey J Rayner, Clinton Robbins, Jason E Fish
Rationale: Inflammation is a key contributor to atherosclerosis. MicroRNA-146a (miR-146a) has been identified as a critical brake on pro-inflammatory NF-κB signalling in several cell types, including endothelial cells and bone marrow-derived cells. Importantly, miR-146a expression is elevated in human atherosclerotic plaques, and polymorphisms in the miR-146a pre-cursor have been associated with risk of coronary artery disease. Objective: To define the role of endogenous miR-146a during atherogenesis. Methods and Results: Paradoxically, Low-density lipoprotein receptor (Ldlr)(-/-) mice deficient in miR-146a develop less atherosclerosis, despite having highly elevated levels of circulating pro-inflammatory cytokines...
June 21, 2017: Circulation Research
https://www.readbyqxmd.com/read/28637782/the-brugada-syndrome-susceptibility-gene-hey2-modulates-cardiac-transmural-ion-channel-patterning-and-electrical-heterogeneity
#19
Christiaan C Veerman, Svitlana Podliesna, Rafik Tadros, Elisabeth M Lodder, Isabella Mengarelli, Berend de Jonge, Leander Beekman, Julien Barc, Ronald Wilders, Arthur A Wilde, Bastiaan J Boukens, Ruben Coronel, Arie Verkerk, Carol Ann Remme, Connie R Bezzina
Rationale: Genome-wide association studies previously identified an association of rs9388451 at chromosome 6q22.3 (near HEY2) with Brugada syndrome (BrS). The causal gene and underlying mechanism remain unresolved. Objective: We used an integrative approach entailing transcriptomic studies in human hearts and electrophysiological studies in Hey2 heterozygous knockout mice (Hey2(+/-) ) to dissect the underpinnings of the 6q22.31 association with BrS. Methods and Results: We queried expression quantitative trait locus (eQTL) data acquired in 190 human left ventricular (LV) samples from the Genotype-Tissue Expression (GTEx) consortium for cis-eQTL effects of rs9388451 which revealed an association between BrS risk allele dosage and HEY2 expression (β=+0...
June 21, 2017: Circulation Research
https://www.readbyqxmd.com/read/28630135/inhibition-of-the-cardiac-fibroblast-enriched-lncrna-meg3-prevents-cardiac-fibrosis-and-diastolic-dysfunction
#20
Maria-Teresa Piccoli, Shashi Gupta, Janika Viereck, Ariana Foinquinos, Sabine Samolovac, Freya Kramer, Ankita Garg, Janet Remke, Karina Zimmer, Sandor Batkai, Thomas Thum
Rationale: Cardiac fibroblasts (CFs) drive extracellular matrix (ECM) remodeling following pressure overload, leading to fibrosis and diastolic dysfunction. Recent studies described the role of long noncoding RNAs (lncRNAs) in cardiac pathologies. Nevertheless, detailed reports on lncRNAs regulating CF biology and describing their implication in cardiac remodeling are still missing. Objective: Here, we aimed at characterizing lncRNA expression in murine CFs following chronic pressure overload, in order to identify CF-enriched lncRNAs and investigate their function and contribution to cardiac fibrosis and diastolic dysfunction...
June 19, 2017: Circulation Research
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