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Cardiac development, cardiac remodelling, cardiac function

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https://www.readbyqxmd.com/read/28329100/long-term-cardiovascular-changes-following-creation-of-arteriovenous-fistula-in-patients-with-end-stage-renal-disease
#1
Yogesh N V Reddy, Masaru Obokata, Patrick G Dean, Vojtech Melenovsky, Karl A Nath, Barry A Borlaug
Aims: Short-term studies have reported left ventricular (LV) dilatation following surgical creation of arteriovenous fistulas (AVF) or arteriovenous grafts (AVGs), but chronic cardiac structural and functional changes have not been examined or related to clinical outcomes following AVF/AVG. We sought to characterize the long-term changes in cardiac structure and function in patients undergoing shunt creation for haemodialysis. Methods and results: A retrospective analysis was performed of patients undergoing echocardiography before and after surgical AVF/AVG creation for the initiation of haemodialysis...
March 6, 2017: European Heart Journal
https://www.readbyqxmd.com/read/28329054/whole-heart-detailed-and-quantitative-anatomy-myofibre-structure-and-vasculature-from-x-ray-phase-contrast-synchrotron-radiation-based-micro-computed-tomography
#2
Anna Gonzalez-Tendero, Chong Zhang, Vedrana Balicevic, Rubén Cárdenes, Sven Loncaric, Constantine Butakoff, Bruno Paun, Anne Bonnin, Patricia Garcia-Cañadilla, Emma Muñoz-Moreno, Eduard Gratacós, Fatima Crispi, Bart Bijnens
Background: While individual cardiac myocytes only have a limited ability to shorten, the heart efficiently pumps a large volume-fraction thanks to a cell organization in a complex 3D fibre structure. Subclinical subtle cardiac structural remodelling is often present before symptoms arise. Understanding and early detection of these subtle changes is crucial for diagnosis and prevention. Additionally, personalized computational modelling requires knowledge on the multi-scale structure of the whole heart and vessels...
March 15, 2017: European Heart Journal Cardiovascular Imaging
https://www.readbyqxmd.com/read/28325835/picomolar-selective-and-subtype-specific-small-molecule-inhibition-of-trpc1-4-5-channels
#3
Hussein N Rubaiy, Melanie J Ludlow, Matthias Henrot, Hannah J Gaunt, Katarina Miteva, Sin Yin Cheung, Yasuyuki Tanahashi, Nurasyikin Hamzah, Katie E Musialowski, Nicola M Blythe, Hollie L Appleby, Marc A Bailey, Lynn McKeown, Roger Taylor, Richard Foster, Herbert Waldmann, Peter Nussbaumer, Mathias Christmann, Robin S Bon, Katsuhiko Muraki, David J Beech
The concentration of free cytosolic Ca(2+) and the voltage across the plasma membrane are major determinants of cell function. Ca(2+)-permeable non-selective cationic channels are known to regulate these parameters but understanding of these channels remains inadequate. Here we focus on Transient Receptor Potential Canonical 4 and 5 proteins (TRPC4 and TRPC5) which assemble as homomers or heteromerize with TRPC1 to form Ca(2+)-permeable non-selective cationic channels in many mammalian cell types. Multiple roles have been suggested including in epilepsy, innate fear, pain and cardiac remodeling but limitations in tools to probe these channels have restricted progress...
March 21, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28315072/direct-myosin-activation-by-omecamtiv-mecarbil-for-heart-failure-with-reduced-ejection-fraction
#4
Mitchell A Psotka, John R Teerlink
Myosin is the indispensable molecular motor that utilizes chemical energy to produce force for contraction within the cardiac myocyte. Myosin activity is gated by intracellular calcium levels which are regulated by multiple upstream signaling cascades that can be altered for clinical utility using inotropic medications. In contrast to clinically available cardiac inotropes, omecamtiv mecarbil is a novel direct myosin activator developed to augment left ventricular systolic function without the undesirable secondary effects of altered calcium homeostasis...
March 18, 2017: Handbook of Experimental Pharmacology
https://www.readbyqxmd.com/read/28303103/multipronged-therapeutic-effects-of-chinese-herbal-medicine-qishenyiqi-in-the-treatment-of-acute-myocardial-infarction
#5
Yong Wang, Weili Lin, Chun Li, Sarita Singhal, Gaurav Jain, Lixin Zhu, Linghui Lu, Ruixin Zhu, Wei Wang
Background: Based on global gene expression profile, therapeutic effects of Qishenyiqi (QSYQ) on acute myocardial infarction (AMI) were investigated by integrated analysis at multiple levels including gene expression, pathways involved and functional group. Methods: Sprague-Dawley (SD) rats were randomly divided into 3 groups: Sham-operated, AMI model (left anterior descending coronary artery ligation) and QSYQ-treated group. Cardiac tissues were obtained for analysing digital gene expression. Sequencing and transcriptome analyses were performed collaboratively, including analyses of differential gene expression, gene co-expression network, targeted attack on network and functional grouping...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28293100/adenosine-a2a-receptor-agonist-prevents-cardiac-remodeling-and-dysfunction-in-spontaneously-hypertensive-male-rats-after-myocardial-infarction
#6
Jaqueline S da Silva, Daniele Gabriel-Costa, Roberto T Sudo, Hao Wang, Leanne Groban, Emanuele B Ferraz, José Hamilton M Nascimento, Carlos Alberto M Fraga, Eliezer J Barreiro, Gisele Zapata-Sudo
BACKGROUND: This work evaluated the hypothesis that 3,4-methylenedioxybenzoyl-2-thienylhydrazone (LASSBio-294), an agonist of adenosine A2A receptor, could be beneficial for preventing cardiac dysfunction due to hypertension associated with myocardial infarction (MI). METHODS: Male spontaneously hypertensive rats (SHR) were randomly divided into four groups (six animals per group): sham-operation (SHR-Sham), and myocardial infarction rats (SHR-MI) were treated orally either with vehicle or LASSBio-294 (10 and 20 mg...
2017: Drug Design, Development and Therapy
https://www.readbyqxmd.com/read/28275592/model-of-human-fetal-growth-in-hypoplastic-left-heart-syndrome-reduced-ventricular-growth-due-to-decreased-ventricular-filling-and-altered-shape
#7
Sukriti Dewan, Adarsh Krishnamurthy, Devleena Kole, Giulia Conca, Roy Kerckhoffs, Michael D Puchalski, Jeffrey H Omens, Heather Sun, Vishal Nigam, Andrew D McCulloch
INTRODUCTION: Hypoplastic left heart syndrome (HLHS) is a congenital condition with an underdeveloped left ventricle (LV) that provides inadequate systemic blood flow postnatally. The development of HLHS is postulated to be due to altered biomechanical stimuli during gestation. Predicting LV size at birth using mid-gestation fetal echocardiography is a clinical challenge critical to prognostic counseling. HYPOTHESIS: We hypothesized that decreased ventricular filling in utero due to mitral stenosis may reduce LV growth in the fetal heart via mechanical growth signaling...
2017: Frontiers in Pediatrics
https://www.readbyqxmd.com/read/28271186/suv39h1-mediated-sirt1-trans-repression-contributes-to-cardiac-ischemia-reperfusion-injury
#8
Guang Yang, Xinjian Zhang, Xinyu Weng, Peng Liang, Xin Dai, Sheng Zeng, Huihui Xu, Hailin Huan, Mingming Fang, Yuehua Li, Dachun Xu, Yong Xu
Ischemic reperfusion (I/R) contributes to deleterious cardiac remodeling and heart failure. The deacetylase SIRT1 has been shown to protect the heart from I/R injury. We examined the mechanism whereby I/R injury represses SIRT1 transcription in the myocardium. There was accumulation of trimethylated histone H3K9 on the proximal SIRT1 promoter in the myocardium in mice following I/R injury and in cultured cardiomyocytes exposed to hypoxia-reoxygenation (H/R). In accordance, the H3K9 trimethyltransferase SUV39H1 bound to the SIRT1 promoter and repressed SIRT1 transcription...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28263709/kchip2-is-a-core-transcriptional-regulator-of-cardiac-excitability
#9
Drew M Nassal, Xiaoping Wan, Haiyan Liu, Danielle Maleski, Angelina Ramirez-Navarro, Christine S Moravec, Eckhard Ficker, Kenneth R Laurita, Isabelle Deschênes
Arrhythmogenesis from aberrant electrical remodeling is a primary cause of death among patients with heart disease. Amongst a multitude of remodeling events, reduced expression of the ion channel subunit KChIP2 is consistently observed in numerous cardiac pathologies. However, it remains unknown if KChIP2 loss is merely a symptom or involved in disease development. Using rat and human derived cardiomyocytes, we identify a previously unobserved transcriptional capacity for cardiac KChIP2 critical in maintaining electrical stability...
March 6, 2017: ELife
https://www.readbyqxmd.com/read/28261787/signalling-mechanisms-underlying-doxorubicin-and-nox2-nadph-oxidase-induced-cardiomyopathy-involvement-of-mitofusin-2
#10
Declan McLaughlin, Youyou Zhao, Karla M O'Neill, Kevin S Edgar, Philip D Dunne, Anna M Kearney, David J Grieve, Barbara J McDermott
BACKGROUND AND PURPOSE: The anthracycline doxorubicin (DOX), although successful as a first-line cancer treatment, induces cardiotoxicity linked with increased production of myocardial reactive oxygen species (ROS), with Nox2 NADPH oxidase-derived superoxide reported to play a key role. The aim of this study was to identify novel mechanisms underlying development of cardiac remodelling/dysfunction further to DOX-stimulated Nox2 activation. EXPERIMENTAL APPROACH: Nox2(-/-) and wild-type (WT) littermate mice were administered DOX (12mg/kg over 3 weeks) prior to study at 4 weeks...
March 6, 2017: British Journal of Pharmacology
https://www.readbyqxmd.com/read/28256242/a-functionally-graded-material-model-for-the-transmural-stress-distribution-of-the-aortic-valve-leaflet
#11
Bruno V Rego, Michael S Sacks
Heterogeneities in structure and stress within heart valve leaflets are of significant concern to their functional physiology, as they affect how the tissue constituents remodel in response to pathological and non-pathological (e.g. exercise, pregnancy) alterations in cardiac function. Indeed, valve interstitial cells (VICs) are known to synthesize and degrade leaflet extracellular matrix (ECM) components in a manner specific to their local micromechanical environment. Quantifying local variations in ECM structure and stress is thus necessary to understand homeostatic valve maintenance as well as to develop predictive models of disease progression and post-surgical outcomes...
February 8, 2017: Journal of Biomechanics
https://www.readbyqxmd.com/read/28242607/invasive-assessment-of-the-coronary-microcirculation-in-reperfused-st-segment-elevation-myocardial-infarction-patients-where-do-we-stand
#12
Heerajnarain Bulluck, Nicolas Foin, Jack W Tan, Adrian F Low, Murat Sezer, Derek J Hausenloy
For patients presenting with an acute ST-segment-elevation myocardial infarction, the most effective therapy for reducing myocardial infarct size and preserving left ventricular systolic function is primary percutaneous coronary intervention (PPCI). However, mortality and morbidity remain significant. This is partly attributed to the development of microvascular obstruction, which occurs in around 50% of ST-segment-elevation myocardial infarction patients post-PPCI, and it is associated with adverse left ventricular remodeling and worse clinical outcomes...
March 2017: Circulation. Cardiovascular Interventions
https://www.readbyqxmd.com/read/28237302/yiqifumai-powder-injection-attenuates-coronary-artery-ligation-induced-myocardial-remodeling-and-heart-failure-through-modulating-mapks-signaling-pathway
#13
Li-Zhi Pang, Ai-Chun Ju, Xian-Jie Zheng, Fang Li, Yun-Fei Song, Yan Zhao, Yuan-Feng Gu, Fei-Leng Chen, Chun-Hua Liu, Jin Qi, Zhen Gao, Jun-Ping Kou, Bo-Yang Yu
ETHNOPHARMACOLOGICAL RELEVANCE: YiQiFuMai Powder Injection (YQFM), a traditional Chinese medicine prescription re-developed based on Sheng-Mai-San, is a classical and traditional therapeutic for clinical heart failure (HF) and angina. However, its potential mechanism against HF remains unclear. AIM OF THE STUDY: The present study observes the therapeutic role of YQFM and mechanisms underlying its effects on coronary artery ligation (CAL)-induced myocardial remodeling (MR) and HF...
February 22, 2017: Journal of Ethnopharmacology
https://www.readbyqxmd.com/read/28231509/a-single-injection-of-protein-loaded-coacervate-gel-significantly-improves-cardiac-function-post-infarction
#14
H K Awada, D W Long, Z Wang, M P Hwang, K Kim, Y Wang
After myocardial infarction (MI), the heart undergoes fibrotic pathological remodeling instead of repair and regeneration. With multiple pathologies developing after MI, treatment using several proteins is expected to address this range of pathologies more effectively than a single-agent therapy. A factorial design of experiments study guided us to combine three complementary factors in one injection: tissue inhibitor of metalloproteinases-3 (TIMP-3) was embedded in a fibrin gel for signaling in the initial phase of the treatment, while basic fibroblast growth factor (FGF-2) and stromal cell-derived factor 1-alpha (SDF-1α) were embedded in heparin-based coacervates for sustained release and distributed within the same fibrin gel to exert their effects over a longer period...
February 17, 2017: Biomaterials
https://www.readbyqxmd.com/read/28225063/targeted-inhibition-of-focal-adhesion-kinase-attenuates-cardiac-fibrosis-and-preserves-heart-function-in-adverse-cardiac-remodeling
#15
Jie Zhang, Guangpu Fan, Hui Zhao, Zhiwei Wang, Fei Li, Peide Zhang, Jing Zhang, Xu Wang, Wei Wang
Cardiac fibrosis in post-myocardial infarction (MI), seen in both infarcted and non-infarcted myocardium, is beneficial to the recovery of heart function. But progressively pathological fibrosis impairs ventricular function and leads to poor prognosis. FAK has recently received attention as a potential mediator of fibrosis, our previous study reported that pharmacological inhibition of FAK can attenuate cardiac fibrosis in post MI models. However, the long-term effects on cardiac function and adverse cardiac remodelling were not clearly investigated...
February 22, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28224334/the-trpm4-channel-is-functionally-important-for-the-beneficial-cardiac-remodeling-induced-by-endurance-training
#16
Mélanie Gueffier, Justin Zintz, Karen Lambert, Amanda Finan, Franck Aimond, Nourdine Chakouri, Christophe Hédon, Mathieu Granier, Pierre Launay, Jérôme Thireau, Sylvain Richard, Marie Demion
Cardiac hypertrophy (CH) is an adaptive process that exists in two distinct forms and allows the heart to adequately respond to an organism's needs. The first form of CH is physiological, adaptive and reversible. The second is pathological, irreversible and associated with fibrosis and cardiomyocyte death. CH involves multiple molecular mechanisms that are still not completely defined but it is now accepted that physiological CH is associated more with the PI3-K/Akt pathway while the main signaling cascade activated in pathological CH involves the Calcineurin-NFAT pathway...
February 21, 2017: Journal of Muscle Research and Cell Motility
https://www.readbyqxmd.com/read/28216385/the-role-of-mitochondria-in-cardiac-development-and-protection
#17
REVIEW
Jaakko L Pohjoismäki, Steffi Goffart
Mitochondria are essential for the development as well as maintenance of the myocardium, the most energy consuming tissue in the human body. Mitochondria are not only a source of ATP energy but also generators of reactive oxygen species (ROS), that cause oxidative damage, but also regulate physiological processes such as the switch from hyperplastic to hypertrophic growth after birth. As excess ROS production and oxidative damage are associated with cardiac pathology, it is not surprising that much of the research focused on the deleterious aspects of free radicals...
February 17, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28213819/conditional-knockout-of-activin-like-kinase-1-alk-1-leads-to-heart-failure-without-maladaptive-remodeling
#18
Kevin J Morine, Xiaoying Qiao, Vikram Paruchuri, Mark J Aronovitz, Emily E Mackey, Lyanne Buiten, Jonathan Levine, Keshan Ughreja, Prerna Nepali, Robert M Blanton, Richard H Karas, S Paul Oh, Navin K Kapur
Activin like kinase-1 (AlK-1) mediates signaling via the transforming growth factor beta (TGFβ) family of ligands. AlK-1 activity promotes endothelial proliferation and migration. Reduced AlK-1 activity is associated with arteriovenous malformations. No studies have examined the effect of global AlK-1 deletion on indices of cardiac remodeling. We hypothesized that reduced levels of AlK-1 promote maladaptive cardiac remodeling. To test this hypothesis, we employed AlK-1 conditional knockout mice (cKO) harboring the ROSA26-CreER knock-in allele, whereby a single dose of intraperitoneal tamoxifen triggered ubiquitous Cre recombinase-mediated excision of floxed AlK-1 alleles...
February 17, 2017: Heart and Vessels
https://www.readbyqxmd.com/read/28192468/matrix-metalloproteinases-are-required-for-membrane-motility-and-lumenogenesis-during-drosophila-heart-development
#19
Qanber S Raza, Jessica L Vanderploeg, J Roger Jacobs
Matrix Metalloproteinases (Mmps) degrade glycoproteins and proteoglycans of the extracellular matrix (ECM) or cell surface and are crucial for morphogenesis. Mmps and their inhibitors are expressed during early stages of cardiac development in vertebrates and expression is altered in multiple congenital cardiomyopathies such as cardia bifida. Drosophila genome encodes two copies of Mmps, Mmp1 and Mmp2 whereas in humans up to 25 Mmps have been identified with overlapping functions. We investigated the role of Mmps during embryonic heart development in Drosophila, a process which is morphogenetically similar to early heart tube formation in vertebrates...
2017: PloS One
https://www.readbyqxmd.com/read/28178567/defective-branched-chain-amino-acid-catabolism-disrupts-glucose-metabolism-and-sensitizes-the-heart-to-ischemia-reperfusion-injury
#20
Tao Li, Zhen Zhang, Stephen C Kolwicz, Lauren Abell, Nathan D Roe, Maengjo Kim, Bo Zhou, Yang Cao, Julia Ritterhoff, Haiwei Gu, Daniel Raftery, Haipeng Sun, Rong Tian
Elevated levels of branched-chain amino acids (BCAAs) have recently been implicated in the development of cardiovascular and metabolic diseases, but the molecular mechanisms are unknown. In a mouse model of impaired BCAA catabolism (knockout [KO]), we found that chronic accumulation of BCAAs suppressed glucose metabolism and sensitized the heart to ischemic injury. High levels of BCAAs selectively disrupted mitochondrial pyruvate utilization through inhibition of pyruvate dehydrogenase complex (PDH) activity...
February 7, 2017: Cell Metabolism
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