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Transverse aortic constriction

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https://www.readbyqxmd.com/read/28718833/coconut-oil-aggravates-pressure-overload-induced-cardiomyopathy-without-inducing-obesity-systemic-insulin-resistance-or-cardiac-steatosis
#1
Ilayaraja Muthuramu, Ruhul Amin, Andrey Postnov, Mudit Mishra, Frank Jacobs, Olivier Gheysens, Paul P Van Veldhoven, Bart De Geest
Studies evaluating the effects of high-saturated fat diets on cardiac function are most often confounded by diet-induced obesity and by systemic insulin resistance. We evaluated whether coconut oil, containing C12:0 and C14:0 as main fatty acids, aggravates pressure overload-induced cardiomyopathy induced by transverse aortic constriction (TAC) in C57BL/6 mice. Mortality rate after TAC was higher (p < 0.05) in 0.2% cholesterol 10% coconut oil diet-fed mice than in standard chow-fed mice (hazard ratio 2.32, 95% confidence interval 1...
July 18, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28713936/epigallocatechin-gallate-attenuates-overload%C3%A2-induced-cardiac-ecm-remodeling-via-restoring-t-cell-homeostasis
#2
Yongsheng Han, Qingtong Wang, Xizhen Fan, Jun Chu, Junfu Peng, Yousheng Zhu, Yan Li, Xiaojing Li, Lei Shen, James Asenso, Shanfeng Li
It has previously been demonstrated that Epigallocatechin gallate (EGCG) has regulatory effects on cellular immunity. The present study explored whether EGCG inhibits the overload‑induced cardiac extracellular matrix (ECM) remodeling through targeting the balance of T cell subpopulations. Sprague‑Dawley rats were subjected to either transverse aortic constriction (TAC) or sham operation. TAC rats were treated with EGCG or valsartan (Val) for 6 weeks. The administration of EGCG or Val ameliorated the overproduction of cardiac collagen, inhibited matrix metalloproteinase (MMP) activity, decreased the expression of tissue inhibitor of MMP‑2, atrial natriuretic peptide and brain natriuretic peptide...
September 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28708271/melatonin-protects-against-the-pathological-cardiac-hypertrophy-induced-by-transverse-aortic-constriction-through-activating-pgc-1%C3%AE-in-vivo-and-in-vitro-studies
#3
Mengen Zhai, Zhenhua Liu, Bin Zhang, Lin Jing, Buying Li, Kaifeng Li, Xiuju Chen, Meng Zhang, Bo Yu, Kai Ren, Yang Yang, Wei Yi, Jian Yang, Jincheng Liu, Dinghua Yi, Hongliang Liang, Zhenxiao Jin, Russel J Reiter, Weixun Duan, Shiqiang Yu
Melatonin, a circadian molecule secreted by the pineal gland, confers a protective role against cardiac hypertrophy induced by hyperthyroidism, chronic hypoxia and isoproterenol. However, its role against pressure overload-induced cardiac hypertrophy and the underlying mechanisms remain elusive. In this study, we investigated the pharmacological effects of melatonin on pathological cardiac hypertrophy induced by transverse aortic constriction (TAC). Male C57BL/6 mice underwent TAC or sham surgery at day 0 and were then treated with melatonin (20 mg/kg/day, via drinking water) for 4 or 8 weeks...
July 14, 2017: Journal of Pineal Research
https://www.readbyqxmd.com/read/28667250/heart-failure-and-mef2-transcriptome-dynamics-in-response-to-%C3%AE-blockers
#4
S W Tobin, S Hashemi, K Dadson, S Turdi, K Ebrahimian, J Zhao, G Sweeney, J Grigull, J C McDermott
Myocyte Enhancer Factor 2 (MEF2) mediates cardiac remodelling in heart failure (HF) and is also a target of β-adrenergic signalling, a front-line treatment for HF. We identified global gene transcription networks involved in HF with and without β-blocker treatment. Experimental HF by transverse aortic constriction (TAC) in a MEF2 "sensor" mouse model (6 weeks) was followed by four weeks of β-blockade with Atenolol (AT) or Solvent (Sol) treatment. Transcriptome analysis (RNA-seq) from left ventricular RNA samples and MEF2A depleted cardiomyocytes was performed...
June 30, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28667100/interleukin-10-inhibits-bone-marrow-fibroblast-progenitor-cell-mediated-cardiac-fibrosis-in-pressure-overloaded-myocardium
#5
Suresh K Verma, Venkata N S Garikipati, Prasanna Krishnamurthy, Sarah M Schumacher-Bass, Laurel A Grisanti, Maria Cimini, Zhongjian Cheng, Mohsin Khan, Yujia Yue, Cindy L Benedict, May M Truongcao, Joseph E Rabinowitz, David A Goukassian, Douglas G Tilley, Walter J Koch, Raj Kishore
Background -Activated fibroblasts (myofibroblasts; myoFBs) play critical role in cardiac fibrosis; however, their origin in the diseased heart remains unclear warranting further investigation. Recent studies suggest the contribution of bone marrow fibroblast progenitor cells (BM-FPC) in pressure overload (PO)-induced cardiac fibrosis. We have earlier shown that interleukin-10 (IL10) suppresses PO-induced cardiac fibrosis; however, the role of IL10 in inhibition of BM-FPC-mediated cardiac fibrosis is not known...
June 30, 2017: Circulation
https://www.readbyqxmd.com/read/28659816/cardioprotective-effects-of-sirt6-in-a-mouse-model-of-transverse-aortic-constriction-induced-heart-failure
#6
Yongming Li, Xianda Meng, Wenguang Wang, Fu Liu, Zhiru Hao, Yang Yang, Jinbo Zhao, Wensi Yin, Lijuan Xu, Ruiping Zhao, Jiang Hu
SIRT6, a member of the NAD (+)-dependent class III deacetylase sirtuin family, plays important roles in the maintenance of cardiovascular homeostasis. Telomere shortening is a risk factor for age-associated diseases, including heart disease. In the present study, we investigated the role of SIRT6 and telomerase in a mouse model of transverse aortic constriction (TAC)-induced heart failure. SIRT6, telomerase reverse transcriptase (TERT), and telomere repeat binding factor (TRF)-1 were significantly downregulated in TAC mice compared with their expression in sham-operated mice...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/28659552/differential-effects-of-myocardial-afadin-on-pressure-overload-induced-compensated-cardiac-hypertrophy
#7
Dimitar P Zankov, Akira Sato, Akio Shimizu, Hisakazu Ogita
BACKGROUND: Pressure overload induces cardiac hypertrophy, which often ends in heart failure. Afadin is an adaptor protein that is ubiquitously expressed and, in the heart, it localizes at intercalated disks. The current study aimed to examine the afadin-mediated cardiac phenotype in mice exposed to different types of pressure overload: transverse aortic constriction (TAC) burden and angiotensin II (Ang II) stimulation.Methods and Results:Conditional knockout mice with selective deletion of afadin (afadin cKO) in cardiomyocytes were generated...
June 28, 2017: Circulation Journal: Official Journal of the Japanese Circulation Society
https://www.readbyqxmd.com/read/28641980/cardiomyocyte-specific-overexpression-of-a-37-amino-acid-domain-of-regulator-of-g-protein-signalling-2-inhibits-cardiac-hypertrophy-and-improves-function-in-response-to-pressure-overload-in-mice
#8
Katherine N Lee, Xiangru Lu, Chau Nguyen, Qingping Feng, Peter Chidiac
Regulator of G protein signalling 2 (RGS2) is known to play a protective role in maladaptive cardiac hypertrophy and heart failure via its ability to inhibit Gq- and Gs- mediated GPCR signalling. We previously demonstrated that RGS2 can also inhibit protein translation and can thereby attenuate cell growth. This G protein-independent inhibitory effect has been mapped to a 37 amino acid domain (RGS2(eb)) within RGS2 that binds to eukaryotic initiation factor 2B (eIF2B). When expressed in neonatal rat cardiomyocytes, RGS2(eb) attenuates both protein synthesis and hypertrophy induced by Gq- and Gs- activating agents...
June 19, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28637784/tnfr2-stimulation-promotes-mitochondrial-fusion-via-stat3-and-nf-kb-dependent-activation-of-opa1-expression
#9
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/28637706/endothelial-mineralocorticoid-receptor-contributes-to-systolic-dysfunction-induced-by-pressure-overload-without-modulating-cardiac-hypertrophy-or-inflammation
#10
Ane M Salvador, M Elizabeth Moss, Mark Aronovitz, Kathleen B Mueller, Robert M Blanton, Iris Z Jaffe, Pilar Alcaide
Heart Failure (HF) is associated with increased circulating levels of aldosterone and systemic inflammation. Mineralocorticoid receptor (MR) antagonists block aldosterone action and decrease mortality in patients with congestive HF However, the molecular mechanisms underlying the therapeutic benefits of MR antagonists remain unclear. MR is expressed in all cell types in the heart, including the endothelial cells (EC), in which aldosterone induces the expression of intercellular adhesion molecule 1 (ICAM-1)...
June 2017: Physiological Reports
https://www.readbyqxmd.com/read/28630135/inhibition-of-the-cardiac-fibroblast-enriched-lncrna-meg3-prevents-cardiac-fibrosis-and-diastolic-dysfunction
#11
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
https://www.readbyqxmd.com/read/28622359/aerobic-exercise-protects-against-pressure-overload-induced-cardiac-dysfunction-and-hypertrophy-via-%C3%AE-3-ar-nnos-no-activation
#12
Bin Wang, Ming Xu, Wenju Li, Xiaoli Li, Qiangsun Zheng, Xiaolin Niu
Aerobic exercise confers sustainable protection against cardiac hypertrophy and heart failure (HF). Nitric oxide synthase (NOS) and nitric oxide (NO) are known to play an important role in exercise-mediated cardioprotection, but the mechanism of NOS/NO stimulation during exercise remains unclear. The aim of this study is to determine the role of β3-adrenergic receptors (β3-ARs), NOS activation, and NO metabolites (nitrite and nitrosothiols) in the sustained cardioprotective effects of aerobic exercise. An HF model was constructed by transverse aortic constriction (TAC)...
2017: PloS One
https://www.readbyqxmd.com/read/28611128/decreased-kcne2-expression-participates-in-the-development-of-cardiac-hypertrophy-by-regulation-of-calcineurin-nfat-nuclear-factor-of-activated-t-cells-and-mitogen-activated-protein-kinase-pathways
#13
Wenjuan Liu, Jianxin Deng, Wenwen Ding, Gang Wang, Yuanyuan Shen, Junmeng Zheng, Xiaoming Zhang, Yizhi Luo, Chifei Lv, Yonghui Wang, Liqing Chen, Dewen Yan, Ryan L Boudreau, Long-Sheng Song, Jie Liu
BACKGROUND: KCNE2 is a promiscuous auxiliary subunit of voltage-gated cation channels. A recent work demonstrated that KCNE2 regulates L-type Ca(2+) channels. Given the important roles of altered Ca(2+) signaling in structural and functional remodeling in diseased hearts, this study investigated whether KCNE2 participates in the development of pathological hypertrophy. METHODS AND RESULTS: We found that cardiac KCNE2 expression was significantly decreased in phenylephrine-induced cardiomyocyte hypertrophy in neonatal rat ventricular myocytes and in transverse aortic constriction-induced cardiac hypertrophy in mice, as well as in dilated cardiomyopathy in human...
June 2017: Circulation. Heart Failure
https://www.readbyqxmd.com/read/28611091/inhibition-of-microrna-146a-and-overexpression-of-its-target-dihydrolipoyl-succinyltransferase-protect-against-pressure-overload-induced-cardiac-hypertrophy-and-dysfunction
#14
Ward A Heggermont, Anna-Pia Papageorgiou, Annelies Quaegebeur, Sophie Deckx, Paolo Carai, Wouter Verhesen, Guy Eelen, Sandra Schoors, Rick van Leeuwen, Sergey Alekseev, Ies Elzenaar, Stefan Vinckier, Peter Pokreisz, Ann-Sophie Walravens, Rik Gijsbers, Chris Van Den Haute, Alexander G Nickel, Blanche Schroen, Marc van Bilsen, Stefan Janssens, Christoph Maack, Yigal M Pinto, Peter Carmeliet, Stephane Heymans
Background -Cardiovascular diseases remain the predominant cause of death worldwide, with the prevalence of heart failure continuing to increase. Despite increased knowledge of the metabolic alterations that occur in heart failure, novel therapies to treat the observed metabolic disturbances are still lacking. Methods -Mice were subjected to pressure overload by means of angiotensin-II infusion or transversal aortic constriction (TAC). MicroRNA-146a was either genetically or pharmacologically knocked out, or genetically overexpressed in cardiomyocytes...
June 13, 2017: Circulation
https://www.readbyqxmd.com/read/28593149/effects-of-a-proteasome-inhibitor-on-cardiomyocytes-in-a-pressure-overload-hypertrophy-rat-model-an-animal-study
#15
In-Sub Kim, Won-Min Jo
BACKGROUND: The ubiquitin-proteasome system (UPS) is an important pathway of proteolysis in pathologic hypertrophic cardiomyocytes. We hypothesize that MG132, a proteasome inhibitor, might prevent hypertrophic cardiomyopathy (CMP) by blocking the UPS. Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and androgen receptor (AR) have been reported to be mediators of CMP and heart failure. This study drew upon pathophysiologic studies and the analysis of NF-κB and AR to assess the cardioprotective effects of MG132 in a left ventricular hypertrophy (LVH) rat model...
June 2017: Korean Journal of Thoracic and Cardiovascular Surgery
https://www.readbyqxmd.com/read/28575410/enhanced-endothelin-1-rho-kinase-signaling-and-coronary-microvascular-dysfunction-in-hypertensive-myocardial-hypertrophy
#16
Shu-Huai Tsai, Guangrong Lu, Xin Xu, Yi Ren, Travis W Hein, Lih Kuo
Aims: Hypertensive cardiac hypertrophy is associated with reduced coronary flow reserve, but its impact on coronary flow regulation and vasomotor function remains incompletely understood and requires further investigation. Methods and results: Left ventricular hypertrophy was induced in mice by transverse aortic coarctation (TAC) for 4 weeks. The left coronary artery blood velocity (LCABV) and myocardium lactate level were measured following the metabolic activation by isoproterenol...
May 29, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28573136/effects-of-wenxin-keli-on-cardiac-hypertrophy-and-arrhythmia-via-regulation-of-the-calcium-calmodulin-dependent-kinase-ii-signaling-pathway
#17
Xinyu Yang, Yu Chen, Yanda Li, Xiaomeng Ren, Yanwei Xing, Hongcai Shang
We investigated the effects of Wenxin Keli (WXKL) on the Calcium/Calmodulin dependent kinase II (CaMK II) signal transduction pathway with transverse aortic constriction (TAC) rats. Echocardiographic measurements were obtained 3 and 9 weeks after the surgery. Meanwhile, the action potentials (APDs) were recorded using the whole-cell patch clamp technique, and western blotting was used to assess components of the CaMK II signal transduction pathway. At both 3 and 9 weeks after treatment, the fractional shortening (FS%) increased in the WXKL group compared with the TAC group...
2017: BioMed Research International
https://www.readbyqxmd.com/read/28554563/left-ventricular-fibrosis-and-systolic-hypertension-persist-in-a-repaired-aortic-coarctation-model
#18
Jie Liu, Douglas Drak, Anish Krishnan, Sing-Young Chen, Carla Canniffe, Shisan Bao, Gareth Denyer, David S Celermajer
BACKGROUND: Despite successful repair in early life, patients with coarctation of the aorta (CoA) are predisposed to several cardiovascular complications in later life related to systemic hypertension or left ventricular (LV) dysfunction, or both, the pathogenesis of which is unclear. METHODS: Three-week-old Sprague-Dawley rats underwent transverse aortic constriction (TAC) or a sham operation, with release of the constriction 3 weeks later. Twenty-five weeks after the repair operation, animals underwent hemodynamic assessment, LV gene profiling, and histologic analysis...
May 27, 2017: Annals of Thoracic Surgery
https://www.readbyqxmd.com/read/28549111/diabetic-db-db-mice-do-not-develop-heart-failure-upon-pressure-overload-a-longitudinal-in-vivo-pet-mri-and-mrs-study-on-cardiac-metabolic-structural-and-functional-adaptations
#19
Desiree Abdurrachim, Miranda Nabben, Verena Hoerr, Michael T Kuhlmann, Philipp Bovenkamp, Jolita Ciapaite, Ilvy M E Geraets, Will Coumans, Joost J F P Luiken, Jan F C Glatz, Michael Schäfers, Klaas Nicolay, Cornelius Faber, Sven Hermann, Jeanine J Prompers
Aim: Heart failure is associated with altered myocardial substrate metabolism and impaired cardiac energetics. Comorbidities like diabetes may influence the metabolic adaptations during heart failure development. We quantified to what extent changes in substrate preference, lipid accumulation, and energy status predict the longitudinal development of hypertrophy and failure in the non-diabetic and the diabetic heart. Methods and results: Transverse aortic constriction (TAC) was performed in non-diabetic ( db /+) and diabetic ( db/db ) mice to induce pressure overload...
May 26, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28548932/lncrna-tincr-attenuates-cardiac-hypertrophy-by-epigenetic-silencing-of-camkii
#20
Mingjing Shao, Guangdong Chen, Fengli Lv, Yanyan Liu, Hongjun Tian, Ran Tao, Ronghuan Jiang, Wei Zhang, Chuanjun Zhuo
In the previous study, we established a mouse model of cardiac hypertrophy using transverse aortic constriction (TAC) and found that the expression of long non-coding RNAs TINCR was downregulated in myocardial tissue. The present study was designed to determine the potential role of TINCR in the pathogenesis of cardiac hypertrophy. Our results showed that enforced expression of TINCR could attenuate cardiac hypertrophy in TAC mice. Angiotensin II (Ang-II) was found to be associated with reduced TINCR expression and increased hypertrophy in cultured neonatal cardiomyocytes...
May 10, 2017: Oncotarget
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