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https://www.readbyqxmd.com/read/28925362/generation-of-a-klf15-homozygous-knockout-human-embryonic-stem-cell-line-using-paired-crispr-cas9n-and-human-cardiomyocytes-derivation
#1
Claudia Noack, Luis Peter Haupt, Wolfram-Hubertus Zimmermann, Katrin Streckfuss-Bömeke, Laura Cecilia Zelarayán
Krueppel-like factor 15 (KLF15) is abundantly expressed in liver, kidney, and muscle, including myocardium. In the adult heart KLF15 is important to maintain homeostasis and to repress hypertrophic remodeling. We generated a homozygous hESC KLF15 knockout (KO) line using paired CRISPR/Cas9n. KLF15-KO cells maintained full pluripotency and differentiation potential as well as genomic integrity. We demonstrated that KLF15-KO cells can be differentiated into morphologically normal cardiomyocytes turning them into a valuable tool for studying human KLF15-mediated mechanisms resulting in human cardiac dysfunction...
August 2017: Stem Cell Research
https://www.readbyqxmd.com/read/28924076/third-and-fourth-heart-sounds-and-myocardial-fibrosis-in-hypertrophic-cardiomyopathy
#2
Yoshimi Sato, Tatsuya Kawasaki, Sakiko Honda, Kuniyasu Harimoto, Shigeyuki Miki, Tadaaki Kamitani, Hirokazu Shiraishi, Satoaki Matoba
BACKGROUND: The 4th heart sound (S4) is commonly heard in patients with hypertrophic cardiomyopathy (HCM). The 3rd heart sound (S3) is also audible in HCM patients regardless of the presence or absence of heart failure. These extra heart sounds may be associated with myocardial fibrosis because myocardial fibrosis has been suggested to affect left ventricular compliance.Methods and Results:The present retrospective study evaluated 53 consecutive HCM patients with sinus rhythm who had no symptoms of heart failure and underwent an initial assessment including phonocardiography, echocardiography, and late gadolinium enhancement (LGE) magnetic resonance imaging (MRI)...
September 16, 2017: Circulation Journal: Official Journal of the Japanese Circulation Society
https://www.readbyqxmd.com/read/28923351/functionally-redundant-control-of-cardiac-hypertrophic-signaling-by-inositol-1-4-5-trisphosphate-receptors
#3
M Iveth Garcia, Anja Karlstaedt, Jessica J Chen, Javier Amione-Guerra, Keith A Youker, Heinrich Taegtmeyer, Darren Boehning
Calcium plays an integral role to many cellular processes including contraction, energy metabolism, gene expression, and cell death. The inositol 1, 4, 5-trisphosphate receptor (IP3R) is a calcium channel expressed in cardiac tissue. There are three IP3R isoforms encoded by separate genes. In the heart, the IP3R-2 isoform is reported to being most predominant with regards to expression levels and functional significance. The functional roles of IP3R-1 and IP3R-3 in the heart are essentially unexplored despite measureable expression levels...
September 15, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28921420/causes-of-an-increased-pressure-gradient-through-the-left-ventricular-outflow-tract-a-west-coast-experience
#4
Sayuki Kobayashi, Yoshihiko Sakai, Isao Taguchi, Hiroto Utsunomiya, Takahiro Shiota
BACKGROUND: Left ventricular outflow tract obstruction (LVOTO) occurs from not only obstructive hypertrophic cardiomyopathy but also other conditions such as sigmoid septum or post mitral valve repair. However, the changes of the LVOT pressure gradient (LVOT PG) in LVOTO with various conditions remain unclear. METHODS: The clinical characteristics and echocardiographic parameters of 73 patients with LVOT PG ≥50 mmHg at rest on Doppler ultrasound were retrospectively investigated...
September 18, 2017: Journal of Echocardiography
https://www.readbyqxmd.com/read/28919046/fgf23-activates-injury-primed-renal-fibroblasts-via-fgfr4-dependent-signalling-and-enhancement-of-tgf-%C3%AE-autoinduction
#5
Edward R Smith, Stephen G Holt, Tim D Hewitson
Bone-derived fibroblast growth factor 23 (FGF23) is an important endocrine regulator of mineral homeostasis with effects transduced by cognate FGF receptor (FGFR)1-α-Klotho complexes. Circulating FGF23 levels rise precipitously in patients with kidney disease and portend to worse renal and cardiovascular outcomes. De novo expression of FGF23 has been found in the heart and kidney following injury but its significance remains unclear. Studies showing that exposure to chronically high FGF23 concentrations activates hypertrophic gene programmes in the cardiomyocyte, has spawned intense interest in other pathological off-target effects of FGF23 excess...
September 14, 2017: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/28916721/loss-of-cardiac-carnitine-palmitoyltransferase-2-results-in-rapamycin-resistant-acetylation-independent-hypertrophy
#6
Andrea S Pereyra, Like Y Hasek, Kate L Harris, Alycia G Berman, Frederick W Damen, Craig J Goergen, Jessica M Ellis
Cardiac hypertrophy is closely linked to impaired fatty acid oxidation, but the molecular basis of this link is unclear. Here, we investigated the loss of an obligate enzyme in mitochondrial long-chain fatty acid oxidation, carnitine palmitoyltransferase 2 (CPT2), on muscle and heart structure, function, and molecular signatures in a muscle- and heart-specific CPT2-deficient mouse (Cpt2M-/-) model. CPT2 loss in heart and muscle reduced complete oxidation of long-chain fatty acids by 87% and 69%, respectively, without altering body weight, energy expenditure, respiratory quotient, or adiposity...
September 15, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28916640/clinical-profile-and-consequences-of-atrial-fibrillation-in-hypertrophic-cardiomyopathy
#7
Ethan J Rowin, Anais Hausvater, Mark S Link, Patrick Abt, William Gionfriddo, Wendy Wang, Hassan Rastegar, N A Mark Estes, Martin S Maron, Barry J Maron
Background -Atrial fibrillation (AF), the most common sustained arrhythmia in hypertrophic cardiomyopathy (HCM), is capable of producing symptoms that impact quality of life and is associated with risk for embolic stroke. However, the influence of AF on clinical course and outcome in HCM remains incompletely resolved. Methods -Records were accessed of 1558 consecutive patients followed at the Tufts Medical Center Hypertrophic Cardiomyopathy Institute for 4.8 ± 3.4 years, from 2004 to 2014. Results -Of the 1558 HCM patients, 304 (20%) had episodes of AF, of which 226 (74%) were confined to symptomatic paroxysmal AF (PAF; average 5 ± 5; range 1 to > 20), while 78 (26%) developed permanent AF, preceded by 7 ± 6 PAF episodes...
September 15, 2017: Circulation
https://www.readbyqxmd.com/read/28916354/abnormal-sodium-channel-mrna-splicing-in-hypertrophic-cardiomyopathy
#8
Adam M Noyes, Anyu Zhou, Ge Gao, Lianzhi Gu, Sharlene Day, J Andrew Wasserstrom, Samuel C Dudley
BACKGROUND: Our previous studies showed that in ischemic and nonischemic heart failure (HF), the voltage-gated cardiac Na(+) channel α subunit (SCN5A) mRNA is abnormally spliced to produce two truncated transcript variants (E28C and D) that activate the unfolded protein response (UPR). We tested whether SCN5A post-transcriptional regulation was abnormal in hypertrophic cardiomyopathy (HCM). MATERIAL AND METHODS: Human heart tissue was obtained from HCM patients...
September 7, 2017: International Journal of Cardiology
https://www.readbyqxmd.com/read/28911943/heterozygous-deletion-of-akt1-rescues-cardiac-contractility-but-not-hypertrophy-in-a-mouse-model-of-noonan-syndrome-with-multiple-lentigines
#9
Rajika Roy, Maike Krenz
Noonan Syndrome with Multiple Lentigines (NSML) is associated with congenital heart disease in form of pulmonary valve stenosis and hypertrophic cardiomyopathy (HCM). Genetically, NSML is primarily caused by mutations in the non-receptor protein tyrosine phosphatase SHP2. Importantly, certain SHP2 mutations such as Q510E can cause a particularly severe form of HCM with heart failure in infancy. Due to lack of insight into the underlying pathomechanisms, an effective custom-tailored therapy to prevent heart failure in these patients has not yet been found...
September 11, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28911804/case-report-left-ventricular-noncompaction-cardiomyopathy-and-rasopathies
#10
John Lynn Jefferies, Carlos Enrique Prada, Juli Ann Sublett
The following is a case report of 6 patients with Noonan syndrome (NS) and/or a related RASsopathy that also have evidence of left ventricular noncompaction cardiomyopathy (LVNC). Noonan syndrome,a type of RASopathy, is an autosomal dominant disorder that is typically associated with congenital heart defects and hypertrophic cardiomyopathy. There have been minimal reports of Noonan syndrome or other RASopathy and the association of LVNC. This report promulgates 6 nonrelated cases of Noonan syndrome or unspecified RASopathy and LVNC...
September 11, 2017: European Journal of Medical Genetics
https://www.readbyqxmd.com/read/28910549/upregulation-of-%C3%AE-enolase-protects-cardiomyocytes-from-phenylephrine-induced-hypertrophy
#11
Si Gao, Xueping Liu, Lihua Wei, Jing Lu, Peiqing Liu
Cardiac hypertrophy often refers to the abnormal growth of heart muscle through a variety of factors. The mechanisms of cardiomyocyte hypertrophy have been extensively investigated using neonatal rat cardiomyocytes treated with phenylephrine. α-Enolase is a glycolytic enzyme with "multifunctional jobs" beyond its catalytic activity. Its possible contribution to cardiac dysfunction remains to be determined. The present study aimed to investigate the change of α-enolase during cardiac hypertrophy and explore its role in this pathological process...
September 14, 2017: Canadian Journal of Physiology and Pharmacology
https://www.readbyqxmd.com/read/28905470/outcomes-of-berlin-heart-excor-%C3%A2-pediatric-ventricular-assist-device-support-in-patients-with-restrictive-and-hypertrophic-cardiomyopathy
#12
Jennifer A Su, Jondavid Menteer
The outcomes of pediatric ventricular assist device support in patients with diastolic heart failure have not been well described. This study reviews the North American experience with Berlin Heart EXCOR(®) ventricular assist device implants in children with such physiology. The Berlin Heart clinical database was reviewed. Patients with primary diastolic dysfunction are included in this study. Twenty pediatric patients with restrictive cardiomyopathy (n = 13), hypertrophic cardiomyopathy (n = 3), or congenital heart disease with restrictive physiology (n = 4) who were supported with EXCOR(®) were identified...
September 14, 2017: Pediatric Transplantation
https://www.readbyqxmd.com/read/28901173/cyclin-d2-is-a-critical-mediator-of-exercise-induced-cardiac-hypertrophy
#13
Stephen W Luckey, Chris D Haines, John P Konhilas, Elizabeth D Luczak, Antke Messmer-Kratzsch, Leslie A Leinwand
A number of signaling pathways underlying pathological cardiac hypertrophy have been identified. However, few studies have probed the functional significance of these signaling pathways in the context of exercise or physiological pathways. Exercise studies were performed on females from six different genetic mouse models that have been shown to exhibit alterations in pathological cardiac adaptation and hypertrophy. These include mice expressing constitutively active glycogen synthase kinase-3β (GSK-3βS9A), an inhibitor of CaMK II (AC3-I), both GSK-3βS9A and AC3-I (GSK-3βS9A/AC3-I), constitutively active Akt (myrAkt), mice deficient in MAPK/ERK kinase kinase-1 (MEKK1(-/-)), and mice deficient in cyclin D2 (cyclin D2(-/-))...
January 1, 2017: Experimental Biology and Medicine
https://www.readbyqxmd.com/read/28900930/cardiac-remodeling-and-disease-soce-and-trpc-signaling-in-cardiac-pathology
#14
Petra Eder
TRPC channels have been suggested as potential candidates mediating store-operated Ca(2+) entry (SOCE) in cardiomyocytes. There is increasing evidence that the TRPC isoforms TRPC1 and TRPC4 might fulfill the function as SOCs, in concert with or in parallel to the key players of SOCE, Orai1, and STIM1. Several other isoforms, e.g., TRPC3, TRPC6, and TRPC7, might rather associate to receptor-activated diacylglycerol (DAG)-sensitive ion channels. However, the exact activation mode has not been elucidated yet, given the characteristic of TRPC channels to heteromerize to unpredictable ion channel assemblies...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28900153/genetic-ablation-of-fgf23-or-klotho-does-not-modulate-experimental-heart-hypertrophy-induced-by-pressure-overload
#15
Svetlana Slavic, Kristopher Ford, Magalie Modert, Amarela Becirovic, Stephan Handschuh, Andreas Baierl, Nejla Katica, Ute Zeitz, Reinhold G Erben, Olena Andrukhova
Left ventricular hypertrophy (LVH) ultimately leads to heart failure in conditions of increased cardiac pre- or afterload. The bone-derived phosphaturic and sodium-conserving hormone fibroblast growth factor-23 (FGF23) and its co-receptor Klotho have been implicated in the development of uremic LVH. Using transverse aortic constriction (TAC) in gene-targeted mouse models, we examine the role of Fgf23 and Klotho in cardiac hypertrophy and dysfunction induced by pressure overload. TAC profoundly increases serum intact Fgf23 due to increased cardiac and bony Fgf23 transcription and downregulation of Fgf23 cleavage...
September 12, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28899782/the-lncrna-gas5-mir-23a-foxo3a-axis-regulates-cardiac-hypertrophy-by-wnt-%C3%AE-catenin-signal-pathway
#16
Wei Wei, Yan Chen, Jing Gao, Chenyi Li
Cardiac hypertrophy (CH) is related to a variety of physiological as well as pathological stimuli and eventually increases the risk of heart failure. lncRNA GAS5 has been identified as a competing endogenous RNA in multiple human biological processes. Whether lncRNA GAS5 is involved in the progress of CH and how it works still remain unknown. Here, we found that the expression of lncRNA-GAS5 was increased in the AngII-induced Cardiac hypertrophy model. lncRNA-GAS5 inhibited the total protein per well, as well as the expression of hypertrophic markers, ANF and β-MHC...
September 9, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28891814/fibroblast-specific-tgf-%C3%AE-smad2-3-signaling-underlies-cardiac-fibrosis
#17
Hadi Khalil, Onur Kanisicak, Vikram Prasad, Robert N Correll, Xing Fu, Tobias Schips, Ronald J Vagnozzi, Ruijie Liu, Thanh Huynh, Se-Jin Lee, Jason Karch, Jeffery D Molkentin
The master cytokine TGF-β mediates tissue fibrosis associated with inflammation and tissue injury. TGF-β induces fibroblast activation and differentiation into myofibroblasts that secrete extracellular matrix proteins. Canonical TGF-β signaling mobilizes Smad2 and Smad3 transcription factors that control fibrosis by promoting gene expression. However, the importance of TGF-β-Smad2/3 signaling in fibroblast-mediated cardiac fibrosis has not been directly evaluated in vivo. Here, we examined pressure overload-induced cardiac fibrosis in fibroblast- and myofibroblast-specific inducible Cre-expressing mouse lines with selective deletion of the TGF-β receptors Tgfbr1/2, Smad2, or Smad3...
September 11, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28888840/teneligliptin-prevents-cardiomyocyte-hypertrophy-fibrosis-and-development-of-hypertensive-heart-failure-in-dahl-salt-sensitive-rats
#18
Masayoshi Yamamoto, Tomoko Ishizu, Yoshihiro Seo, Yoshimi Suto, Seika Sai, Dongzhu Xu, Nobuyuki Murakoshi, Taizo Kimura, Yasushi Kawakami, Kazutaka Aonuma
BACKGROUND: We investigated the effects of the DPP4 inhibitor, teneligliptin, on cardiac function and hemodynamics during heart failure in hypertensive model rats. METHODS AND RESULTS: Fifty-five male Dahl salt-sensitive rats were divided into four groups: control group (0.3% NaCl chow, n=13), hypertension (HT) group (8% NaCl chow, n=20), HT-early TNL group (8% NaCl chow and teneligliptin from 6 weeks, n=10), and HT-late TNL group (8% NaCl chow and teneligliptin from 10 weeks, n=12)...
September 6, 2017: Journal of Cardiac Failure
https://www.readbyqxmd.com/read/28888352/high-fat-diet-aggravates-atrial-and-ventricular-remodeling-of-hypertensive-heart-disease-in-aging-rats
#19
Yi-Lin Shiou, I-Chieh Huang, Hsin-Ting Lin, Hsiang-Chun Lee
BACKGROUND/PURPOSE: Left ventricular hypertrophy is a major cause of heart failure in aging population. This study is to determine whether an excess dietary fat is lipotoxic or lipoprotein to the hypertrophic aging heart. METHODS: At 44-week-old, a normal chow (12% fat) was replaced a high-fat diet (HFD; 45% fat) for randomly selective spontaneously hypertensive rats (SHR + HFD, n = 6) and Wistar-Kyoto rats (WKY + HFD, n = 6, normotensive control). Others (SHR, n = 11; WKY, n = 10) were continuously fed with normal diets...
September 6, 2017: Journal of the Formosan Medical Association, Taiwan Yi Zhi
https://www.readbyqxmd.com/read/28888041/supplementation-with-the-methyl-donor-betaine-prevents-congenital-defects-induced-by-prenatal-alcohol-exposure
#20
Ganga Karunamuni, Megan M Sheehan, Yong Qiu Doughman, Shi Gu, Jiayang Sun, Youjun Li, James P Strainic, Andrew M Rollins, Michael W Jenkins, Michiko Watanabe
BACKGROUND: Despite decades of public education about dire consequences of prenatal alcohol exposure, drinking alcohol during pregnancy remains prevalent. As high as 40% of live-born infants exposed to alcohol during gestation and diagnosed with Fetal Alcohol Syndrome have congenital heart defects that can be life-threatening. In animal models, the methyl donor betaine, found in foods such as wheat bran, quinoa, beets and spinach, ameliorated neurobehavioral deficits associated with prenatal alcohol exposure (PAE) but effects on heart development are unknown...
September 9, 2017: Alcoholism, Clinical and Experimental Research
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