• mice
  • Studies have shown that knockdown of tafazzin results in cardiac and skeletal muscle defects and prenatal cardiomyopathy in mice ( 1 , 58 ), retarded cardiac development and bradycardia in zebrafish ( 40 ), and impaired motor activity in Drosophila ( 72 ). (physiology.org)
  • Cardiac function, morphology and miR expression profiles were determined in neonatal, 4 weeks, 6 months and 19 months old normotensive male healthy C57/Bl6N mice. (biomedsearch.com)
  • Knockout of kinin B2 receptor (B2R) signaling causes dilated and failing cardiomyopathy in 129/J mice, and a 9-bp deletion polymorphism of human B2R is associated with reduced receptor expression and exaggerated left ventricular growth response to physical stress. (ahajournals.org)
  • This phenotype was not observed in wild-type mice with CKD or in hBAC-S100 mice lacking the receptor for advanced glycation end products with CKD, suggesting that the inflammatory milieu mediated by S100/receptor for advanced glycation end products promotes pathological cardiac hypertrophy in CKD. (ahajournals.org)
  • The 5-HT2B receptor subtype is involved in: CNS: presynaptic inhibition, behavioural effects Vascular: pulmonary vasoconstriction Cardiac: The 5-HT2B receptor regulates cardiac structure and functions as demonstrated by the abnormal cardiac development observed in 5-HT2B receptor null mice. (wikipedia.org)
  • Using AT1a knockout (KO) mice, we examined whether Ang II is indispensable for pressure overload-induced cardiac hypertrophy in the present study. (ahajournals.org)
  • Moreover, we have recently observed that chronic pressure overload produced by constricting the abdominal aorta induces cardiac hypertrophy with the expression of fetal genes not only in WT mice but also in AT1a KO mice, 19 in which signaling pathways through AT1a are genetically deleted, suggesting that Ang II is not required for the development of pressure overload-induced cardiac hypertrophy (authors' unpublished data, 1998). (ahajournals.org)
  • In the present study, to confirm that Ang II is not required for the development of pressure overload-induced cardiac hypertrophy and to gain insight into the mechanism by which pressure overload induces cardiac hypertrophy without Ang II−evoked signaling pathways, we examined acute hypertrophic responses in the hearts of AT1a KO mice by using a different pressure-overload model. (ahajournals.org)
  • In mice, aortic banding-induced pressure overload leads to cardiac hypertrophy and heart failure. (wikidot.com)
  • 14 ] showed that shunt-induced volume-overload congestive heart failure (CHF) resulted in cardiac hypertrophy with compromised left ventricular hypertrophy in mice. (wikidot.com)
  • Induced ischemia via coronary artery ligation of the left anterior descending artery in mice has been shown to produce myocyte death and eventual cardiac dysfunction. (wikidot.com)
  • Cardiac remodelling of the ECM is also regulated by the CNP/NPR-B pathway as demonstrated by the improved outcomes in transgenic mice with CNP over-expression subjected to myocardial infarction. (wikipedia.org)
  • Further support was gained from in vivo studies in which mice expressing a mutant cTnI (Serine43/45Alanine) exhibited enhanced cardiac contractility. (wikipedia.org)
  • In agreement with this, mice with ablation of N-cadherin in adult hearts via a cardiac-specific tamoxifen-inducible Cre N-cadherin transgene showed disrupted assembly of intercalated discs, dilated cardiomyopathy, impaired cardiac function, decreased sarcomere length, increased Z-line thickness, decreases in connexin 43, and a loss in muscular tension. (wikipedia.org)
  • Mice died within two months of transgene expression, mainly due to spontaneous ventricular tachycardia. (wikipedia.org)
  • A more aggressive overexpression of β-tropomyosin (to over 75% of total tropomyosin) in the heart causes death of mice 10-14 days old, along with cardiac abnormalities, suggesting that the normal distribution of tropomyosin isoforms is critical to normal cardiac function. (wikipedia.org)
  • congestive heart f
  • It provides independent prognostic information in the general population, free of clinical signs of heart failure ( 1 ), as well as in different clinical settings, including essential hypertension ( 2 ), congestive heart failure ( 3 ), myocardial infarction ( 4 ), and left ventricular hypertrophy (LVH), and in the elderly ( 5 ). (diabetesjournals.org)
  • 13 If it is true that IGF-I supports cardiac function, low circulating IGF-I levels may be one of the direct reasons for increased mortality in patients with congestive heart failure. (ahajournals.org)
  • vitro
  • Additionally, in vitro study of human fibroblasts demonstrates that CD-NP reduces TGF-beta 1 induced collagen production. (wikipedia.org)
  • These tissues provide a unique in vitro model to study cardiac physiology with a species-specific advantage over cultured animal cells in experimental studies. (wikipedia.org)
  • These studies were further supported by those performed in isolated, skinned cardiac muscle fibers, showing that in vitro phosphorylation of cTnI by PKCε or Serine-43/45 mutation to Glutamate to mimic phosphorylation desensitized myofilaments to calcium and decreased maximal tension and filament sliding speed. (wikipedia.org)
  • myocardium
  • PF is an ultrafiltrate of plasma, 18 but it also reflects the composition of cardiac interstitium, at least in cardiac ischemia, 19 and the production and release of macromolecules (including growth factors) in normal and diseased myocardium. (ahajournals.org)
  • 22 However, whether human PF contains growth factors and peptides specifically synthesized within the myocardium and whether its characteristics reflect cardiac adaptation to chronic overload have not yet been established. (ahajournals.org)
  • induces
  • Treatment with hydralazine abolished the induction of IGF-I mRNA, which indicates that Ang II induces cardiac IGF-I mRNA expression through a pressor-mediated mechanism. (ahajournals.org)
  • 16 ] When increased myotrophin induces significant overexpression of proto-oncogenes and hypertrophy marker genes in the heart, it can lead to hypertrophy and heart failure. (wikidot.com)
  • reactive
  • In primary cultures of neonatal ventricular fibroblasts (NVFs) transduced with a tafazzin short hairpin RNA adenovirus, tafazzin knockdown increased production of reactive oxygen species and activation of mitogen-activated protein kinases and induced protein and DNA synthesis via cell cycle regulators. (physiology.org)
  • alterations
  • In human heart failure, there are characteristic alterations in the cardiac β-adrenoceptor system: selective downregulation of β 1 -adrenoceptors with little or no change in β 2 -adrenoceptors, reduced adenylyl cyclase activity, increased G protein-coupled receptor kinases (GRKs) activity, and reduced neuronal noradrenaline transporter. (ahajournals.org)
  • genes
  • TGFbeta mediated activation of p38 MAPK decreases KLF15 permitting the upreg of myocardin and stimulate the expression of serum response factor target genes, such as atrial natriuretic factor eventually leading to left ventricular hypertrophy which often progresses to heart failure. (wikipedia.org)
  • hECTs also express key cardiac genes (α-MHC, SERCA2a and ACTC1) nearing the levels seen in the adult heart. (wikipedia.org)
  • protein
  • This is associated with characteristic changes in right ventricular β-adrenoceptors (β-AR), neuronal noradrenaline transporter (NAT) density and activity (uptake 1 ), and G protein-coupled receptor kinase (GRK) activity. (ahajournals.org)
  • Numerous perturbations affecting the cardiac neural crest have been associated with persistent truncus arteriosus, some of which include growth factors (fibroblast growth factor 8 and bone morphogenetic protein), transcription factors (T-box, Pax, Nkx2-5, GATA-6, and Forkhead), and gap junction proteins (Connexin). (wikipedia.org)
  • Cardiac Organellar Protein Atlas Knowledgebase (COPaKB). (wikipedia.org)
  • trophic effects
  • 01). These trophic effects of PF were mimicked by exogenous basic fibroblast growth factor (FGF2) and inhibited by anti-FGF2 antibodies and transforming growth factor-β (TGF-β), suggesting a relationship to FGF2. (ahajournals.org)
  • tissue
  • Fibroblasts constitute over 90% of nonmyocyte cells in the heart ( 2 ), yet occupy only one third of cardiac tissue ( 9 ). (physiology.org)
  • Studies have also shown that the expression of galectin-3 is implicated in a variety of processes associated with heart failure, including myofibroblast proliferation, fibrogenesis, tissue repair, inflammation, and ventricular remodeling. (wikipedia.org)
  • N-cadherin, originally named for its role in neural tissue, plays a role in neurons and later was found to also play a role in cardiac muscle and in cancer metastasis. (wikipedia.org)
  • 0.01
  • Within 13 to 19 days after MCT application (group A), RV weight (222±6 versus 147±5 mg) and RV/left ventricular (LV) weight ratio (0.42±0.01 versus 0.29±0.01) were significantly increased, whereas plasma noradrenaline, RV β-AR density, RV NAT density and activity, and RV GRK activity were not significantly altered. (ahajournals.org)
  • adult
  • Studies in the 1970s and 1980s from Zak and Nag defined and quantified the cellular populations of the adult rat left ventricle based on morphological characteristics using transmission electron microscopy of rat left ventricular sections, as well as gradient centrifugation. (ahajournals.org)
  • A study overexpressing β-tropomyosin in adult cardiac muscle evoked a 34-fold increase in expression of β-tropomyosin, resulting in preferential formation of the αβ-tropomyosin heterodimer. (wikipedia.org)
  • mRNA
  • 12 13 In addition, it has been demonstrated that mRNA levels of cardiac ACE, 14 angiotensinogen, 10 and local synthesis of Ang II 14 are increased in the hypertrophied heart. (ahajournals.org)
  • proteins
  • In cardiac muscle cells, PKCε regulates muscle contraction through its actions at sarcomeric proteins, and PKCε modulates cardiac cell metabolism through its actions at mitochondria. (wikipedia.org)
  • cardiovascular
  • 2007 ). The incidence of cardiovascular disease increases dramatically with advanced age, therefore elucidation of the molecular mechanisms contributing to cardiac aging in healthy heart would help to identify early pathophysiological changes in the heart. (biomedsearch.com)
  • Left ventricular hypertrophy and failure constitute major risks of cardiovascular complications and sudden death among hypertensive subjects. (ahajournals.org)
  • Interest in these bioengineered cardiac tissues has risen due to their potential use in cardiovascular research and clinical therapies. (wikipedia.org)
  • stimulation
  • In cardiac muscle, PKCε translocates to sarcomeres at Z-lines following α-adrenergic and endothelin (ET)A-receptor stimulation. (wikipedia.org)