ライフサイエンスコーパス: myocyte hypertrophy

1 ting increased calcineurin/NFAT signaling in myocyte hypertrophy.

2 ntricular myocytes and inducing compensatory myocyte hypertrophy.

3 een implicated in the development of cardiac myocyte hypertrophy.

4 II (Ang II) triggers cell death and promotes myocyte hypertrophy.

5 he mouse cardiac myocyte and perturbation of myocyte hypertrophy.

6 of the signaling pathway leading to cardiac myocyte hypertrophy.

7 orm was involved in myotrophin-induced adult myocyte hypertrophy.

8 nlargement and hyperchromasia, indicative of myocyte hypertrophy.

9 of the most distinctive features of cardiac myocyte hypertrophy.

10 ates, but JNK suppresses, the development of myocyte hypertrophy.

11 ess the role of this small GTPase in cardiac myocyte hypertrophy.

12 essential for 8,12-iso-iPF2alpha-III-induced myocyte hypertrophy.

13 tivity is required for p70S6K activation and myocyte hypertrophy.

14 36 weeks and was associated with significant myocyte hypertrophy.

15 her capillary density, and less compensatory myocyte hypertrophy.

16 t to adult cardiac fibroblasts that promoted myocyte hypertrophy.

17 rt responds to pathological overload through myocyte hypertrophy.

18 of cAMP second messenger controlling cardiac myocyte hypertrophy.

19 Integrins appear to be necessary for cardiac myocyte hypertrophy.

20 titial fibrosis, endothelial dysfunction and myocyte hypertrophy.

21 lts in a myopathy characterized by organ and myocyte hypertrophy.

22 Rac1 mediate hypertrophic signals in cardiac myocyte hypertrophy.

23 fficient to trigger neonatal rat ventricular myocyte hypertrophy.

24 ve been linked to the development of cardiac myocyte hypertrophy.

25 oliferation, increased apoptosis and cardiac myocyte hypertrophy.

26 es, and stimulation of protein synthesis and myocyte hypertrophy.

27 decreased AngII-induced O2*- production and myocyte hypertrophy.

28 tor tyrosine kinase Src in signaling cardiac myocyte hypertrophy.

29 and gene expression associated with cardiac myocyte hypertrophy.

30 Our data dissociate myocyte hypertrophy, a consistent response in HCM, from

31 Myocyte hypertrophy accompanies many forms of heart dise

32 lecule, referred to as pyridine activator of myocyte hypertrophy, acts as a selective agonist for 5-H

33 r this pathway in the development of cardiac myocyte hypertrophy, alpha1-adrenergic stimulation simil

34 lass I and II HDACs primarily causes cardiac myocyte hypertrophy and also induces modest cell death.

35 AC6mut reduced phenylephrine-induced cardiac myocyte hypertrophy and apoptosis (p < 0.001), expressio

36 re linked to MAPK activation, namely cardiac myocyte hypertrophy and apoptosis.

37 AdCnA infection, which induced myocyte hypertrophy and atrial natriuretic factor expres

38 nduce a molecular program leading to cardiac myocyte hypertrophy and cardiomyopathy.

39 hat explains how Ca(2+) discretely regulates myocyte hypertrophy and contraction.

40 However, ventricular dilation, myocyte hypertrophy and death, and depressed cardiac pum

41 The histological features of HCM include myocyte hypertrophy and disarray, as well as interstitia

42 onse to sustained pressure overload involves myocyte hypertrophy and dysfunction along with interstit

43 hways by which sarcomeric mutations engender myocyte hypertrophy and electrophysiological abnormaliti

44 pha develop cardiomyopathy, characterized by myocyte hypertrophy and extensive myocardial fibrosis.

45 AT have been implicated in the regulation of myocyte hypertrophy and fiber type specificity.

46 Histological examination revealed myocyte hypertrophy and fibrosis in 4- to 16-week PKCbet

47 topathological examination demonstrated that myocyte hypertrophy and fibrosis were already present in

48 Cardiac myocyte hypertrophy and fibrosis were assessed by morpho

49 d followed by tissue analysis for changes in myocyte hypertrophy and fibrosis.

50 roach for the specific inhibition of cardiac myocyte hypertrophy and for the development of novel str

51 of a fetal gene program in association with myocyte hypertrophy and heart failure.

52 d cardiac mass results from a combination of myocyte hypertrophy and hyperplasia.

53 prevented phenylephrine induced pathological myocyte hypertrophy and hypertrophic marker expression i

54 ion of stretch response proteins, attenuates myocyte hypertrophy and improves SR calcium cycling.

55 ed cardiac alpha-actin, reversed cardiac and myocyte hypertrophy and interstitial fibrosis, reduced t

56 ion of systolic function in association with myocyte hypertrophy and interstitial fibrosis.

57 , or cardiac transplants (n=2) showed marked myocyte hypertrophy and iron deposits with or without in

58 ctivity between calcineurin-mediated cardiac myocyte hypertrophy and p38 MAPK signaling in vitro and

59 5N may further contribute to the severity of myocyte hypertrophy and related prognosis of the disease

60 tch for a negative feedback circuit for both myocyte hypertrophy and survival.

61 scriptional changes occurring during cardiac myocyte hypertrophy and that Ras and Raf may be downstre

62 MAPK activity are associated with changes in myocyte hypertrophy and viability, suggesting a potentia

63 rial dilatation, mitral valve regurgitation, myocyte hypertrophy, and atrial fibrosis occurred progre

64 r with increased ventricular wall thickness, myocyte hypertrophy, and disarray.

65 OS3(-/-) TAC hearts developed less fibrosis, myocyte hypertrophy, and fetal gene re-expression (B-nat

66 nhibitor (sildenafil) suppresses chamber and myocyte hypertrophy, and improves in vivo heart function

67 uppression of Ca(2+)-induced Ca(2+) release, myocyte hypertrophy, and premature death by 16 weeks of

68 pregulation of transcription factors, induce myocyte hypertrophy, and prepare the cell for entry into

69 ho) families have been implicated in cardiac myocyte hypertrophy, and this may involve the extracellu

70 response to the known stimulators of cardiac myocyte hypertrophy, angiotensin II (Ang II) and phenyle

71 B(DeltaI)/B(DeltaI) mice developed cardiac myocyte hypertrophy between 7 months and 11 months of ag

72 their ventricular myocytes and showed a 28% myocyte hypertrophy; both phenomena were prevented by IG

73 This phenotype does not appear to involve myocyte hypertrophy but is associated with dephosphoryla

74 DF11 did not reduce neonatal rat ventricular myocytes hypertrophy, but instead induced hypertrophy.

75 reover, 5 of 5 B(DeltaI)/B(-) mice developed myocyte hypertrophy by 1 month; B(DeltaI)/B(-) mice also

76 We observed corresponding myocyte hypertrophy by light microscopy.

77 pathways include those that regulate cardiac myocyte hypertrophy, calcium homoeostasis, energetics, a

78 a (IL-1beta) induces a novel form of cardiac myocyte hypertrophy characterized by an increase in prot

79 II-B results in a marked increase in cardiac myocyte hypertrophy compared with the NM II-B hypomorphi

80 betaIPKC, also inhibited PMA-induced cardiac myocyte hypertrophy, demonstrating that both betaI- and

81 t correlation (r=0.85) between the extent of myocyte hypertrophy (determined by computer imaging) and

82 A phorbol ester that also causes myocyte hypertrophy did not increase ROS generation, and

83 n caused cardiac histopathologic findings of myocyte hypertrophy, disarray and replacement fibrosis.

84 ardly appear similar to conditions with true myocyte hypertrophy (e.g., hypertrophic cardiomyopathy,

85 11-15 months, characterized by reduced LVEF, myocyte hypertrophy, fibrosis, and apoptosis.

86 Adverse cardiac remodeling includes myocyte hypertrophy, fibrosis, and electrical remodeling

87 and pathophysiological processes, including myocyte hypertrophy, fibrosis, inflammation and epitheli

88 to investigate the relative contribution of myocyte hypertrophy, hemodynamic load, severity of AS, a

89 n of ERK1/2 has been associated with cardiac myocyte hypertrophy (ie, increased cell size and myofibr

90 a remodeling process that is accompanied by myocyte hypertrophy, impaired contractility, and pump fa

91 x DNp38alpha MAPK mice, and failed to reduce myocyte hypertrophy in either group.

92 on, the betaIIV5-3 peptide inhibited cardiac myocyte hypertrophy in PMA-treated cells.

93 heart growth in pythons is characterized by myocyte hypertrophy in the absence of cell proliferation

94 r the effects of IGF-1 on cell viability and myocyte hypertrophy in the nonpathological and pathologi

95 ects them from apoptosis and interferes with myocyte hypertrophy in the normal and pathological heart

96 independent mechanism, in part by decreasing myocyte hypertrophy in the remote myocardium.

97 aryl coenzyme A inhibitors (statins) inhibit myocyte hypertrophy in vitro and ameliorate the progress

98 ZBTB17 also regulated cardiac myocyte hypertrophy in vitro and in vivo in a calcineuri

99 duces myogenic differentiation and generates myocyte hypertrophy in vitro and in vivo.

100 ated PE-mediated/FAK-dependent initiation of myocyte hypertrophy in vivo Collectively, these findings

101 rinking water had a small effect in reducing myocyte hypertrophy in WT mice and no effect in betaRM m

102 vo and the mechanisms by which adult cardiac myocytes hypertrophy in vivo are less clear.

103 y in heterozygous MYBPC3(+/-) individuals is myocyte hypertrophy (increased cell size), whereas the m

104 llmarks of cardiovascular aging (progressive myocyte hypertrophy, increased myocardial fibrosis and a

105 etion in the mouse attenuated the concentric myocyte hypertrophy induced by pressure overload and cat

106 n the regulation of cardiac gene expression, myocyte hypertrophy, inflammation, energetic metabolism,

107 Ventricular myocyte hypertrophy is an important compensatory growth

108 Cardiac myocyte hypertrophy is associated with cell growth and c

109 Cardiac myocyte hypertrophy is regulated by an extensive intrace

110 Cardiac myocyte hypertrophy is the main compensatory response to

111 m the sham-operated group (P<0.05), regional myocyte hypertrophy (myocyte volume per nucleus, 14 183+

112 a remodeling process that is associated with myocyte hypertrophy, myocyte death, and fibrosis.

113 diomyopathy with prominent histopathology of myocyte hypertrophy, myofibrillar disarray, fibrosis, an

114 proteins demonstrate that PGF2alpha-induced myocyte hypertrophy occurs independent of either PKC, p3

115 nical stretch, a potent stimulus for cardiac myocyte hypertrophy, on GRK2 activity and beta-AR signal

116 myocardial specimens from humans either with myocyte hypertrophy or with no pathological changes.

117 Myocyte hypertrophy, possibly related to subcellular inj

118 o a dilated myopathy in which cell death and myocyte hypertrophy predominate.

119 mitogen-activated protein kinase), increased myocyte hypertrophy, reduced SERCA2a activity with uncha

120 nflammation, collagen deposition and cardiac myocyte hypertrophy, regenerated 80-90% of lost myocardi

121 density returned to normal, whereas regional myocyte hypertrophy regressed.

122 ession of cardiac stretch response proteins, myocyte hypertrophy, sarcoplasmic reticulum Ca2+-ATPase

123 iferation, angiogenesis, collagen synthesis, myocyte hypertrophy, scar contraction, and, ultimately,

124 veloped a computational model of the cardiac myocyte hypertrophy signaling network to determine how t

125 generated a model of persistent, functional myocyte hypertrophy using a tissue-restricted transgene

126 PGF2alpha and 8,12-iso-iPF2alpha-III induce myocyte hypertrophy via discrete signaling pathways.

127 Reversal of myocyte hypertrophy was produced in hypertensive/heart f

128 resulted in increased ventricular growth and myocyte hypertrophy when treated embryos were compared t

129 in wall thickness with partial resolution of myocyte hypertrophy, whereas calorie-restricted mice had

130 erted opposing effects on the development of myocyte hypertrophy, which is an adaptive physiological

131 age, these animals demonstrated compensatory myocyte hypertrophy with an increase in the cardiac coll

132 cal increases in cardiac afterload result in myocyte hypertrophy with changes in myocyte electrical a

133 on of RLC phosphorylation led to ventricular myocyte hypertrophy with histological evidence of necros

134 Both ligands induce myocyte hypertrophy with overlapping potencies.

135 Histological analysis reveals marked cardiac myocyte hypertrophy, with accompanying cellular infiltra

136 ity, inhibit 8,12-iso-iPF2alpha-III -induced myocyte hypertrophy, with IC50 values of 60 +/- 12 and 3

137 5) improves regional function by stimulating myocyte hypertrophy without increasing myocardial perfus