ライフサイエンスコーパス: myocyte hypertrophy

1 regulatory pathway controlling pathological myocyte hypertrophy.

2 een implicated in the development of cardiac myocyte hypertrophy.

3 ident beta1ARs prevents NE dependent 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 ting increased calcineurin/NFAT signaling in myocyte hypertrophy.

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

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

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

14 tivity is required for p70S6K activation and myocyte hypertrophy.

15 36 weeks and was associated with significant myocyte hypertrophy.

16 other ion channel gene expression or atrial myocyte hypertrophy.

17 rt responds to pathological overload through myocyte hypertrophy.

18 fficient to trigger neonatal rat ventricular myocyte hypertrophy.

19 ntricular myocytes and inducing compensatory myocyte hypertrophy.

20 her capillary density, and less compensatory myocyte hypertrophy.

21 t to adult cardiac fibroblasts that promoted myocyte hypertrophy.

22 of cAMP second messenger controlling cardiac myocyte hypertrophy.

23 Integrins appear to be necessary for cardiac myocyte hypertrophy.

24 titial fibrosis, endothelial dysfunction and myocyte hypertrophy.

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

26 Rac1 mediate hypertrophic signals in cardiac myocyte hypertrophy.

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

28 oliferation, increased apoptosis and cardiac myocyte hypertrophy.

29 2D-dependent gene expression and ventricular myocyte hypertrophy.

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

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

32 tor tyrosine kinase Src in signaling cardiac myocyte hypertrophy.

33 and gene expression associated with cardiac myocyte hypertrophy.

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

35 Myocyte hypertrophy accompanies many forms of heart dise

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

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

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

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

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

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

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

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

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

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

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

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

48 Myocyte hypertrophy and endocardial thickening were nega

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

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

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

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

53 Cardiac myocyte hypertrophy and fibrosis were assessed by morpho

54 D mice expression in other lines caused mild myocyte hypertrophy and fibrosis, did not affect lifespa

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

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

57 lar geometry in conjunction with improved RV myocyte hypertrophy and function independent of reduced

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

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

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

61 ic constriction and exercise-induced cardiac myocyte hypertrophy and impaired cardiac function, demon

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

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

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

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

66 caused RV dilatation, systolic dysfunction, myocyte hypertrophy and LV compression which improved af

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

68 -independent histone variant H3.3a inhibited myocyte hypertrophy and prevented phenylephrine-induced

69 5N may further contribute to the severity of myocyte hypertrophy and related prognosis of the disease

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

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

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

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

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

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

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

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

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

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

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

81 differentiation and neonatal rat ventricular myocyte hypertrophy are inhibited by mAKAPbeta signaloso

82 ular disease, including heart contractility, myocyte hypertrophy, arterial stiffness, and systemic re

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

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

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

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

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

88 We observed corresponding myocyte hypertrophy by light microscopy.

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

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

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

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

93 a) is required for induction of pathological myocyte hypertrophy, despite calcineurin Aalpha expressi

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

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

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

97 Myocyte hypertrophy, disarray, and myocardial fibrosis c

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

99 t contributes to increased oxidative stress, myocyte hypertrophy, ECM remodeling, and inflammation, i

100 ventricular (LV) compression; biventricular myocyte hypertrophy, fibrosis and dysfunction.

101 11-15 months, characterized by reduced LVEF, myocyte hypertrophy, fibrosis, and apoptosis.

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

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

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

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

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

107 se calcineurin is a key regulator of cardiac myocyte hypertrophy in disease.

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

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

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

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

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

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

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

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

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

117 lear factor of activated T cells pathway and myocyte hypertrophy in vitro.

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

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

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

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

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

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

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

125 Ventricular myocyte hypertrophy is an important compensatory growth

126 Cardiac myocyte hypertrophy is associated with cell growth and c

127 We report that asymmetrical cardiac myocyte hypertrophy is modulated by SRF (serum response

128 Cardiac myocyte hypertrophy is regulated by an extensive intrace

129 Cardiac myocyte hypertrophy is the main compensatory response to

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

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

132 by multiple pathological features including myocyte hypertrophy, myocyte disarray, and interstitial

133 Myocyte hypertrophy, myocyte disarray, interstitial fibr

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

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

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

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

138 Myocyte hypertrophy (p < 0.001), myocyte disarray (p < 0

139 Myocyte hypertrophy, possibly related to subcellular inj

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

141 LV myocyte hypertrophy (r = 0.58, P = 0.016) and collagen v

142 RV myocyte hypertrophy (r = 0.75, P < 0.001) but not collag

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

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

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

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

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

148 odel, older age (p < 0.001), lower degree of myocyte hypertrophy (severe vs. mild hazard ratio: 0.41;

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

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

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

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

153 terations in Ca(2+) handling at baseline and myocyte hypertrophy were present throughout the left ven

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

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

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

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

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

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

160 Both ligands induce myocyte hypertrophy with overlapping potencies.

161 cise, both of which promote adaptive cardiac myocyte hypertrophy with preserved cardiac function.

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

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

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

165 umol/mg tissue/min), increased inflammation, myocyte hypertrophy (WT, 19.8 mum; CatA-TG, 21.9 mum), c