ライフサイエンスコーパス: cardiomyocyte hypertrophy

1 roved microvascular formation and attenuated cardiomyocyte hypertrophy).

2 feration and vascular density, and decreased cardiomyocyte hypertrophy.

3 ed angiotensin II- and phenylephrine-induced cardiomyocyte hypertrophy.

4 ckdown) had a significant negative effect on cardiomyocyte hypertrophy.

5 cate increased RAS signaling in pathological cardiomyocyte hypertrophy.

6 xpression induced the fetal gene program and cardiomyocyte hypertrophy.

7 ida toxin, a Galpha(q) agonist that promotes cardiomyocyte hypertrophy.

8 ilation, decreased infarct size, and reduced cardiomyocyte hypertrophy.

9 ogram, it does not appear to be critical for cardiomyocyte hypertrophy.

10 ognition by intrinsic Toll-like receptors to cardiomyocyte hypertrophy.

11 P complex show that anchored ERK5 can induce cardiomyocyte hypertrophy.

12 failure, we hypothesized that IL-18 induces cardiomyocyte hypertrophy.

13 ta is a negative regulator of stress-induced cardiomyocyte hypertrophy.

14 ces agonist-induced calcineurin activity and cardiomyocyte hypertrophy.

15 positive or negative roles in the control of cardiomyocyte hypertrophy.

16 (NF)-kappaB signaling has been implicated in cardiomyocyte hypertrophy.

17 ts as an inhibitor of cell proliferation and cardiomyocyte hypertrophy.

18 actory to hypertrophic signaling and inhibit cardiomyocyte hypertrophy.

19 ith NKX2-5, is essential for stretch-induced cardiomyocyte hypertrophy.

20 ve action, gp130-dependent signaling induces cardiomyocyte hypertrophy.

21 (i)-coupled receptors do not directly effect cardiomyocyte hypertrophy.

22 f p38-MAPK alone is not sufficient to induce cardiomyocyte hypertrophy.

23 ys an essential role in ET-1- and PE-induced cardiomyocyte hypertrophy.

24 that couple to Gq class proteins can induce cardiomyocyte hypertrophy.

25 sis and protein accumulation associated with cardiomyocyte hypertrophy.

26 bol 12-myristate 13-acetate (PMA) results in cardiomyocyte hypertrophy.

27 ted the effect of IL-1beta on alpha1-induced cardiomyocyte hypertrophy.

28 ription during contraction-mediated neonatal cardiomyocyte hypertrophy.

29 macitentan decreased the aldosterone-induced cardiomyocyte hypertrophy.

30 (Ser473)/p70-S6K(Thr389) phosphorylation and cardiomyocyte hypertrophy.

31 ma at the Golgi or PM blocked ET-1-dependent cardiomyocyte hypertrophy.

32 th subsequent organ growth occurring through cardiomyocyte hypertrophy.

33 ckdown of PRMT5 induced GATA4 activation and cardiomyocyte hypertrophy.

34 t paracrine-acting RNA molecule that induces cardiomyocyte hypertrophy.

35 regulated during myocyte differentiation and cardiomyocyte hypertrophy.

36 aling is necessary and sufficient to promote cardiomyocyte hypertrophy.

37 t of apoptotic caspase pathways in mediating cardiomyocyte hypertrophy.

38 ssment of extracellular matrix expansion and cardiomyocyte hypertrophy.

39 be both necessary and sufficient to repress cardiomyocyte hypertrophy.

40 xpression of miR-22 was sufficient to induce cardiomyocyte hypertrophy.

41 resonance provides a noninvasive measure of cardiomyocyte hypertrophy.

42 rdiomyocyte resting tension (F(passive)) and cardiomyocyte hypertrophy.

43 eart growth involves primarily physiological cardiomyocyte hypertrophy.

44 pivotal point linking sustained overload to cardiomyocyte hypertrophy.

45 rexpression of CIP repressed agonist-induced cardiomyocyte hypertrophy.

46 the regulation of cellular responses such as cardiomyocyte hypertrophy.

47 5 inhibits cardiac fetal gene expression and cardiomyocyte hypertrophy.

48 screen for previously unknown regulators of cardiomyocyte hypertrophy.

49 of metalloproteases, and for stress-induced cardiomyocyte hypertrophy.

50 after pressure overload results mainly from cardiomyocyte hypertrophy.

51 nversion into smooth muscle cells as well as cardiomyocyte hypertrophy.

52 differentiation, a program with parallels to cardiomyocyte hypertrophy.

53 lates miR-133a that targets SP1 and inhibits cardiomyocytes hypertrophy.

54 yclic stress conditioning markedly increases cardiomyocyte hypertrophy (2.2-fold) and proliferation r

55 ated endothelial proliferation, and enhanced cardiomyocyte hypertrophy after infarction.

56 direct Galpha(q) agonist that induces robust cardiomyocyte hypertrophy, also activates the PKD-CREB-S

57 tional coactivators, called CAMTAs, promotes cardiomyocyte hypertrophy and activates the ANF gene, at

58 nockdown studies revealed that IL-18 induced cardiomyocyte hypertrophy and ANF gene transcription via

59 Cardiomyocyte hypertrophy and apoptosis have been implic

60 gical changes that include chamber dilation, cardiomyocyte hypertrophy and apoptosis, and ultimately

61 the role of AKT and JUN in TNF-alpha-induced cardiomyocyte hypertrophy and apoptosis.

62 eurin inhibitory domain of AKAP79 attenuated cardiomyocyte hypertrophy and atrial natriuretic factor

63 ment for p8 in key cellular events linked to cardiomyocyte hypertrophy and cardiac fibroblast MMP pro

64 rdial capillary density and an inhibition of cardiomyocyte hypertrophy and cardiac fibrosis.

65 es uncover miR-22 as a critical regulator of cardiomyocyte hypertrophy and cardiac remodeling.

66 fy CHAMP as a cardiac-specific suppressor of cardiomyocyte hypertrophy and cell cycle progression and

67 The impact of ERK(Thr188) phosphorylation on cardiomyocyte hypertrophy and cell survival was analyzed

68 Cardiomyocyte hypertrophy and ERK activation were also i

69 Cardiomyocyte hypertrophy and extracellular matrix remod

70 Results showed development of cardiomyocyte hypertrophy and fibrosis in mouse hearts.

71 thelin- and alpha-adrenergic agonist-induced cardiomyocyte hypertrophy and for tumor necrosis factor-

72 Biomechanical strain is a stimulus for cardiomyocyte hypertrophy and heart failure, but the und

73 previously been shown to effectively prevent cardiomyocyte hypertrophy and heart failure.

74 ion in TAUlocal was increased and related to cardiomyocyte hypertrophy and increased mitochondrial de

75 in the knockouts coincident with increasing cardiomyocyte hypertrophy and interstitial and perivascu

76 or 1-nitrosocyclohexylacetate (1-NCA) limits cardiomyocyte hypertrophy and LV diastolic dysfunction i

77 d with bosentan showed significantly less LV cardiomyocyte hypertrophy and LV volume fraction of inte

78 The development of posttransplant cardiomyocyte hypertrophy and myocardial fibrosis likely

79 e the degree and time course over 6 years of cardiomyocyte hypertrophy and myocardial fibrosis of the

80 ed in a phenocopy of endurance exercise with cardiomyocyte hypertrophy and proliferation.

81 ure overload, Gata4 regulates the pattern of cardiomyocyte hypertrophy and protects the heart from lo

82 y that HDAC9 acts as a negative regulator of cardiomyocyte hypertrophy and skeletal muscle differenti

83 Six1 induced cardiomyocyte hypertrophy and skeletal muscle gene expre

84 bstitute for hypertrophic signals and induce cardiomyocyte hypertrophy and the fetal cardiac gene pro

85 cts of cardiac remodeling, such as fibrosis, cardiomyocyte hypertrophy, and calcium handling (Col1a2,

86 fingolimod decreased interstitial fibrosis, cardiomyocyte hypertrophy, and chronic activation of Akt

87 ly HFpEF was associated with LA enlargement, cardiomyocyte hypertrophy, and enhanced LA contractile f

88 yofibril maturation, enhancing the extent of cardiomyocyte hypertrophy, and facilitating the coordina

89 s and fibrosis, with attenuated compensatory cardiomyocyte hypertrophy, and further impaired function

90 tion, higher LV end-diastolic pressure, more cardiomyocyte hypertrophy, and higher mortality but simi

91 ssary for the development of agonist-induced cardiomyocyte hypertrophy, and suggest that in response

92 nisms downstream of PLCbeta1b culminating in cardiomyocyte hypertrophy, and that the hypertrophic res

93 n of numerous signaling cascades, leading to cardiomyocyte hypertrophy, apoptosis, and ultimately, he

94 the signal transduction pathways leading to cardiomyocyte hypertrophy are strongly influenced by and

95 , extracellular signal-regulated kinase, and cardiomyocyte hypertrophy; AYPGKF and thrombin, but not

96 onstrate that H-Ras, but not K-Ras, promotes cardiomyocyte hypertrophy both in vivo and in vitro.

97 Inhibition of cardiomyocyte hypertrophy by CHAMP requires the conserve

98 Overexpression of iex-1 abolished cardiomyocyte hypertrophy by mechanical strain, phenylep

99 e of hydrogen peroxide generated by MAO A in cardiomyocyte hypertrophy by serotonin.

100 Unlike WT-TAC controls, G4D-TAC cardiomyocytes hypertrophied by increasing in length mor

101 These abnormalities are associated with cardiomyocyte hypertrophy, cardiac chamber dilation and

102 Adverse ventricular remodeling including cardiomyocyte hypertrophy (cardiomyocyte cross-sectional

103 amine toxicity with contractile dysfunction, cardiomyocyte hypertrophy, cardiomyocyte death, and N-te

104 ther GATA4 or GATA6 was sufficient to induce cardiomyocyte hypertrophy characterized by enhanced sarc

105 ranscriptional responses and agonist-induced cardiomyocyte hypertrophy, demonstrating that cardiac-ex

106 Cardiomyocyte hypertrophy downstream of Gq-coupled recep

107 junctures led to a significant inhibition of cardiomyocyte hypertrophy during agonist stimulation, wi

108 bition of cardiomyocyte proliferation and to cardiomyocyte hypertrophy during embryonic development.

109 s that heart growth should occur entirely by cardiomyocyte hypertrophy during preadolescence when, in

110 ly induced in response to T. cruzi, promotes cardiomyocyte hypertrophy early in the infective process

111 n was associated with increased LV fibrosis, cardiomyocyte hypertrophy, elevated NT-proBNP plasma lev

112 intron of the alphaMHC gene is required for cardiomyocyte hypertrophy, fibrosis, and expression of b

113 structural features of cardiac remodeling - cardiomyocyte hypertrophy, fibrosis, microvasculature ch

114 PMCA4b overexpression inhibited cultured cardiomyocyte hypertrophy following agonist stimulation,

115 n of MK2 partially but significantly reduced cardiomyocyte hypertrophy, improved contractile performa

116 c extracellular matrix and the regulation of cardiomyocyte hypertrophy in a mouse model of heart fibr

117 ditis-like foci, cardiomyocyte necrosis, and cardiomyocyte hypertrophy in all cases.

118 AP13 Rho-GEF and PKD-binding domains mediate cardiomyocyte hypertrophy in cell culture.

119 XO1 overexpression suppressed stress-induced cardiomyocyte hypertrophy in CIP-deficient cardiomyocyte

120 rth American ginseng can reverse established cardiomyocyte hypertrophy in cultured myocytes as well a

121 pertrophy-associated genes, miR-1 attenuated cardiomyocyte hypertrophy in cultured neonatal rat cardi

122 M-stimulated PDE1 in regulating pathological cardiomyocyte hypertrophy in neonatal and adult rat vent

123 -9 in RAS function we assessed its action in cardiomyocyte hypertrophy in rat neonatal H9c2 and prima

124 logic effector caspase inhibitor p35 blunted cardiomyocyte hypertrophy in response to agonist stimula

125 hat calcineurin is an important regulator of cardiomyocyte hypertrophy in response to certain agonist

126 eurin plays a central role in the control of cardiomyocyte hypertrophy in response to pathological st

127 ine key upstream signaling events leading to cardiomyocyte hypertrophy in response to T. cruzi infect

128 rdiomyocytes by 15%, resulting in comparable cardiomyocyte hypertrophy in the 2 strains.

129 diastolic dysfunction, cardiac fibrosis, and cardiomyocyte hypertrophy in the pressure-overloaded hea

130 Absence of osteoglycin did not affect cardiomyocyte hypertrophy in the remodeling remote myoca

131 at GATA factors are sufficient regulators of cardiomyocyte hypertrophy in vitro and in vivo.

132 BET inhibition potently suppresses cardiomyocyte hypertrophy in vitro and pathologic cardia

133 hy in Raf1(L613V)-expressing ECs that drives cardiomyocyte hypertrophy in vitro.

134 nt protein kinase (PKG) activity and thereby cardiomyocyte hypertrophy in vitro.

135 gh the sufficiency of calcineurin to promote cardiomyocyte hypertrophy in vivo and in vitro is establ

136 normalizes the increased wall thickness and cardiomyocyte hypertrophy in vivo.

137 egulatory circuits, which directly influence cardiomyocyte hypertrophy, in part, through membrane bou

138 of stretch response proteins, attenuation of cardiomyocyte hypertrophy, increased affinity of the pum

139 ective in transcriptional activation, blocks cardiomyocyte hypertrophy induced by hypertrophic agonis

140 During neonatal cardiomyocyte hypertrophy induced by norepinephrine or s

141 to determine whether p70S6K plays a role in cardiomyocyte hypertrophy induced by the alpha 1-adrener

142 set of lethal cardiomyopathy associated with cardiomyocyte hypertrophy, interstitial fibrosis, and co

143 Cardiomyocyte hypertrophy is a complex cellular behavior

144 Cardiomyocyte hypertrophy is a critical precursor to the

145 Moreover, cardiomyocyte hypertrophy is blunted with cardiac fibrob

146 s studies established that T. cruzi-elicited cardiomyocyte hypertrophy is mediated by interleukin-1be

147 One potential regulator of cardiomyocyte hypertrophy is the calcium-sensitive phosp

148 Cardiomyocyte hypertrophy is the cellular response that

149 integrity, in the context of enabling foetal cardiomyocyte hypertrophy, maintenance of contractile fu

150 rDNA transcription observed during neonatal cardiomyocyte hypertrophy mediated by both phorbol ester

151 nt is refractory to PKC signaling and blocks cardiomyocyte hypertrophy mediated by pharmacological ac

152 Human myocardium with extensive fibrosis and cardiomyocyte hypertrophy obtained from explanted hearts

153 CSQ mice revealed biventricular dilatation, cardiomyocyte hypertrophy, patchy interstitial fibrosis

154 llowing TAC, cyclin D2 expression attenuated cardiomyocyte hypertrophy, reduced cardiomyocyte apoptos

155 d3+/- animals were associated with decreased cardiomyocyte hypertrophy, reduced collagen deposition,

156 the mechanisms by which the hormones induce cardiomyocyte hypertrophy remain uncharacterized.

157 Cardiomyocyte hypertrophy requires a source of Ca(2+) di

158 rated protein accumulation characteristic of cardiomyocyte hypertrophy results from increased cellula

159 Overexpression of SMAD2 attenuated cardiomyocyte hypertrophy similar to GDF15 treatment, wh

160 cell nuclear antigen expression and induces cardiomyocyte hypertrophy, suggesting that p66Shc exerts

161 miR-21* as a paracrine signaling mediator of cardiomyocyte hypertrophy that has potential as a therap

162 We demonstrate that TRPC promotes cardiomyocyte hypertrophy through activation of calcineu

163 Here, we report tight control of cardiomyocyte hypertrophy through miR-378.

164 In early-stage hypertensive HFpEF, LA cardiomyocyte hypertrophy, titin hyperphosphorylation, a

165 Here, we investigate the contribution of cardiomyocyte hypertrophy to cardiac chamber emergence,

166 The effect of beta-adrenergic signalling on cardiomyocyte hypertrophy underwent a developmental tran

167 neurin, MAPK, and PKC isoforms in regulating cardiomyocyte hypertrophy using three separate approache

168 rticularly PDE1A, in regulating pathological cardiomyocyte hypertrophy via a cGMP/PKG-dependent mecha

169 shown that dysbindin is a potent inducer of cardiomyocyte hypertrophy via activation of Rho-dependen

170 the local Ca2+ signals involved in reactive cardiomyocyte hypertrophy via calcineurin regulation.

171 rovide the first evidence that IL-18 induces cardiomyocyte hypertrophy via PI3K-dependent signaling,

172 Since phenylephrine stimulates cardiomyocyte hypertrophy via protein kinase C (PKC), th

173 behavior during chamber emergence: although cardiomyocyte hypertrophy was prevalent, many cells did

174 Compensatory cardiomyocyte hypertrophy was reduced in border and remo

175 Cardiomyocyte hypertrophy was stimulated with AngII or v

176 ed as a potent paracrine factor that induces cardiomyocyte hypertrophy when shuttled through exosomes

177 r PKC alpha as a mediator of agonist-induced cardiomyocyte hypertrophy, whereas dominant negative PKC

178 cardiac fibrosis and pathological growth of cardiomyocytes (hypertrophy), which contribute to heart

179 Our data identify miR-378 as a regulator of cardiomyocyte hypertrophy, which exerts its activity by

180 Furthermore, we demonstrate that cardiomyocyte hypertrophy, which is initiated by live in

181 ependent hypertrophic response and can blunt cardiomyocyte hypertrophy, which may have important impl

182 ammation resulted in attenuated fibrosis and cardiomyocyte hypertrophy, which thereby improved global

183 E2 replacement limited TAC-induced LV and cardiomyocyte hypertrophy while attenuating deterioratio

184 Finally, induction of cardiomyocyte hypertrophy with an activated MEK1-express

185 a catalytically inactive PTEN mutant led to cardiomyocyte hypertrophy, with increased protein synthe