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

1 roved microvascular formation and attenuated cardiomyocyte hypertrophy).

2 a causal role of elevated aspartate level in cardiomyocyte hypertrophy.

3 le for m6A methylation in the development of cardiomyocyte hypertrophy.

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

5 after pressure overload results mainly from cardiomyocyte hypertrophy.

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

7 differentiation, a program with parallels to cardiomyocyte hypertrophy.

8 feration and vascular density, and decreased cardiomyocyte hypertrophy.

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

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

11 cate increased RAS signaling in pathological cardiomyocyte hypertrophy.

12 s of the epigenetic program for pathological cardiomyocyte hypertrophy.

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

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

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

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

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

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

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

20 ces agonist-induced calcineurin activity and cardiomyocyte hypertrophy.

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

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

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

24 actory to hypertrophic signaling and inhibit cardiomyocyte hypertrophy.

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

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

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

28 th subsequent organ growth occurring through cardiomyocyte hypertrophy.

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

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

31 sis and protein accumulation associated with cardiomyocyte hypertrophy.

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

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

34 ription during contraction-mediated neonatal cardiomyocyte hypertrophy.

35 protein kinase II phosphorylation of CREB in cardiomyocyte hypertrophy.

36 drugs and downstream pathways that modulate cardiomyocyte hypertrophy.

37 DNA synthesis pathways play a direct role in cardiomyocyte hypertrophy.

38 45), indicating reduced myocardial edema and cardiomyocyte hypertrophy.

39 4 protein levels and increased resistance to cardiomyocyte hypertrophy.

40 lactylation suppressed phenylephrine-induced cardiomyocyte hypertrophy.

41 ine osmolality, increased pulse pressure and cardiomyocyte hypertrophy.

42 m mishandling, ventricular fibrillation, and cardiomyocyte hypertrophy.

43 ft ventricle volume increases as a result of cardiomyocyte hypertrophy.

44 ered in a previous compound screen attenuate cardiomyocyte hypertrophy.

45 protein kinase II phosphorylation of CREB in cardiomyocyte hypertrophy.

46 constriction as a model of pressure overload cardiomyocyte hypertrophy.

47 xpression induced the fetal gene program and cardiomyocyte hypertrophy.

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

49 macitentan decreased the aldosterone-induced cardiomyocyte hypertrophy.

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

51 n the LV weight-to-tibia length ratio due to cardiomyocyte hypertrophy.

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

53 ckdown of PRMT5 induced GATA4 activation and cardiomyocyte hypertrophy.

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

55 regulated during myocyte differentiation and cardiomyocyte hypertrophy.

56 aling is necessary and sufficient to promote cardiomyocyte hypertrophy.

57 t of apoptotic caspase pathways in mediating cardiomyocyte hypertrophy.

58 ssment of extracellular matrix expansion and cardiomyocyte hypertrophy.

59 be both necessary and sufficient to repress cardiomyocyte hypertrophy.

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

61 ied nitrogen for nucleotide synthesis during cardiomyocyte hypertrophy.

62 resonance provides a noninvasive measure of cardiomyocyte hypertrophy.

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

64 eart growth involves primarily physiological cardiomyocyte hypertrophy.

65 pivotal point linking sustained overload to cardiomyocyte hypertrophy.

66 te several cardiac genes and stretch-induced cardiomyocyte hypertrophy.

67 rexpression of CIP repressed agonist-induced cardiomyocyte hypertrophy.

68 the regulation of cellular responses such as cardiomyocyte hypertrophy.

69 se chain reaction analysis confirmed reduced cardiomyocyte hypertrophy.

70 5 inhibits cardiac fetal gene expression and cardiomyocyte hypertrophy.

71 screen for previously unknown regulators of cardiomyocyte hypertrophy.

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

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

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

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

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

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

78 Furthermore, IL-21 could directly induce cardiomyocyte hypertrophy and apoptosis and exacerbate I

79 Cardiomyocyte hypertrophy and apoptosis have been implic

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

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

82 g, likely contributing to conditions such as cardiomyocyte hypertrophy and apoptosis.

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

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

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

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

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

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

89 The P710R mutation also caused cardiomyocyte hypertrophy and cytoskeletal remodeling as

90 Cardiomyocyte hypertrophy and ERK activation were also i

91 Cardiomyocyte hypertrophy and extracellular matrix remod

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

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

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

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

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

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

98 rmalized heart and left ventricular weights, cardiomyocyte hypertrophy and interstitial fibrosis furt

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

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

101 The development of posttransplant cardiomyocyte hypertrophy and myocardial fibrosis likely

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

103 Finally, AKAP6 is required for cardiomyocyte hypertrophy and osteoclast bone resorption

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

105 rtmentalized Gbetagamma signaling attenuates cardiomyocyte hypertrophy and prostate tumorigenesis, in

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

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

108 Six1 induced cardiomyocyte hypertrophy and skeletal muscle gene expre

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

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

111 ac pathology and that diastolic dysfunction, cardiomyocyte hypertrophy, and cardiac phospholamban pho

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

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

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

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

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

117 emodeling, decreased myocardial fibrosis and cardiomyocyte hypertrophy, and improved LV systolic func

118 t leads to rupturing of cardiac capillaries, cardiomyocyte hypertrophy, and pathological cardiac remo

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

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

121 d with adverse remodeling, including loss of cardiomyocytes, hypertrophy, and alterations in cell-cel

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

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

124 Additionally, cardiomyocytes hypertrophy, augmented myocyte apoptosis,

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

126 While Dex triggered cardiomyocyte hypertrophy, Beta promoted a decrease in c

127 A methylase METTL3 was sufficient to promote cardiomyocyte hypertrophy both in vitro and in vivo.

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

129 Inhibition of cardiomyocyte hypertrophy by CHAMP requires the conserve

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

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

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

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

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

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

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

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

138 usive whether substrate metabolism regulates cardiomyocyte hypertrophy directly or via a secondary ef

139 Cardiomyocyte hypertrophy downstream of Gq-coupled recep

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

141 cardiac function and energetics, and reduces cardiomyocyte hypertrophy during cardiac stresses.

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

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

144 This pathway impeded uncontrolled cardiomyocyte hypertrophy during pregnancy, and mice wit

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

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

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

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

149 PMCA4b overexpression inhibited cultured cardiomyocyte hypertrophy following agonist stimulation,

150 They also had cardiomyocyte hypertrophy, glomerulomegaly, and tubular

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

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

153 Further, escitalopram reduced cardiomyocyte hypertrophy in a mouse model of hypertroph

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

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

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

157 n capillary dysfunction and TNFalpha driving cardiomyocyte hypertrophy in CKD, which was validated in

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

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

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

161 demonstrated that diastolic dysfunction and cardiomyocyte hypertrophy in preclinical HFpEF were T ce

162 -9 in RAS function we assessed its action in cardiomyocyte hypertrophy in rat neonatal H9c2 and prima

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

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

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

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

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

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

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

170 ice induced left ventricular dysfunction and cardiomyocyte hypertrophy in uninjured mice without TAC.

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

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

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

174 cardiac, renal, and fat cells and inhibited cardiomyocyte hypertrophy in vitro.

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

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

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

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

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

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

181 During neonatal cardiomyocyte hypertrophy induced by norepinephrine or s

182 zation and tubular membrane proliferation in cardiomyocyte hypertrophy induced by pressure overload.

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

184 These groups with maladapted RVs had marked cardiomyocyte hypertrophy, interstitial fibrosis, and ca

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

186 hallmark features of the disease, including cardiomyocyte hypertrophy, interstitial fibrosis, and le

187 Cardiomyocyte hypertrophy is a complex cellular behavior

188 Cardiomyocyte hypertrophy is a critical precursor to the

189 Cardiomyocyte hypertrophy is a key clinical predictor of

190 Moreover, cardiomyocyte hypertrophy is blunted with cardiac fibrob

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

192 Although cardiomyocyte hypertrophy is often associated with these

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

194 Cardiomyocyte hypertrophy is the cellular response that

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

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

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

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

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

200 In the murine model, cardiomyocyte hypertrophy positively correlated with 2 u

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

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

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

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

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

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

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

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

209 dated a logic-based systems biology model of cardiomyocyte hypertrophy that, for the first time, inco

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

211 ass IIa histone deacetylases (HDACs) repress cardiomyocyte hypertrophy through association with the p

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

213 oves mitochondrial abnormalities and reduces cardiomyocyte hypertrophy through regulation of the nduf

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

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

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

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

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

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

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

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

222 in vivo, while Tgfb2 overexpression promoted cardiomyocyte hypertrophy via PI3K/AKT/mTOR (mechanistic

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

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

225 Compensatory cardiomyocyte hypertrophy was reduced in border and remo

226 Cardiomyocyte hypertrophy was stimulated with AngII or v

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

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

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

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

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

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

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

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

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

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