ライフサイエンスコーパス: hypertrophy

1 cular formation and attenuated cardiomyocyte hypertrophy).

2 in reducing myofiber strain associated with hypertrophy.

3 organ growth occurring through cardiomyocyte hypertrophy.

4 that targets SP1 and inhibits cardiomyocytes hypertrophy.

5 ell fusion during physiological adult muscle hypertrophy.

6 am for cardiomyocyte homeostasis and cardiac hypertrophy.

7 inconsistently linked with left ventricular hypertrophy.

8 a clinically relevant large animal model of hypertrophy.

9 and increases its expression during cardiac hypertrophy.

10 nalogs for treatment of pathological cardiac hypertrophy.

11 tion of excess collagen synthesis in cardiac hypertrophy.

12 increased significantly in overload-induced hypertrophy.

13 IRT1-regulated pathways and overload-induced hypertrophy.

14 ncomitant with ameliorated cardiac and renal hypertrophy.

15 ator, is critical for stress-induced cardiac hypertrophy.

16 hologic (i.e., pressure overload) myocardial hypertrophy.

17 n the dynamic adaptation of cardiac cells to hypertrophy.

18 ures, cardiac fibrosis, and left ventricular hypertrophy.

19 ing development of pressure overload-induced hypertrophy.

20 c remodeling, failed to attenuate Cpt2M(-/-) hypertrophy.

21 howed stress-induced nucleus accumbens (NAc) hypertrophy.

22 e hypertrophy while IHH promoted chondrocyte hypertrophy.

23 ced the fetal gene program and cardiomyocyte hypertrophy.

24 ression and improves cardiac function during hypertrophy.

25 bosome biogenesis central to skeletal muscle hypertrophy.

26 274L, N276S, and D326N failed to rescue this hypertrophy.

27 togenic diet, yet it did not improve cardiac hypertrophy.

28 ty and cardiac contractility without causing hypertrophy.

29 ved a complete reduction of overload-induced hypertrophy.

30 isplay diffuse myocarditis with fibrosis and hypertrophy.

31 thickness, as well as increased chondrocyte hypertrophy.

32 sin II (Ang II)-induced pathological cardiac hypertrophy.

33 reexpression of fetal genes and pathological hypertrophy.

34 pposite metabolic phenotype due to adipocyte hypertrophy.

35 ceptor (IP3R) affects progression to cardiac hypertrophy.

36 % black, and 11% (n=142) baseline concentric hypertrophy.

37 n a number of diseases, including myocardial hypertrophy.

38 es, heart failure, myocardial ischaemia, and hypertrophy.

39 factors necessary for gene transcription and hypertrophy.

40 ther increase in cardiac mass is achieved by hypertrophy.

41 l negative regulator of pathological cardiac hypertrophy.

42 arization, and amelioration of apoptosis and hypertrophy.

43 trial natriuretic peptide message of cardiac hypertrophy.

44 reased calcineurin/NFAT signaling in myocyte hypertrophy.

45 s is sufficient to ensure long-term myofiber hypertrophy.

46 es respond to AC progression by pathological hypertrophy.

47 icular systolic pressure and right ventricle hypertrophy.

48 o the investigation of aging-related cardiac hypertrophy.

49 erload promotes oxidative stress and cardiac hypertrophy.

50 entions in aging- and stress-induced cardiac hypertrophy.

51 tunnel EVH displayed the lowest longitudinal hypertrophy (1% versus 13.5% versus 3%; P=0.001).

52 .001), attenuated the development of cardiac hypertrophy (-14+/-6% heart weight/tibia length; P<0.05)

53 Pathological cardiac hypertrophy, a dynamic remodeling process, is a major ri

54 adigm of the progression of left ventricular hypertrophy, a thick-walled left ventricle (LV) ultimate

55 ss of SRC-2 (SRC-2 CKO) results in a blunted hypertrophy accompanied by a rapid, progressive decrease

56 Ras proteins are thought to promote cardiac hypertrophy, an important risk factor for cardiovascular

57 Left ventricular (LV) hypertrophy and abnormal myocardial strain predict morta

58 llite cell activity and muscle repair during hypertrophy and aging.

59 elated processes like myocarditis, fibrosis, hypertrophy and arrhythmia.

60 Cardiac hypertrophy and associated heart fibrosis remain a major

61 thood myogenesis (regeneration) and myofibre hypertrophy and atrophy, processes associated with muscl

62 ardiac dysfunction, characterized by reduced hypertrophy and biomarkers of fibrosis, remodeling, infl

63 al transduction, and its knockdown repressed hypertrophy and calcineurin/NFAT activity.

64 ts to detect myocardial deformation, cardiac hypertrophy and capillary density via non-invasive imagi

65 tify PABPC1 as a direct regulator of cardiac hypertrophy and define a new paradigm of gene regulation

66 atal cardiomyoblasts resulted in ventricular hypertrophy and dilation, supporting a functional requir

67 histological features of HCM include myocyte hypertrophy and disarray, as well as interstitial fibros

68 onokiol exerts beneficial effects on cardiac hypertrophy and doxorubicin (Dox)-cardiotoxicity via dea

69 w that Herpud1-knockout mice exhibit cardiac hypertrophy and dysfunction and that decreased Herpud1 p

70 in wild-type mice protected against cardiac hypertrophy and dysfunction in vivo.

71 them to pressure overload to induce cardiac hypertrophy and dysfunction.

72 epigenetic regulator at the onset of cardiac hypertrophy and enables an improved understanding about

73 -Ras in modulating stress-induced myocardial hypertrophy and failure.

74 MT1/2 was sufficient to promote pathological hypertrophy and fetal gene reexpression, while suppressi

75 Sirt2 knockout markedly exaggerated cardiac hypertrophy and fibrosis and decreased cardiac ejection

76 ed the hearts against Ang II-induced cardiac hypertrophy and fibrosis and rescued cardiac function.

77 lays a crucial role in stress/injury-induced hypertrophy and fibrosis development that can ultimately

78 cy increased cardiac necrosis, inflammation, hypertrophy and fibrosis following MI, accompanied by ex

79 Chronic cardiac stress induces pathologic hypertrophy and fibrosis of the myocardium.

80 of platelets, and the development of cardiac hypertrophy and fibrosis.

81 ) mice with Angiotensin II induced extensive hypertrophy and fibrotic cardiomyopathy, with increased

82 GDF8 inhibition, leads to pronounced muscle hypertrophy and force production in mice and monkeys.

83 t mechano-sensors are integrated to modulate hypertrophy and gene expression in cardiomyocytes remain

84 tening pathological conditions, like cardiac hypertrophy and heart failure (HF).

85 and K-Ras have divergent effects on cardiac hypertrophy and heart failure in response to pressure ov

86 aortic constriction model of murine cardiac hypertrophy and heart failure over 5 weeks.

87 utic target in treating pathological cardiac hypertrophy and heart failure.

88 ve over 5 weeks in a murine model of cardiac hypertrophy and heart failure.

89 ed with numerous diseases, including cardiac hypertrophy and heart failure.

90 how that AGGF1 can effectively treat cardiac hypertrophy and heart failure.

91 attractive paradigm for treatment of cardiac hypertrophy and heart failure.Endoplasmic reticulum (ER)

92 nsequences of obesity-related adipose tissue hypertrophy and hyperplasia for health, critical pathway

93 lts in defects in muscle differentiation and hypertrophy and identify primary downstream targets: Igf

94 mouse hearts with pressure overload-induced hypertrophy and in human hearts with dilated cardiomyopa

95 eys, but manifested with concomitant cardiac hypertrophy and increased cardiac glycogen without appar

96 eliorates AngII-induced hypertension, medial hypertrophy and inflammation in vivo in mice.

97 iet-induced obesity (DIO) promotes adipocyte hypertrophy and inflammation, thereby contributing to me

98 and signaling Ca(2+) occurs in pathological hypertrophy and is central to myocyte remodeling.

99 oRNA-146a in cardiomyocytes provoked cardiac hypertrophy and left ventricular dysfunction in vivo, wh

100 tilage discs underwent progressive deep-zone hypertrophy and mineralization.

101 t the levels of miR1 and miR133a decrease in hypertrophy and negatively correlate with muscle mass, S

102 4-1 therapy significantly suppressed cardiac hypertrophy and progression to heart failure in both vit

103 sclerosis 2 (Tsc2) was sufficient to induce hypertrophy and proliferation, resulting in excessive gr

104 n a localized regeneration instead of global hypertrophy and proliferation.

105 the metformin-mediated reduction of cardiac hypertrophy and protection of cardiac function.

106 Furthermore, C1-Ten causes podocyte hypertrophy and proteinuria by increasing mTORC1 activit

107 ular systolic pressure and right ventricular hypertrophy and pulmonary vascular remodeling in monocro

108 knockout mice displayed attenuated astrocyte hypertrophy and reactive remodeling; astrocytes largely

109 A combination of cardiac hypertrophy and reduced capillary density likely contrib

110 that endurance exercise can attenuate muscle hypertrophy and strength but the mechanistic underpinnin

111 stopathologic findings of smooth muscle cell hypertrophy and stroma-like cells, consistently observed

112 tially enhances nephrocyte function, causing hypertrophy and subsequent cell death.

113 Cpt2M(-/-) mice developed cardiac hypertrophy and systolic dysfunction, evidenced by a 5-f

114 mice showed an increase in oxidative stress, hypertrophy and systolic dysfunction.

115 Gray matter hypertrophy and thickening were associated with hypoxemi

116 C was associated with increased pathological hypertrophy and with key abnormalities in both cardiac p

117 till generic descriptors, such as thickness (hypertrophy) and function (diastolic or systolic), which

118 tes aging-related and Ang II-induced cardiac hypertrophy, and blunts metformin-mediated cardioprotect

119 remodeling, such as fibrosis, cardiomyocyte hypertrophy, and calcium handling (Col1a2, Nppa, and Ser

120 reticulum stress-induced apoptosis, cardiac hypertrophy, and heart failure, providing an attractive

121 ed aging-/diet-associated obesity, adipocyte hypertrophy, and liver steatosis.

122 truction than G- probands, however, had more hypertrophy, and nonsustained ventricular tachycardia.

123 ey regulators of smooth muscle tone, cardiac hypertrophy, and other physiological processes.

124 ting heart failure, inhibits stretch-induced hypertrophy, and predict further efficacious pairs of dr

125 mice show HF diet-induced obesity, adipocyte hypertrophy, and present with non-alcoholic fatty liver

126 olved in metabolic regulation, activation of hypertrophy, and survival pathways.

127 Furthermore, these mice lacked eccentric hypertrophy, and their cardiomyocytes exhibited markedly

128 increases in myotube size, in type IIb fiber hypertrophy, and ultimately in muscle strength.

129 ction; arterial stiffening; left ventricular hypertrophy; and worsened metrics of diabetes, hypertens

130 of sudden cardiac death, and severe cardiac hypertrophy are major risk factors for sudden cardiac de

131 cardiomyocyte number and exaggerated cardiac hypertrophy, as indicated by increased septum thickness.

132 vel the mechanism of AA action in regressing hypertrophy-associated cardiac fibrosis by assigning a r

133 susceptible to isoproterenol-induced cardiac hypertrophy at both young and advanced ages.

134 that CPT2-deficient hearts are impervious to hypertrophy attenuators, that mitochondrial metabolism r

135 this pathway protected against pathological hypertrophy both in vitro and in mice.

136 Inhibition of Chronos induces myofiber hypertrophy both in vitro and in vivo, in part, through

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

138 odel for bile acid overload, display cardiac hypertrophy, bradycardia, and exercise intolerance.

139 uggest that STIM1 may play a role in cardiac hypertrophy, but its role in electrical and mechanical p

140 mTORC1 hyperactivation leads to podocyte hypertrophy, but the detailed mechanism of how mTORC1 ac

141 lity testing strategy using left ventricular hypertrophy by ECG, coronary artery calcium, N-terminal

142 nd underwent measurement of left ventricular hypertrophy by ECG, coronary artery calcium, N-terminal

143 SJYD suppressed hypertension-induced cardiac hypertrophy by inhibiting the expression of ERK pathway.

144 pud1 acts as a negative regulator of cardiac hypertrophy by regulating IP3R protein levels.

145 Moreover, G9a promoted cardiac hypertrophy by repressing antihypertrophic genes.

146 al overload model to induce plantaris muscle hypertrophy by surgically removing the soleus and gastro

147 s, such as undifferentiated left ventricular hypertrophy, cardio-oncology, aortic stenosis, and ische

148 with contractile dysfunction, cardiomyocyte hypertrophy, cardiomyocyte death, and N-terminal pro B-t

149 cardiovascular regulator involved in cardiac hypertrophy, cardiorenal fibrosis, and inflammation.

150 el of pressure overload-induced heart muscle hypertrophy caused by transverse aortic constriction (TA

151 KEY POINTS: At the cellular level cardiac hypertrophy causes remodelling, leading to changes in io

152 sed by macrophages clustered around enlarged hypertrophied, dead, and dying adipocytes, forming crown

153 ion and promoted a more pathological form of hypertrophy devoid of transcriptional activation of the

154 ft ventricular afterload leads to myocardial hypertrophy, diastolic dysfunction, cellular remodelling

155 l abnormalities, defined as left ventricular hypertrophy, dilation or dysfunction, or significant val

156 These data suggest that if concentric hypertrophy does progress to a dilated cardiomyopathy, s

157 uced cardiac stress induces left ventricular hypertrophy driven by increased cardiomyocyte mass.

158 tenuated the activation of SRF signaling and hypertrophy due to dysbindin, whereas TRIM24 promoted th

159 The heart hypertrophies during pregnancy, but its metabolic adapta

160 iomyocyte proliferation and to cardiomyocyte hypertrophy during embryonic development.

161 ed with increased LV fibrosis, cardiomyocyte hypertrophy, elevated NT-proBNP plasma levels, fluid and

162 Cardiac hypertrophy, fibrosis, and cardiac function were examine

163 inflammatory cardiomyopathy characterized by hypertrophy, fibrosis, and myocarditis.

164 turn lead to a reduction in cardiac injury, hypertrophy, fibrosis, remodeling, and systolic dysfunct

165 were associated with higher left ventricular hypertrophy, glycemic traits, interleukin 6, and circula

166 In hypertrophy, H3K9me2 was reduced following a miR-217-med

167 the molecular mechanism for skeletal muscle hypertrophy has been well studied, it still is not compl

168 ificance of this process during adult muscle hypertrophy has not been explored.

169 Inhibiting IF1 in the hypertrophied heart not only prevents cell death from ex

170 altered electromechanical properties of the hypertrophied heart.

171 Reduced fat oxidation in hypertrophied hearts coincides with a shift of carnitine

172 hypertensive patients with left ventricular hypertrophy (HTN LVH) and hypertensive patients without

173 Hypertensive left ventricular hypertrophy (HTN-LVH) is a leading cause of heart failur

174 ose tissue, possibly related to adipose cell hypertrophy, hypoxia, and/or intestinal leakage of bacte

175 Cardiac hypertrophy in 12-month old Hfe-deficient mice was consi

176 r matrix and the regulation of cardiomyocyte hypertrophy in a mouse model of heart fibrosis.

177 assay, and significantly ameliorated cardiac hypertrophy in cell culture studies and in animal models

178 daily rapamycin exposure failed to attenuate hypertrophy in Cpt2M(-/-) mice.

179 RH(1-44)NH2 attenuates phenylephrine-induced hypertrophy in H9c2 cardiac cells, adult rat ventricular

180 s, and reduced cell apoptosis, fibrosis, and hypertrophy in H9c2 cells.

181 our findings suggest that baseline cortical hypertrophy in medication-free patients likely represent

182 In vivo, MR-409 mitigated cardiac hypertrophy in mice subjected to transverse aortic const

183 muscle growth and overload-induced myofiber hypertrophy in mice.

184 on changes during the development of cardiac hypertrophy in mice.

185 ts protection against stress-induced cardiac hypertrophy in mice.

186 left ventricular dysfunction, fibrosis, and hypertrophy in naive recipient mice.

187 The pathogenesis of left ventricular hypertrophy in patients with CKD is incompletely underst

188 t muscle growth in mice, but less impressive hypertrophy in primates, including man.

189 o investigate the function of TNC in cardiac hypertrophy in response to pressure overload.

190 elopment of multi-cystic kidneys and cardiac hypertrophy in some mice.

191 r qualitatively similar activation profiles, hypertrophy in the anterior temporal region was associat

192 The atlas comparison revealed central gland hypertrophy in the Bx- subpopulation, resulting in signi

193 plasia that occurs much later than adipocyte hypertrophy in the development of obesity.

194 e in determining protein synthesis rates and hypertrophy in the heart.

195 s associated with improving behaviour, while hypertrophy in the precentral gyrus was associated with

196 (rRNA) production and IGF-1-mediated myotube hypertrophy in vitro Primary skeletal myotubes were trea

197 be a prerequisite for IGF-1-induced myotube hypertrophy in vitro.

198 3V)-expressing ECs that drives cardiomyocyte hypertrophy in vitro.

199 mediated/FAK-dependent initiation of myocyte hypertrophy in vivo Collectively, these findings identif

200 mice, knockdown of AK017368 promoted muscle hypertrophy in vivo RNA molecules of AK017368 acted mech

201 e increased wall thickness and cardiomyocyte hypertrophy in vivo.

202 models tested the association of concentric hypertrophy (increased LV mass and LV mass/volume(0.67))

203 ctional residual capacity, right ventricular hypertrophy index, and total cell count in BALF.

204 Pathological cardiac hypertrophy induced by stresses such as aging and neuroh

205 The hypertrophy-inducing mammalian target of rapamycin compl

206 es considerable cardiac remodelling, such as hypertrophy, interstitial fibrosis, and abnormal activit

207 Cardiac hypertrophy (interventricular septum, 12+/-4 [7-23] mm;

208 Treated mice developed severe medial wall hypertrophy, intima proliferation, and various forms of

209 lum stress signaling pathway causing cardiac hypertrophy involves endoplasmic reticulum stress sensor

210 s commonly asymmetrical with the most severe hypertrophy involving the basal interventricular septum.

211 Hypertrophy is a prominent feature of damaged podocytes

212 In contrast, physiologically induced hypertrophy is adaptive, resulting in improved cardiac f

213 The hypertrophy is also frequently associated with left vent

214 Cardiac hypertrophy is an adaptive response triggered by patholo

215 Moreover, cardiomyocyte hypertrophy is blunted with cardiac fibroblast-specific

216 Cardiac hypertrophy is closely linked to impaired fatty acid oxi

217 Here, we report that FGF23-induced cardiac hypertrophy is reversible in vitro and in vivo upon remo

218 ) signaling, which is linked to pathological hypertrophy, is observed during AC progression, as evide

219 hs revealed concentric left ventricular (LV) hypertrophy, left atrial (LA) enlargement and dysfunctio

220 1(DT-cKO) mice) resulted in left ventricular hypertrophy (LVH) and decreased kidney expression of alp

221 arcomere mutations and left ventricular (LV) hypertrophy (LVH) are cardinal features of hypertrophic

222 iteria for the diagnosis of left ventricular hypertrophy (LVH) have low sensitivity.

223 ore lowering of the risk of left ventricular hypertrophy (LVH) in patients with hypertension and whet

224 owth and the development of left ventricular hypertrophy (LVH) in rodents.

225 idosis, asymmetrical septal left ventricular hypertrophy (LVH) was present in 79% of patients with AT

226 ically develop pathological left ventricular hypertrophy (LVH), which is reproduced in Raf1(L613V/+)

227 orse allograft function and left ventricular hypertrophy (LVH).

228 plays an important role in left ventricular hypertrophy (LVH).

229 Golgi stacks in the border cells have hypertrophied margins, reflecting elevated biosynthetic

230 strates, especially in the gray zone of mild hypertrophy (maximum wall thickness </=16 mm) or normal

231 nthase and GLUT4 levels were also induced in hypertrophied muscles, and SIRT1 levels correlated with

232 Hypertrophied myocytes had increased STIM1 expression an

233 Exposure of hypertrophied myocytes to the Orai channel blocker BTP2

234 Underestimation was because of focal LV hypertrophy (n=10; 10.3%) or poor acoustic windows (n=22

235 ergetic demand and cardiomyocyte size during hypertrophy necessitate increased fuel and oxygen delive

236 right ventricular hypokinesis, dilation, and hypertrophy observed on echocardiography, and 40% reduct

237 ortic constriction in which left ventricular hypertrophy occurred by 2 weeks without functional decli

238 n together, we demonstrate that pathological hypertrophy occurs in AC and is secondary to cardiomyocy

239 ations occurring in SBMA muscles and induced hypertrophy of both glycolytic and oxidative fibers.

240 ere, we show that miR-29 promotes pathologic hypertrophy of cardiac myocytes and overall cardiac dysf

241 ce underlies obesity and occurs through both hypertrophy of existing cells and increased differentiat

242 response is not required for IGF-1-mediated hypertrophy of human primary myotubes.

243 sorption of globally sclerotic glomeruli and hypertrophy of remaining nephrons.

244 well-defined borders, resembling congenital hypertrophy of retinal pigment epithelium (CHRPE) lesion

245 ay a crucial causal role in overload-induced hypertrophy of skeletal muscle.

246 d pathway, regulates anabolic process in the hypertrophy of skeletal muscle.

247 Other CT findings included hypertrophy of the bronchial arteries along the mediasti

248 s a genetic disorder characterized by marked hypertrophy of the myocardium.

249 gnaling in normal or cachectic mice leads to hypertrophy or prevention of muscle loss, perhaps sugges

250 Hypertrophy progresses further during the chronic diseas

251 ytes from physiologically and pathologically hypertrophied rat hearts, and correlated these marks wit

252 yclin D2 expression attenuated cardiomyocyte hypertrophy, reduced cardiomyocyte apoptosis, fibrosis,

253 ls, aged HCM females exhibited adrenal gland hypertrophy, reduced volume in mood-related brain region

254 e mechanisms underlying pathological cardiac hypertrophy remain largely unknown.

255 The I-BET drug restored the hypertrophy response suggesting that the non-response of

256 ulmonary inflammation totally inhibited this hypertrophy response under both normoxic and hypoxic con

257 histone acetylation signaling in the altered hypertrophy response.

258 angiogenesis, reduced fibrosis, and improved hypertrophy, resulting in improved cardiac function; how

259 contractility, and reduced RV stiffness, RV hypertrophy, RV fibrosis, RV inflammation, and RV alpha-

260 PPARalpha knockdown during AA treatment in hypertrophy samples, including angiotensin II-treated ad

261 Inhibition of these two ligands mimics the hypertrophy seen with broad TGF-beta blockers, while avo

262 upplying the area of the contact between the hypertrophied septum and the anterior leaflet of the mit

263 FG+ relatives with HCM had less hypertrophy, smaller left atria, and less systolic and d

264 K9me2 as a conserved feature of pathological hypertrophy that was associated with reexpression of fet

265 cardiomyocytes promote the progression from hypertrophy to heart failure in mice with increased pres

266 prevent or slow progression of pathological hypertrophy to heart failure.

267 Asymmetrical hypertrophy, traditionally associated with hypertrophic

268 letion in the heart (SRF(HKO)) or of cardiac hypertrophy triggered by transverse aorta constriction.

269 the pathogenesis of DKD by inducing podocyte hypertrophy under high glucose conditions.

270 lcineurin is known to be critical in cardiac hypertrophy under normoxia, but its role in the heart un

271 sification holds that chondrocytes mature to hypertrophy, undergo apoptosis and new bone forms by inv

272 er that is characterized by left ventricular hypertrophy unexplained by secondary causes and a nondil

273 Because coupling is maintained by hypertrophy until the end stage of the disease, when pro

274 effects of iron overload and age on cardiac hypertrophy using 1-, 5- and 12-month old Hfe-deficient

275 sbindin is a potent inducer of cardiomyocyte hypertrophy via activation of Rho-dependent serum-respon

276 subclinical myocardial deformation, cardiac hypertrophy via elevated expression of pro-hypertrophic

277 st-translational regulation of dysbindin and hypertrophy via TRIM24 and TRIM32 and show the importanc

278 erited myocardial disease defined by cardiac hypertrophy (wall thickness >/=15 mm) that is not explai

279 VEDV in those with versus without concentric hypertrophy was 1 mL (-9 to 12) versus -2 mL (-11 to 7),

280 sion was blunted in PAI-1(-/-) mice, cardiac hypertrophy was accelerated.

281 Cardiac hypertrophy was also induced by Ang II (1.3 mg/kg/d for

282 f interval myocardial infarction, concentric hypertrophy was associated with a small, but significant

283 ein analysis indicated that this substantial hypertrophy was associated with both the complete inhibi

284 ariable linear regression models, concentric hypertrophy was associated with larger follow-up LVEDV (

285 beta-oxidation through beta-catenin, whereas hypertrophy was dependent on mammalian target of rapamyc

286 METHODS AND Cardiac hypertrophy was induced by slow progressive pressure ove

287 tes, CBS and miR-133a were downregulated and hypertrophy was induced.

288 Muscle hypertrophy was initiated by bilateral ablation of soleu

289 At month 24, left ventricular hypertrophy was present in 41.7% versus 37.7% of everoli

290 Analyses indicated that hypertrophy was primarily driven by an increase in prote

291 progressive left ventricular dilatation and hypertrophy, whereas adoptive transfer of splenic CD4(+)

292 B men >30 years of age had left ventricular hypertrophy, which was mainly asymmetrical, and had simi

293 ature chondrocytes but inhibited chondrocyte hypertrophy while IHH promoted chondrocyte hypertrophy.

294 22 deficiency resulted in thymic and splenic hypertrophy, while excessive IL-22 induced atrophy in th

295 that wild-type PTEN can rescue the neuronal hypertrophy, while PTEN H93R, F241S, D252G, W274L, N276S

296 s, particularly younger patients with severe hypertrophy, who do not uniformly experience complete re

297 eases in cardiac afterload result in myocyte hypertrophy with changes in myocyte electrical and mecha

298 ase in the severity of left ventricular (LV) hypertrophy, with a concentric rather than asymmetric ap

299 atients showed asymmetrical left ventricular hypertrophy, with maximal left ventricular thickness in

300 /endocardial (EC) Raf1(L613V) causes cardiac hypertrophy without affecting contractility.