ライフサイエンスコーパス: cardiac hypertrophy

1 a context-specific model of beta-adrenergic cardiac hypertrophy.

2 various in vivo models of human pathological cardiac hypertrophy.

3 evated atrial natriuretic peptide message of cardiac hypertrophy.

4 ic regulator, is critical for stress-induced cardiac hypertrophy.

5 fed a ketogenic diet, yet it did not improve cardiac hypertrophy.

6 s a novel negative regulator of pathological cardiac hypertrophy.

7 jected to the investigation of aging-related cardiac hypertrophy.

8 iron overload promotes oxidative stress and cardiac hypertrophy.

9 c interventions in aging- and stress-induced cardiac hypertrophy.

10 al program for cardiomyocyte homeostasis and cardiac hypertrophy.

11 ARalpha) and increases its expression during cardiac hypertrophy.

12 of its analogs for treatment of pathological cardiac hypertrophy.

13 amelioration of excess collagen synthesis in cardiac hypertrophy.

14 angiotensin II (Ang II)-induced pathological cardiac hypertrophy.

15 phate receptor (IP3R) affects progression to cardiac hypertrophy.

16 constitute a therapeutic target to regulate cardiac hypertrophy.

17 al delay, intellectual disability as well as cardiac hypertrophy.

18 act significantly reduced blood pressure and cardiac hypertrophy.

19 key role in the development of pathological cardiac hypertrophy.

20 itors improved contractility and ameliorated cardiac hypertrophy.

21 al to deactivate a key negative regulator of cardiac hypertrophy.

22 ), which is necessary for the development of cardiac hypertrophy.

23 at the promoter regions of genes involved in cardiac hypertrophy.

24 hypertrophy but also reverses preestablished cardiac hypertrophy.

25 of NSML-associated SHP2 induced adult-onset cardiac hypertrophy.

26 ided evidence that these loci play a role in cardiac hypertrophy.

27 switch, angiotensin I-to-II conversion, and cardiac hypertrophy.

28 ing in response to pressure overload-induced cardiac hypertrophy.

29 ocardia phenotype and amplified pathological cardiac hypertrophy.

30 c gene transcription leading to pathological cardiac hypertrophy.

31 eoglycan previously described as a marker of cardiac hypertrophy.

32 h variable severity, which may co-occur with cardiac hypertrophy.

33 rmacologically and pressure overload-induced cardiac hypertrophy.

34 e of RNA polymerase II, respectively, during cardiac hypertrophy.

35 higher systolic blood pressure, and signs of cardiac hypertrophy.

36 lysis on the development of exercise-induced cardiac hypertrophy.

37 that angiotensin II receptor blockers reduce cardiac hypertrophy.

38 jury and prevented pressure overload-induced cardiac hypertrophy.

39 s that drives the increase of biomass during cardiac hypertrophy.

40 roteins associated with energy metabolism in cardiac hypertrophy.

41 specialized versus housekeeping genes during cardiac hypertrophy.

42 rmacologically and pressure overload-induced cardiac hypertrophy.

43 nd function in a mouse model of pathological cardiac hypertrophy.

44 into new-found crosstalks in beta-adrenergic cardiac hypertrophy.

45 plasia, pulmonary arterial hypertension, and cardiac hypertrophy.

46 e cardiomyocyte cytoplasm, where it promotes cardiac hypertrophy.

47 ainst pressure overload-induced pathological cardiac hypertrophy.

48 , von Willebrand factor(vWF), and CD31 after cardiac hypertrophy.

49 xidative stress response, cell survival, and cardiac hypertrophy.

50 AS variants on pathogenesis of NS-associated cardiac hypertrophy.

51 overlapping and distinct roles in modulating cardiac hypertrophy.

52 d in various age-related pathologies such as cardiac hypertrophy.

53 g pathogenic MRAS variants, displayed severe cardiac hypertrophy.

54 clear translocation of GRK5 and promotion of cardiac hypertrophy.

55 ment suppressed CKD-induced hypertension and cardiac hypertrophy.

56 and HDAC9 are not required for inhibition of cardiac hypertrophy.

57 d RNA-binding protein Lin28a in pathological cardiac hypertrophy.

58 cellular pathway signaling characteristic of cardiac hypertrophy.

59 down Pck2 attenuated norepinephrine-induced cardiac hypertrophy.

60 efine an in vitro phenotype of MRAS-mediated cardiac hypertrophy.

61 pathogenicity of p.Gly23Val-MRAS in NS with cardiac hypertrophy.

62 =29; P<0.001), attenuated the development of cardiac hypertrophy (-14+/-6% heart weight/tibia length;

63 Pathological cardiac hypertrophy, a dynamic remodeling process, is a

64 due to pressure overload led to accelerated cardiac hypertrophy, accompanied by "super"-induction of

65 Compensatory cardiac hypertrophy activates ER stress and ATF6, which

66 ptor-associated microdomains occurs in early cardiac hypertrophy, affects cGMP-mediated contractility

67 lectin-3 knockout mice exhibited accelerated cardiac hypertrophy after 7 days of pressure overload, w

68 determinant of the progression of pathologic cardiac hypertrophy after aortic banding in mice.

69 erestingly, Tsg101-KD mice failed to develop cardiac hypertrophy after intense treadmill training.

70 general, Ras proteins are thought to promote cardiac hypertrophy, an important risk factor for cardio

71 ncreased titin phosphorylation and prevented cardiac hypertrophy and a decline in diastolic function,

72 njection of Ad-Nur77 substantially inhibited cardiac hypertrophy and ameliorated cardiac dysfunction

73 Cardiac hypertrophy and associated heart fibrosis remain

74 ike diabetes, atherosclerosis, hypertension, cardiac hypertrophy and atrial fibrillation, are also br

75 e patients to detect myocardial deformation, cardiac hypertrophy and capillary density via non-invasi

76 ir skeletal muscle and reverses pathological cardiac hypertrophy and cardiac dysfunction.

77 echocardiographic analysis revealed massive cardiac hypertrophy and chamber dilation, albeit with in

78 clerosis, damage from ischaemia-reperfusion, cardiac hypertrophy and decompensated heart failure.

79 ngs identify PABPC1 as a direct regulator of cardiac hypertrophy and define a new paradigm of gene re

80 ical features of diabetic cardiomyopathy are cardiac hypertrophy and diastolic dysfunction, which lea

81 the heart that harmonizes the progression of cardiac hypertrophy and dilation.

82 nt (Carabin(-/-)) mice developed exaggerated cardiac hypertrophy and displayed a strong decrease in f

83 e that Honokiol exerts beneficial effects on cardiac hypertrophy and doxorubicin (Dox)-cardiotoxicity

84 o determine the mechanistic role of STIM1 in cardiac hypertrophy and during the transition to heart f

85 and FYN-deficient mice displayed exacerbated cardiac hypertrophy and dysfunction and increased ROS pr

86 ults show that Herpud1-knockout mice exhibit cardiac hypertrophy and dysfunction and that decreased H

87 of DLST in wild-type mice protected against cardiac hypertrophy and dysfunction in vivo.

88 TAC-induced cardiac hypertrophy and dysfunction was mitigated in MHC

89 ation in the diabetic hearts correlated with cardiac hypertrophy and dysfunction, suggesting a potent

90 ubjected them to pressure overload to induce cardiac hypertrophy and dysfunction.

91 f pressure overload substantially attenuates cardiac hypertrophy and dysfunction.

92 on, TP-10 is able to reverse pre-established cardiac hypertrophy and dysfunction.

93 ncoding epigenetic regulator at the onset of cardiac hypertrophy and enables an improved understandin

94 ard K(+) current (Ito) is well documented in cardiac hypertrophy and failure both in animal models an

95 tablished model of pressure overload-induced cardiac hypertrophy and failure in mice.

96 ng tissue ischemia and reperfusion injuries, cardiac hypertrophy and failure, and cancer progression.

97 estosterone contribute to the development of cardiac hypertrophy and failure.

98 Sirt2 knockout markedly exaggerated cardiac hypertrophy and fibrosis and decreased cardiac e

99 on of miR-29 or antimiR-29 infusion prevents cardiac hypertrophy and fibrosis and improves cardiac fu

100 cent cells using senolytic drugs ameliorated cardiac hypertrophy and fibrosis and may inform novel ap

101 protected the hearts against Ang II-induced cardiac hypertrophy and fibrosis and rescued cardiac fun

102 wide association study for genes influencing cardiac hypertrophy and fibrosis in a large panel of inb

103 anced infarct neovascularization, diminished cardiac hypertrophy and fibrosis, altered metabolic enzy

104 om a transaortic-constriction mouse model of cardiac hypertrophy and fibrosis, and from a heart-on-a-

105 gical analysis revealed only mild effects on cardiac hypertrophy and fibrosis, but a significant incr

106 cy also provided dramatic protection against cardiac hypertrophy and fibrosis, hepatic steatosis, and

107 iency of GzmB reduced angiotensin II-induced cardiac hypertrophy and fibrosis, independently of perfo

108 29 in cardiac myocytes in vivo also prevents cardiac hypertrophy and fibrosis, indicating that the fu

109 s to HFpEF, including diastolic dysfunction, cardiac hypertrophy and fibrosis, pulmonary edema, and i

110 ctivity of platelets, and the development of cardiac hypertrophy and fibrosis.

111 hanced angiotensin II production, leading to cardiac hypertrophy and fibrosis.

112 t production of angiotensin II that promotes cardiac hypertrophy and fibrosis.

113 monstrates that Lin28a promotes pathological cardiac hypertrophy and glycolytic reprograming, at leas

114 fe-threatening pathological conditions, like cardiac hypertrophy and heart failure (HF).

115 has recently emerged as a key contributor of cardiac hypertrophy and heart failure but the relevance

116 that H- and K-Ras have divergent effects on cardiac hypertrophy and heart failure in response to pre

117 gements that occur during the development of cardiac hypertrophy and heart failure in well-defined mo

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

119 nder hemodynamic stress induces pathological cardiac hypertrophy and heart failure through persistent

120 Sike-deficient mice develop cardiac hypertrophy and heart failure, whereas Sike-over

121 CICR is disrupted in cardiac hypertrophy and heart failure, which is associat

122 associated with numerous diseases, including cardiac hypertrophy and heart failure.

123 therapeutic target in treating pathological cardiac hypertrophy and heart failure.

124 effective over 5 weeks in a murine model of cardiac hypertrophy and heart failure.

125 P, and show that AGGF1 can effectively treat cardiac hypertrophy and heart failure.

126 nt a therapeutic target for the treatment of cardiac hypertrophy and heart failure.

127 s been reported in pressure overload-induced cardiac hypertrophy and heart failure.

128 ttention as a possible therapeutic target in cardiac hypertrophy and heart failure.

129 s as a promising target for the treatment of cardiac hypertrophy and heart failure.

130 ly novel therapeutic strategy for preventing cardiac hypertrophy and heart failure.

131 ding an attractive paradigm for treatment of cardiac hypertrophy and heart failure.Endoplasmic reticu

132 ci (2 well-characterized genes implicated in cardiac hypertrophy and homeostasis) for enhanced transc

133 in cardiomyocytes that was downregulated in cardiac hypertrophy and human heart failure.

134 TAC surgery resulted in cardiac hypertrophy and impaired cardiac function.

135 ermline deletion of Grb14 in mice results in cardiac hypertrophy and impaired systolic function, whic

136 sociated virus gene therapy vector inhibited cardiac hypertrophy and improved systolic function after

137 olism for energy production, thus preventing cardiac hypertrophy and improving myocardial energetics.

138 sus monkeys, but manifested with concomitant cardiac hypertrophy and increased cardiac glycogen witho

139 MyBP-C dephosphorylation produced cardiac hypertrophy and increased wall thickness in MyBP

140 of microRNA-146a in cardiomyocytes provoked cardiac hypertrophy and left ventricular dysfunction in

141 The cardioGRKO mice spontaneously developed cardiac hypertrophy and left ventricular systolic dysfun

142 ed by left-ventricular systolic dysfunction, cardiac hypertrophy and myocardial fibrosis.

143 e remodeling, the concomitant attenuation of cardiac hypertrophy and oxidative stress allowed myocard

144 ure overload models substantially attenuated cardiac hypertrophy and pathological manifestations.

145 ation, which can be manipulated to attenuate cardiac hypertrophy and preserve cardiac function by imp

146 nd exerts cardioprotective effects, reducing cardiac hypertrophy and preserving diastolic function in

147 expressing phospho-ablated MyBP-C displayed cardiac hypertrophy and prevented full acceleration of p

148 re, VDR 4-1 therapy significantly suppressed cardiac hypertrophy and progression to heart failure in

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

150 veal that PMCA4 regulates the development of cardiac hypertrophy and provide proof of principle for a

151 A combination of cardiac hypertrophy and reduced capillary density likely

152 ansverse aortic constriction (TAC) developed cardiac hypertrophy and reduced ventricular function ass

153 s that drives physiological and pathological cardiac hypertrophy and remodeling, as well as the trans

154 rocess of pathological gene induction during cardiac hypertrophy and remodeling, but the underlying r

155 ed in old mice, indicating that aging causes cardiac hypertrophy and remodeling.

156 We found that YAP-CHKO mice had attenuated cardiac hypertrophy and significant increases in CM apop

157 insulin signaling and those associated with cardiac hypertrophy and stress including insulin recepto

158 206 in cardiomyocytes attenuated YAP-induced cardiac hypertrophy and survival, suggesting that miR-20

159 of a PDE9a inhibitor reverses preestablished cardiac hypertrophy and systolic dysfunction in mice sub

160 Cpt2M(-/-) mice developed cardiac hypertrophy and systolic dysfunction, evidenced

161 ling in animal models promotes hypertension, cardiac hypertrophy, and atherosclerosis.

162 n, promotes aging-related and Ang II-induced cardiac hypertrophy, and blunts metformin-mediated cardi

163 rdiomyopathy, characterized by hypertension, cardiac hypertrophy, and fibrosis, is a complication of

164 effects on the development of hypertension, cardiac hypertrophy, and fibrosis.

165 (TAC), a model for pressure overload-induced cardiac hypertrophy, and followed it by cancer cell impl

166 domain causes reduced contractile function, cardiac hypertrophy, and heart failure without changes i

167 oplasmic reticulum stress-induced apoptosis, cardiac hypertrophy, and heart failure, providing an att

168 d mitochondrial protein hyperacetylation and cardiac hypertrophy, and improved cardiac function in re

169 motes coronary arteriogenesis, physiological cardiac hypertrophy, and ischemia resistance, could be a

170 CS includes dilated vasculature, marked cardiac hypertrophy, and other cardiovascular abnormalit

171 s) are key regulators of smooth muscle tone, cardiac hypertrophy, and other physiological processes.

172 stent with lower risk for hepatic steatosis, cardiac hypertrophy, and premature death.

173 Concentric and eccentric cardiac hypertrophy are associated with pressure and vol

174 history of sudden cardiac death, and severe cardiac hypertrophy are major risk factors for sudden ca

175 patho-physiologies such as atherosclerosis, cardiac hypertrophy, arrhythmias, contractile dysfunctio

176 ease in cardiomyocyte number and exaggerated cardiac hypertrophy, as indicated by increased septum th

177 eart-enriched long noncoding (lnc)RNA, named cardiac-hypertrophy-associated epigenetic regulator (Cha

178 nd less susceptible to isoproterenol-induced cardiac hypertrophy at both young and advanced ages.

179 ice, a model for bile acid overload, display cardiac hypertrophy, bradycardia, and exercise intoleran

180 ging cell type crosstalk during pathological cardiac hypertrophy but also shed light on strategies fo

181 knockout mice developed a similar degree of cardiac hypertrophy but exhibited significantly improved

182 treatment did not prevent the development of cardiac hypertrophy, but did prevent the decline in left

183 eports suggest that STIM1 may play a role in cardiac hypertrophy, but its role in electrical and mech

184 have elevated Ca(2+) handling and increased cardiac hypertrophy, but RAD is expressed also in noncar

185 Many gene abnormalities are associated with cardiac hypertrophy, but their function in cardiac devel

186 ll population that can be regulated to treat cardiac hypertrophy by improving neovascularization and

187 sion of Nur77 markedly inhibited ISO-induced cardiac hypertrophy by inducing nuclear translocation of

188 usion, BSJYD suppressed hypertension-induced cardiac hypertrophy by inhibiting the expression of ERK

189 that Herpud1 acts as a negative regulator of cardiac hypertrophy by regulating IP3R protein levels.

190 Moreover, G9a promoted cardiac hypertrophy by repressing antihypertrophic genes

191 is a calcium (Ca(2+)) sensor that regulates cardiac hypertrophy by triggering store-operated Ca(2+)

192 master cardiovascular regulator involved in cardiac hypertrophy, cardiorenal fibrosis, and inflammat

193 KEY POINTS: At the cellular level cardiac hypertrophy causes remodelling, leading to chang

194 s mechanism is involved in the regulation of cardiac hypertrophy (CH), an antecedent condition to HF

195 Here we show that SUN2-null mice display cardiac hypertrophy coincident with enhanced AKT/MAPK si

196 In wild-type mice, cardiac hypertrophy, diastolic dysfunction (end diastoli

197 rease in mechanical load in the heart causes cardiac hypertrophy, either physiologically (heart devel

198 gated MYOCD siRNA resulted in attenuation of cardiac hypertrophy, fibrosis and restoration of the lef

199 Gfat1 exacerbates pressure overload-induced cardiac hypertrophy, fibrosis, and cardiac dysfunction.

200 Cardiac hypertrophy, fibrosis, and cardiac function were

201 a PDE10A-regualted transcriptome involved in cardiac hypertrophy, fibrosis, and cardiomyopathy.

202 encing showed beneficial effects by rescuing cardiac hypertrophy, fibrosis, size and function in a ca

203 Propionate significantly attenuated cardiac hypertrophy, fibrosis, vascular dysfunction, and

204 Development of physiologic cardiac hypertrophy has primarily been ascribed to the I

205 (HCM), a heritable disease characterized by cardiac hypertrophy, heart failure, and sudden cardiac d

206 in several diseases, including hypertensive cardiac hypertrophy, Hirschsprung disease and blood vess

207 heart, both lines developed WPW syndrome and cardiac hypertrophy; however, these effects were indepen

208 c mice treated with MK-0626 exhibited modest cardiac hypertrophy, impairment of cardiac function, and

209 Cardiac hypertrophy in 12-month old Hfe-deficient mice w

210 the progression of pressure overload-induced cardiac hypertrophy in a mouse model, we characterized t

211 inatal DDT exposure induces hypertension and cardiac hypertrophy in adult mice.

212 ys of transverse aortic banding that induced cardiac hypertrophy in adult mouse hearts and was also e

213 atal exposure to DDT causes hypertension and cardiac hypertrophy in adult offspring.

214 d provide a therapeutic approach to mitigate cardiac hypertrophy in cases of CS.

215 er gene assay, and significantly ameliorated cardiac hypertrophy in cell culture studies and in anima

216 s, which we have addressed here by analyzing cardiac hypertrophy in gene-targeted mice deficient in B

217 increases expression of molecular markers of cardiac hypertrophy in iPSC-CMs.

218 Deletion of Cul4a results in cardiac hypertrophy in male mice that can be partially r

219 In vivo, MR-409 mitigated cardiac hypertrophy in mice subjected to transverse aort

220 expression changes during the development of cardiac hypertrophy in mice.

221 and exerts protection against stress-induced cardiac hypertrophy in mice.

222 r tyrosine kinase, has been shown to inhibit cardiac hypertrophy in mice.

223 The development of cardiac hypertrophy in response to hemodynamic overload

224 dy was to investigate the function of TNC in cardiac hypertrophy in response to pressure overload.

225 interferon pathway, attenuates pathological cardiac hypertrophy in rodents and non-human primates in

226 d in development of multi-cystic kidneys and cardiac hypertrophy in some mice.

227 PDE2 emerges as a novel key regulator of cardiac hypertrophy in vitro and in vivo, and its inhibi

228 diomyocytes and in pressure overload-induced cardiac hypertrophy in vivo.

229 egulated RHEB, activated mTORC1, and induced cardiac hypertrophy in wild type mouse hearts but not in

230 27) showed less cardiac arrhythmogenesis and cardiac hypertrophy index compared to AV-Shunt(Scr).

231 loss of P2Y6 receptor enhanced pathological cardiac hypertrophy induced after isoproterenol injectio

232 icarboxylic acid (ATA) inhibits and reverses cardiac hypertrophy induced by pressure overload in mice

233 Pathological cardiac hypertrophy induced by stresses such as aging an

234 Using a rat model of cardiac hypertrophy induced by thoracic aortic banding,

235 ontributes to vasoconstriction, vascular and cardiac hypertrophy, inflammation, and to the developmen

236 f transcriptional regulation by FoxO1 during cardiac hypertrophy, information that is essential for i

237 d R wave amplitudes, sinus node dysfunction, cardiac hypertrophy, interstitial fibrosis, multi-focal

238 Cardiac hypertrophy (interventricular septum, 12+/-4 [7-

239 c reticulum stress signaling pathway causing cardiac hypertrophy involves endoplasmic reticulum stres

240 Pressure overload-induced pathological cardiac hypertrophy is a common predecessor of heart fai

241 Cardiac hypertrophy is a context-dependent phenomenon wh

242 Cardiac hypertrophy is a major risk factor for heart fai

243 Cardiac hypertrophy is an adaptive response triggered by

244 Cardiac hypertrophy is an early hallmark during the clin

245 Cardiac hypertrophy is closely linked to impaired fatty

246 Understanding cardiac hypertrophy is critical to comprehending the mec

247 The study of the mechanisms leading to cardiac hypertrophy is essential to better understand ca

248 NPPA and GATA4 is initiated and pathological cardiac hypertrophy is established.

249 Cardiac hypertrophy is often initiated as an adaptive re

250 Here, we report that FGF23-induced cardiac hypertrophy is reversible in vitro and in vivo u

251 e found that angiotensin II (Ang II)-induced cardiac hypertrophy is significantly reduced in mice def

252 However, aldosterone-induced cardiac hypertrophy is totally prevented in Grk5 KO mice

253 on of local Ca(2+) signaling in pathological cardiac hypertrophy is unclear.

254 senchymal-endothelial transition (MEndoT) in cardiac hypertrophy is unclear.

255 Thus, cardiac hypertrophy is uncoupled from profibrotic signal

256 transverse aortic constriction and in vitro cardiac hypertrophy models to characterize the role of a

257 overexpressing mice and in vivo and in vitro cardiac hypertrophy models to determine the essential re

258 Cardiac hypertrophy often causes impairment of cardiac f

259 alth and during pathological remodeling (eg, cardiac hypertrophy or failure) forms an exciting target

260 34a in male mice in settings of pathological cardiac hypertrophy or ischaemia protects the heart agai

261 hat absence of these lincRNAs did not affect cardiac hypertrophy or left ventricular function post-st

262 increase oxidative stress, or are linked to cardiac hypertrophy or neurodegenerative diseases in mam

263 with aging was associated with pathological cardiac hypertrophy (PCH) and restoring GDF11 to normal

264 These TG mice exhibited a physiologic-like cardiac hypertrophy phenotype at 8 wk evidenced by: 1) t

265 is both necessary and sufficient to elicit a cardiac hypertrophy phenotype in iPSC-CMs that includes

266 expression, we recapitulated the anticipated cardiac hypertrophy phenotype.

267 hypoplastic spleen, thymus, and bone marrow, cardiac hypertrophy, placental distress, and small size

268 rts partially rescued the cryoinjury-induced cardiac hypertrophy, promoted cardiomyocyte replication

269 ever, the mechanisms underlying pathological cardiac hypertrophy remain largely unknown.

270 Although pathological cardiac hypertrophy represents a leading cause of morbid

271 loration of the molecular causes of enhanced cardiac hypertrophy revealed significant activation of b

272 Pressure overload-induced cardiac hypertrophy, such as that caused by hypertension

273 inhibition of LCZ696 on cardiac fibrosis and cardiac hypertrophy than either stand-alone neprilysin i

274 fractional shortening associated with a mild cardiac hypertrophy that resorbed with age.

275 ed that activation of TAK1 promoted adaptive cardiac hypertrophy through a cross-talk between calcine

276 iomyocyte mechanosensor that is required for cardiac hypertrophy through a mechanism that involves st

277 as a novel positive regulator of physiologic cardiac hypertrophy through facilitating the FIP3-mediat

278 Tsg101 positively regulates physiologic-like cardiac hypertrophy through FIP3-mediated endosomal recy

279 sm in human and mouse models of pathological cardiac hypertrophy through hypoxia-inducible factor 1al

280 l negative regulator for the beta-AR-induced cardiac hypertrophy through inhibiting the NFATc3 and GA

281 perimental and genetic mouse models of human cardiac hypertrophy to identify transcripts revealing en

282 mportance of endothelial leptin signaling in cardiac hypertrophy, transverse aortic constriction was

283 ctor depletion in the heart (SRF(HKO)) or of cardiac hypertrophy triggered by transverse aorta constr

284 Calcineurin is known to be critical in cardiac hypertrophy under normoxia, but its role in the

285 ated the effects of iron overload and age on cardiac hypertrophy using 1-, 5- and 12-month old Hfe-de

286 op early subclinical myocardial deformation, cardiac hypertrophy via elevated expression of pro-hyper

287 s an inherited myocardial disease defined by cardiac hypertrophy (wall thickness >/=15 mm) that is no

288 hypertension was blunted in PAI-1(-/-) mice, cardiac hypertrophy was accelerated.

289 Cardiac hypertrophy was also induced by Ang II (1.3 mg/k

290 Cardiac hypertrophy was increased by voluntary exercise

291 METHODS AND Cardiac hypertrophy was induced by slow progressive pres

292 Volume-overload cardiac hypertrophy was produced in 7-day-old rabbits vi

293 pe switching, a key event at middle-stage of cardiac hypertrophy, was successfully targeted by Dapagl

294 Molecular markers of insulin signaling and cardiac hypertrophy were analyzed.

295 d m6A RNA methylation results in compensated cardiac hypertrophy, whereas diminished m6A drives eccen

296 lcineurin is a key regulator of pathological cardiac hypertrophy whose therapeutic targeting in heart

297 we present a novel pathway for pathological cardiac hypertrophy, whose inhibition is a long-term the

298 We found that db/db mice developed cardiac hypertrophy with normal cardiac function at 6 we

299 VMs is mediated by hyperadrenergic drive in cardiac hypertrophy, with functional effects on the chan

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