ライフサイエンスコーパス: cardiac hypertrophy

1 evated atrial natriuretic peptide message of cardiac hypertrophy.

2 itors improved contractility and ameliorated cardiac hypertrophy.

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

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

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

6 hypertrophy but also reverses preestablished cardiac hypertrophy.

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

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

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

10 s a novel negative regulator of pathological cardiac hypertrophy.

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

12 ocardia phenotype and amplified pathological cardiac hypertrophy.

13 c gene transcription leading to pathological cardiac hypertrophy.

14 eoglycan previously described as a marker of cardiac hypertrophy.

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

16 rmacologically and pressure overload-induced cardiac hypertrophy.

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

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

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

20 that angiotensin II receptor blockers reduce cardiac hypertrophy.

21 jury and prevented pressure overload-induced cardiac hypertrophy.

22 roteins associated with energy metabolism in cardiac hypertrophy.

23 specialized versus housekeeping genes during cardiac hypertrophy.

24 rmacologically and pressure overload-induced cardiac hypertrophy.

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

26 hearts subjected to volume overload-induced cardiac hypertrophy.

27 echanism of Shp2 inhibition that may promote cardiac hypertrophy.

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

29 ide a target to attenuate the development of cardiac hypertrophy.

30 vation suppresses Ang II-induced signals for cardiac hypertrophy.

31 regulation of miRNAs is poorly understood in cardiac hypertrophy.

32 s, which are critical for the development of cardiac hypertrophy.

33 TAT3 signaling, which has been implicated in cardiac hypertrophy.

34 e with insulin in signaling inflammation and cardiac hypertrophy.

35 iron overload promotes oxidative stress and cardiac hypertrophy.

36 ent work, we elucidated the role of Erbin in cardiac hypertrophy.

37 mildly increased arterial wall thickness and cardiac hypertrophy.

38 ng cardiac energy homeostasis and preventing cardiac hypertrophy.

39 fight-or-flight response and development of cardiac hypertrophy.

40 potential therapeutic target in pathological cardiac hypertrophy.

41 yopathy, characterized by muscle wasting and cardiac hypertrophy.

42 as a nuclear effector of insulin, promoting cardiac hypertrophy.

43 trol cell size are prominent in pathological cardiac hypertrophy.

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

45 al program for cardiomyocyte homeostasis and cardiac hypertrophy.

46 ARalpha) and increases its expression during cardiac hypertrophy.

47 of its analogs for treatment of pathological cardiac hypertrophy.

48 amelioration of excess collagen synthesis in cardiac hypertrophy.

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

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

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

52 constitute a therapeutic target to regulate cardiac hypertrophy.

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

54 act significantly reduced blood pressure and cardiac hypertrophy.

55 key role in the development of pathological cardiac hypertrophy.

56 =29; P<0.001), attenuated the development of cardiac hypertrophy (-14+/-6% heart weight/tibia length;

57 as a transcriptional repressor of pathologic cardiac hypertrophy, a direct role for the KLF family in

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

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

60 Cardiac hypertrophy accompanies many forms of heart dise

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

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

63 ession of NKA-alpha2 significantly decreased cardiac hypertrophy after pressure overload in mice at 2

64 natriuretic peptide/cGMP signaling in early cardiac hypertrophy after transverse aortic constriction

65 In a mild model of cardiac hypertrophy after transverse aortic constriction

66 Pathological cardiac hypertrophy (an increase in cardiac mass resulti

67 Cardiac hypertrophy, an adaptive process that responds t

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

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

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

71 Cardiac hypertrophy and associated heart fibrosis remain

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

73 not been reported despite its involvement in cardiac hypertrophy and cancer causation.

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

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

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

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

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

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

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

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

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

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

84 tate disease, potently reverses pathological cardiac hypertrophy and dysfunction in mice and might be

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

86 f pressure overload substantially attenuates cardiac hypertrophy and dysfunction.

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

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

89 Whereas Epac1 overexpression can lead to cardiac hypertrophy and Epac2 activation can be arrhythm

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

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

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

93 and implicates Carabin in the development of cardiac hypertrophy and failure.

94 ings on long noncoding RNAs and microRNAs in cardiac hypertrophy and failure.

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

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

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

98 he cause of Klotho deficiency, the extent of cardiac hypertrophy and fibrosis correlated tightly with

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

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

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

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

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

104 29 in cardiac myocytes in vivo also prevents cardiac hypertrophy and fibrosis, indicating that the fu

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

106 ndothelial dysfunction on the development of cardiac hypertrophy and fibrosis.

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

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

109 athetic activity in addition to unloading on cardiac hypertrophy and function.

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

111 Hyperinsulinemia contributes to cardiac hypertrophy and heart failure in patients with t

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

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

114 f InsP3R2 mRNA and protein expression during cardiac hypertrophy and heart failure is not known.

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

116 n signaling in the adult murine heart caused cardiac hypertrophy and heart failure, partially recapit

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

118 In arrhythmogenic conditions, such as cardiac hypertrophy and heart failure, Wnt signalling is

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

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

121 function and the development of pathological cardiac hypertrophy and heart failure.

122 l therapeutic approach for the prevention of cardiac hypertrophy and heart failure.

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

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

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

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

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

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

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

130 h heart failure is associated with decreased cardiac hypertrophy and improvements in both cardiac ins

131 -regulated in several experimental models of cardiac hypertrophy and in patients with heart failure.

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

133 nically exposed to isoproterenol showed less cardiac hypertrophy and increased threshold for arrhythm

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

135 Increased miR-206 expression induced cardiac hypertrophy and inhibited cell death in cultured

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

137 cardiomyopathy that involved a reduction in cardiac hypertrophy and lipotoxicity, adipose inflammati

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

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

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

141 tion of AMP-activated kinase in vivo rescued cardiac hypertrophy and prevented enhanced glycolytic fl

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

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

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

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

146 A combination of cardiac hypertrophy and reduced capillary density likely

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

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

149 shed pathological and physiological forms of cardiac hypertrophy and served as robust markers for the

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

151 ad box protein P1 attenuated miR-206-induced cardiac hypertrophy and survival, suggesting that Forkhe

152 206 in cardiomyocytes attenuated YAP-induced cardiac hypertrophy and survival, suggesting that miR-20

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

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

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

156 dystrophic mice also developed hypertension, cardiac hypertrophy, and cardiac dysfunction.

157 RyR2 interaction may occur in heart failure, cardiac hypertrophy, and catecholaminergic polymorphic v

158 rbin(-/-) mice rapidly develop decompensated cardiac hypertrophy, and following severe pressure overl

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

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

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

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

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

164 usion, Erbin is an inhibitor of pathological cardiac hypertrophy, and this inhibition is mediated, at

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

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

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

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

169 f miR-21* in a mouse model of Ang II-induced cardiac hypertrophy attenuated pathology.

170 ay be extrapolated to design novel drugs for cardiac hypertrophy based on this biased signal pathway.

171 lome for an adaptive (physiological) form of cardiac hypertrophy because of endurance exercise traini

172 compensated and decompensated (HF) forms of cardiac hypertrophy because of pressure overload.

173 glycoproteins in the discovery of potential cardiac hypertrophy biomarkers.

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

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

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

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

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

179 ew molecular co-mediator of exercise-induced cardiac hypertrophy by inducing nonproliferative cardiom

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

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

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

183 Moreover, G9a promoted cardiac hypertrophy by repressing antihypertrophic genes

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

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

186 Although TZD-induced cardiac hypertrophy (CH) has been attributed to an incre

187 infusion in wild type (WT) mice resulted in cardiac hypertrophy characterized by significant reducti

188 TAK1DeltaN transgenic mice developed greater cardiac hypertrophy compared with control mice after tra

189 Cardiac hypertrophy, coronary artery disease (CAD), coro

190 risingly and paradoxically, DKO mice develop cardiac hypertrophy driven by excessive activation of en

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

192 In this study, patients with HFpEF had more cardiac hypertrophy, epicardial CAD, coronary microvascu

193 eart failure in diabetics is associated with cardiac hypertrophy, fibrosis and diastolic dysfunction.

194 Cardiac hypertrophy, fibrosis, and cardiac function were

195 egulatable transgenic mouse model aggravated cardiac hypertrophy, fibrosis, and contractile dysfuncti

196 e heart disease and significantly attenuated cardiac hypertrophy, fibrosis, and contractile dysfuncti

197 Smad3 mediates diabetic cardiac hypertrophy, fibrosis, and diastolic dysfunction

198 fic EcSOD transgenic mice are protected from cardiac hypertrophy, fibrosis, and dysfunction under the

199 containing an average of 14 genes, affecting cardiac hypertrophy, fibrosis, and surrogate traits rele

200 gin-1 targets signaling proteins involved in cardiac hypertrophy for degradation.

201 atherosclerosis, pulmonary hypertension and cardiac hypertrophy have been linked to aberrant BMP sig

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

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

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

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

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

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

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

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

210 Likewise, calcineurin inhibition prevents cardiac hypertrophy in DKO.

211 , aortic banding induced a similar degree of cardiac hypertrophy in Epac1 KO; however, lack of Epac1

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

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

214 nullifies the protective effects of IRF8 on cardiac hypertrophy in IRF8-overexpressing mice.

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

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

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

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

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

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

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

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

223 ction and decreased apoptosis and attenuated cardiac hypertrophy in the hearts of mice subjected to p

224 c subpressor Ang II infusion induced greater cardiac hypertrophy in transgenic than wild-type mice bu

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

226 activity and expression are increased during cardiac hypertrophy, in heart failure, and under conditi

227 phic responses, and ameliorates pre-existing cardiac hypertrophy, in mice.

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

229 beta expression in mice is important for the cardiac hypertrophy induced by pressure overload and cat

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

231 Pathological cardiac hypertrophy induced by stresses such as aging an

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

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

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

235 e have found that GRK5-mediated pathological cardiac hypertrophy involves the activation of the nucle

236 promotes the development of exercise-induced cardiac hypertrophy involving the lipokine C16:1n7 palmi

237 Cardiac hypertrophy is a major risk factor for heart fai

238 Therefore, although induction of cardiac hypertrophy is a multifaceted process, inhibitio

239 Cardiac hypertrophy is a multifactorial disease characte

240 Cardiac hypertrophy is an adaptive response triggered by

241 Cardiac hypertrophy is an early hallmark during the clin

242 Pathological cardiac hypertrophy is characterized by subcellular remo

243 Cardiac hypertrophy is closely linked to impaired fatty

244 Understanding cardiac hypertrophy is critical to comprehending the mec

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

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

247 Cardiac hypertrophy is often initiated as an adaptive re

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

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

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

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

252 However, whether IRF8 can influence cardiac hypertrophy is unknown.

253 e that, for the initial phase of AII-induced cardiac hypertrophy, lack of cardiomyocyte cGKI activity

254 Sustained Akt activation induces cardiac hypertrophy (LVH), which may lead to heart failu

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

256 34a in male mice in settings of pathological cardiac hypertrophy or ischaemia protects the heart agai

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

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

259 In two animal models of cardiac hypertrophy, PIP2 levels were significantly redu

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

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

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

263 Although pathological cardiac hypertrophy represents a leading cause of morbid

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

265 eptor signaling, endothelin 1 signaling, and cardiac hypertrophy signaling.

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

267 vel GPCR-dependent pathway for regulation of cardiac hypertrophy that depends on Golgi phosphatidylin

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

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

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

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

272 ognition in the progression from compensated cardiac hypertrophy to HF.

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

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

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

276 orm of human cardiomyopathy characterized by cardiac hypertrophy, ventricular preexcitation, and glyc

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

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

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

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

281 Notably, mild cardiac hypertrophy was also observed in nude mice impla

282 nction was improved in HF AAC LF mice, while cardiac hypertrophy was decreased and accompanied by dec

283 Cardiac hypertrophy was increased by voluntary exercise

284 METHODS AND Cardiac hypertrophy was induced by slow progressive pres

285 Cardiac hypertrophy was induced in mice either by isopro

286 Cardiac hypertrophy was present in 57.9% (77 of 133), an

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

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

289 No signs of pathological cardiac hypertrophy were detected in TG(S282A) hearts by

290 diac dysfunction and increased apoptosis and cardiac hypertrophy, whereas Hrd1 overexpression preserv

291 are resistant to aortic banding (AB)-induced cardiac hypertrophy, whereas mice lacking IRF8 either gl

292 ed to pressure overload-induced pathological cardiac hypertrophy, which challenges protein-folding ca

293 Both genotypes developed cardiac hypertrophy, which was more pronounced in Ctr an

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

295 Cardiac hypertrophy with Ang-II treatment was diminished

296 MPK-mTOR interacting molecule, causes severe cardiac hypertrophy with deregulated energy homeostasis

297 erformance, DKO mice show an exaggeration of cardiac hypertrophy with increased expression of the cal

298 ented transverse aortic constriction-induced cardiac hypertrophy with preserved fractional shortening

299 myocyte-specific deletion of ST2 exacerbated cardiac hypertrophy with pressure overload.

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