ライフサイエンスコーパス: hypertrophy

1 xt-specific model of beta-adrenergic cardiac hypertrophy.

2 of elevated aspartate level in cardiomyocyte hypertrophy.

3 oprotein oxidation, and prevented myocardial hypertrophy.

4 rives the increase of biomass during cardiac hypertrophy.

5 ity, hypertrophic gene response and cellular hypertrophy.

6 -found crosstalks in beta-adrenergic cardiac hypertrophy.

7 s adaptability to growth signals and induced hypertrophy.

8 abetes mellitus, and 59 had left ventricular hypertrophy.

9 pulmonary arterial hypertension, and cardiac hypertrophy.

10 nduction system disease and left ventricular hypertrophy.

11 myocyte cytoplasm, where it promotes cardiac hypertrophy.

12 0% were male, and 82 patients had asymmetric hypertrophy.

13 f systemic hypertension and left ventricular hypertrophy.

14 despite a lack of effect on skeletal muscle hypertrophy.

15 well-tolerated without weight loss or organ hypertrophy.

16 d a faster growth rate and developed myotube hypertrophy.

17 essure overload-induced pathological cardiac hypertrophy.

18 or nucleotide synthesis during cardiomyocyte hypertrophy.

19 ich dysregulation yields to tumorigenesis or hypertrophy.

20 , suggesting that KGN does not obstruct BMSC hypertrophy.

21 opathy with early SCD even in the absence of hypertrophy.

22 ssion in Ras(V12)-glands favors unrestricted hypertrophy.

23 llebrand factor(vWF), and CD31 after cardiac hypertrophy.

24 stress response, cell survival, and cardiac hypertrophy.

25 onsistent with the development of concentric hypertrophy.

26 urther, dichloroacetate prevented myocardial hypertrophy.

27 pressed CKD-induced hypertension and cardiac hypertrophy.

28 udies suggest KLF15 as a key regulator of CM hypertrophy.

29 diac genes and stretch-induced cardiomyocyte hypertrophy.

30 pid storage genes concomitant with adipocyte hypertrophy.

31 load indices correlate more strongly with LV hypertrophy.

32 RC1 is necessary for mechanical load-induced hypertrophy.

33 ibrillary acidic protein (GFAP) and cellular hypertrophy.

34 skeletal muscle mass gains in some models of hypertrophy.

35 and has been attributed to regression of LV hypertrophy.

36 ion analysis confirmed reduced cardiomyocyte hypertrophy.

37 dent gene expression and ventricular myocyte hypertrophy.

38 recovery from atrophy/injury, anabolism and hypertrophy.

39 ores were applied to assess the impact of LV hypertrophy.

40 ase (CDK) complex that promotes fibrosis and hypertrophy.

41 ory pathway controlling pathological myocyte hypertrophy.

42 , intellectual disability as well as cardiac hypertrophy.

43 t-to-tibia length ratio due to cardiomyocyte hypertrophy.

44 ationship between training volume and muscle hypertrophy.

45 h, which positively correlate with extent of hypertrophy.

46 -induced expression and to prevent premature hypertrophy.

47 lower oxidative phosphorylation (moderate RV hypertrophy, 287.6+/-19.75 versus RV failure, 137.8+/-11

48 ant of the progression of pathologic cardiac hypertrophy after aortic banding in mice.

49 ly, Tsg101-KD mice failed to develop cardiac hypertrophy after intense treadmill training.

50 FC overexpression reduced the development of hypertrophy, albuminuria, loss of GEnC fenestrations and

51 elination has been associated with astrocyte hypertrophy and aging has been implicated as a basis for

52 dysfunction, vascular oxidative stress, and hypertrophy and attenuates Ang II (angiotensin II) and d

53 t to recapitulate the age-dependent lymphoid hypertrophy and autoinflammation seen in animals with a

54 c disorder characterized by left ventricular hypertrophy and cardiac hyper-contractility.

55 phy revealed that banding induced concentric hypertrophy and diastolic dysfunction (early diastolic t

56 tures of diabetic cardiomyopathy are cardiac hypertrophy and diastolic dysfunction, which lead to hea

57 ological and molecular phenotypes: nucleolar hypertrophy and disorganization, overaccumulation of 5.8

58 apamycin can attenuate bladder smooth muscle hypertrophy and dysfunction during the genesis of partia

59 0 is able to reverse pre-established cardiac hypertrophy and dysfunction.

60 ciated with human skeletal muscle anabolism, hypertrophy and epigenetic memory.

61 t to pressure overload stress, leading to RV hypertrophy and eventually RV failure.

62 votal roles in inhibiting renal fibrosis and hypertrophy and exerts protective effects involving cGMP

63 of high glucose, resulting in mesangial cell hypertrophy and expression of fibronectin and collagen I

64 nt form of oxidative stress, in mediating RV hypertrophy and failure in congenital heart disease is u

65 on metabolic health and particularly muscle hypertrophy and fat loss are well established, but the u

66 d molecule for adrenal stimulation of muscle hypertrophy and fat loss.

67 required for TGFbeta-induced mesangial cell hypertrophy and fibronectin and collagen I (alpha2) prod

68 ls using senolytic drugs ameliorated cardiac hypertrophy and fibrosis and may inform novel approaches

69 icated in maladaptive right ventricular (RV) hypertrophy and fibrosis associated with pulmonary hyper

70 nsaortic-constriction mouse model of cardiac hypertrophy and fibrosis, and from a heart-on-a-chip mod

71 nation of the substrate (regional myocardial hypertrophy and fibrosis, Purkinje fibers) and the trigg

72 ntly emerged as a key contributor of cardiac hypertrophy and heart failure but the relevance of Orai1

73 odynamic stress induces pathological cardiac hypertrophy and heart failure through persistent activat

74 cted Mef2d, which when overexpressed, led to hypertrophy and heart failure, and Klf15, which is lowly

75 CICR is disrupted in cardiac hypertrophy and heart failure, which is associated with

76 romising target for the treatment of cardiac hypertrophy and heart failure.

77 asts, as well as preclinical mouse models of hypertrophy and heart failure.

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

79 )-CaMKIIdeltaC axis contributes to eccentric hypertrophy and HF.

80 ral Ca(2+) handling and CaMKII activation in hypertrophy and HF.

81 ll-characterized genes implicated in cardiac hypertrophy and homeostasis) for enhanced transcription.

82 silencing induced expansion of dWAT through hypertrophy and hyperplasia.

83 adipose depots indicative of both adipocyte hypertrophy and hyperplasia.

84 riction and exercise-induced cardiac myocyte hypertrophy and impaired cardiac function, demonstrating

85 deletion of Grb14 in mice results in cardiac hypertrophy and impaired systolic function, which could

86 duces contractility but also causes cellular hypertrophy and impairs cardiomyocytes' ability to adapt

87 nociceptive hypersensitivity and nerve fiber hypertrophy and improved behavioral parameters without a

88 earts exhibited reduced cardiac fibrosis and hypertrophy and improved cardiac function.

89 e dehydrogenase expression, RV fibrosis, and hypertrophy and improved RV function.

90 virus gene therapy vector inhibited cardiac hypertrophy and improved systolic function after pressur

91 d make mTORC1 constitutively active, causing hypertrophy and improving muscle function.

92 r energy production, thus preventing cardiac hypertrophy and improving myocardial energetics.

93 CTRND05 induces skeletal muscle hypertrophy and increases lean body mass, effects not pr

94 anation for the specific role of CaNAbeta in hypertrophy and its selective activation under condition

95 ion Cardiac MRI findings of left ventricular hypertrophy and late gadolinium enhancement can be used

96 dioGRKO mice spontaneously developed cardiac hypertrophy and left ventricular systolic dysfunction an

97 ral disc degeneration and extensive synovial hypertrophy and loss of articular cartilage in the knees

98 slowed contractile deterioration, attenuated hypertrophy and lung congestion, and prevented apoptosis

99 etylation to regulate kidney glomerular cell hypertrophy and matrix expansion is not known.

100 RAS40 phosphorylation to spur mesangial cell hypertrophy and matrix protein accumulation.

101 nonical kinase cascades regulates glomerular hypertrophy and matrix protein deposition, which are ear

102 ise and is sufficient to cause physiological hypertrophy and mitigate adverse ventricular remodeling

103 s cartilage degeneration through suppressing hypertrophy and MMP-13 in a mouse osteoarthritis model.

104 Nephron hypertrophy and nephrosclerosis may be important determi

105 Finally, AKAP6 is required for cardiomyocyte hypertrophy and osteoclast bone resorption activity.

106 expression of genes involved in chondrocyte hypertrophy and osteogenesis.

107 ling, the concomitant attenuation of cardiac hypertrophy and oxidative stress allowed myocardial ener

108 hich can be manipulated to attenuate cardiac hypertrophy and preserve cardiac function by improving t

109 aortic constriction (TAC) developed cardiac hypertrophy and reduced ventricular function associated

110 d mice, indicating that aging causes cardiac hypertrophy and remodeling.

111 nd that YAP-CHKO mice had attenuated cardiac hypertrophy and significant increases in CM apoptosis an

112 een displayed clear benefit of MOD on muscle hypertrophy and sixteen showed clear benefit of MOD on m

113 Suppression of hypertrophy and stimulation of autophagy in cardiomyocyt

114 clear benefits in response to MOD on muscle hypertrophy and strength.

115 in hearts of patients with NS by exhibiting hypertrophy and structural defects.

116 Greater SDB severity was associated with LV hypertrophy and subclinical markers of LV diastolic dysf

117 9a inhibitor reverses preestablished cardiac hypertrophy and systolic dysfunction in mice subjected t

118 ated that KO mice developed less ventricular hypertrophy and that contractile function is better pres

119 has deleterious long-term effects leading to hypertrophy and the development of heart failure.

120 creased metabolic requirements, and cellular hypertrophy and the etiological fraction (0.93 [95% CI,

121 echanical loading can induce skeletal muscle hypertrophy, and a long standing model in the field indi

122 isoform (encoded by Myh4) is an indicator of hypertrophy, and both porcine MYH4-promoter activity and

123 al mitochondrial abnormalities (hyperplasia, hypertrophy, and crystalline arrays) consistent with a m

124 llowed myocardial energetics, left ventricle hypertrophy, and diastolic dysfunction to recover.

125 MCB-613 decreases infarct size, apoptosis, hypertrophy, and fibrosis while maintaining significant

126 athy, characterized by hypertension, cardiac hypertrophy, and fibrosis, is a complication of chronic

127 on the development of hypertension, cardiac hypertrophy, and fibrosis.

128 model for pressure overload-induced cardiac hypertrophy, and followed it by cancer cell implantation

129 ression in mice with obstruction-induced BSM hypertrophy, and in men with benign prostatic hyperplasi

130 AP/TAZ deletion results in reduced fibrosis, hypertrophy, and increased angiogenesis, leading to impr

131 ion, myocardial infarction, left ventricular hypertrophy, and left bundle branch block were strongly

132 Histological abnormalities, left ventricular hypertrophy, and left ventricular dysfunctions were demo

133 res relative to TGF-beta1, does not obstruct hypertrophy, and may not be a viable alternative to grow

134 includes dilated vasculature, marked cardiac hypertrophy, and other cardiovascular abnormalities.

135 ous secreted Klotho prevented heart failure, hypertrophy, and remodeling in both old mice and KL (-/-

136 Concentric and eccentric cardiac hypertrophy are associated with pressure and volume over

137 These contrasting forms of hypertrophy are characterized by asymmetrical growth of

138 tiation and neonatal rat ventricular myocyte hypertrophy are inhibited by mAKAPbeta signalosome targe

139 hysiologies such as atherosclerosis, cardiac hypertrophy, arrhythmias, contractile dysfunction and th

140 ease, including heart contractility, myocyte hypertrophy, arterial stiffness, and systemic resistance

141 molecular LAM program, leading to adipocyte hypertrophy as well as systemic hypercholesterolemia, bo

142 d perivascular fibrosis and left ventricular hypertrophy associated with diastolic dysfunction and pr

143 terized by unexplained left ventricular (LV) hypertrophy associated with dynamic LV outflow tract obs

144 Left ventricular hypertrophy became less marked over time (maximum wall t

145 elevation of circulating AKG induces muscle hypertrophy, brown adipose tissue (BAT) thermogenesis, a

146 by which CAV gene expression is repressed in hypertrophied BSM in obstructive bladder disease.

147 l type crosstalk during pathological cardiac hypertrophy but also shed light on strategies for cell t

148 mTORC1 promotes skeletal muscle hypertrophy, but also drives organismal aging.

149 proves the contractile reserve and decreases hypertrophy by augmenting carbohydrate metabolism in por

150 n-contraction coupling while not stimulating hypertrophy by calcineurin in the normal heart.

151 o 0.97) among patients with left ventricular hypertrophy by ECG criteria and 0.95 (95% CI: 0.90 to 1.

152 ation that can be regulated to treat cardiac hypertrophy by improving neovascularization and altering

153 and mixed-chain FAs and induced pathological hypertrophy by phenylephrine.

154 Regression of athletic LV hypertrophy can be detected after just 1 month of comple

155 ficiency significantly attenuated myocardial hypertrophy, cardiac fibrosis, and dysfunction induced b

156 ricular systolic pressure, right ventricular hypertrophy, cardiac fibrosis, and vascular remodeling.

157 regulation from the formation of compensated hypertrophy (CH) until signs of heart failure (HF) are a

158 ism is involved in the regulation of cardiac hypertrophy (CH), an antecedent condition to HF where NQ

159 es became swollen and rounded in shape, with hypertrophied contractile vacuoles and intense cytoplasm

160 Two weeks later, hypertrophy decreased with the decline of oxidative stre

161 action and excluding patients with severe LV hypertrophy, defined as wall thickness greater than 1.5

162 quired for induction of pathological myocyte hypertrophy, despite calcineurin Aalpha expression in th

163 omyopathy, characterized by left ventricular hypertrophy, diastolic dysfunction, and impaired myocard

164 AISE) that used left ventricular remodeling (hypertrophy/diastolic dysfunction), age, injury (high-se

165 ed a ~50% decrease in fractional shortening, hypertrophy, dilatation, and premature death.

166 substrate metabolism regulates cardiomyocyte hypertrophy directly or via a secondary effect of improv

167 in cats, and is characterized by myocardial hypertrophy, disarray and fibrosis, as in humans.

168 on and energetics, and reduces cardiomyocyte hypertrophy during cardiac stresses.

169 cardiomyocyte (CM) apoptosis and impaired CM hypertrophy during chronic myocardial infarction (MI) in

170 known features of lipoedema, such as adipose hypertrophy, dysfunction of blood and lymphatic vessels,

171 butes to increased oxidative stress, myocyte hypertrophy, ECM remodeling, and inflammation, implicati

172 xacerbates pressure overload-induced cardiac hypertrophy, fibrosis, and cardiac dysfunction.

173 -regualted transcriptome involved in cardiac hypertrophy, fibrosis, and cardiomyopathy.

174 control remodeling associated processes like hypertrophy, fibrosis, and energy metabolism.

175 Propionate significantly attenuated cardiac hypertrophy, fibrosis, vascular dysfunction, and hyperte

176 t which differs by causing enormous cellular hypertrophy followed by cleavage of the cell into numero

177 ntricular function, blunted left ventricular hypertrophy, greater preservation of viable myocardium i

178 and chronic resistance exercise (RE) induced hypertrophy have been extensively determined in the lite

179 lice variant of alpha(1C) upregulated in the hypertrophied heart.

180 ral diseases, including hypertensive cardiac hypertrophy, Hirschsprung disease and blood vessel forma

181 gonist enhances skeletal muscle strength and hypertrophy; however, its clinical utility is limited by

182 C3KO muscles resulted in significant muscle hypertrophy; however, there were no improvements in musc

183 Previous studies have shown that the LM is hypertrophied in hummingbirds, and that LM cell response

184 ression of pressure overload-induced cardiac hypertrophy in a mouse model, we characterized the spati

185 ressures, vascular remodeling, as well as RV hypertrophy in a rat model of PH and may be appropriate

186 in PPP3R1 to be associated with ventricular hypertrophy in AA hypertensive patients.

187 d sympathetic activity, and left ventricular hypertrophy in Ang II rats, as well as in the SHR.

188 surgical model of pressure overload-induced hypertrophy in C57BL/6J mice produced by suprarenal aort

189 se to elevated subchondral bone turnover and hypertrophy in calcified cartilage, yet additional mecha

190 ADF4(C16)-RGD coatings, which did not induce hypertrophy in cardiomyocytes, but allowed response to h

191 expression, and reverses molecular events of hypertrophy in cardiomyocytes.

192 e a therapeutic approach to mitigate cardiac hypertrophy in cases of CS.

193 ing a competing peptide inhibited concentric hypertrophy in cultured myocytes; disruption of anchorin

194 neurin is a key regulator of cardiac myocyte hypertrophy in disease.

195 after chronic electrical stimulation-induced hypertrophy in rats in vivo, without increases in MuRF1/

196 on of PKD-associated signaling pathways, and hypertrophy in tubule segments along the affected nephro

197 es may also modulate MSC-derived chondrocyte hypertrophy in vitro.

198 ion of LTCC were studied in left ventricular hypertrophy in vivo and in cultured adult feline and rat

199 During compensated hypertrophy in vivo fractional shortening (FS) remains c

200 tes and in pressure overload-induced cardiac hypertrophy in vivo.

201 d to an increase in LV wall thickness and LV hypertrophy in young American Indians with a low burden

202 vascular diagnoses, such as left ventricular hypertrophy, in 28 participants (4.6%).

203 Interestingly, muscle hypertrophy increased the transport of high molecular we

204 es endothelial cadherin, stimulates vascular hypertrophy, increases vascular permeability and vascula

205 ed less cardiac arrhythmogenesis and cardiac hypertrophy index compared to AV-Shunt(Scr).

206 -10, attenuated cardiac myocyte pathological hypertrophy induced by Angiotensin II, phenylephrine, an

207 , apoptosis, and fibrosis, while attenuating hypertrophy induced by chronic isoproterenol infusion.

208 did not affect cardiac myocyte physiological hypertrophy induced by IGF-1 (insulin-like growth factor

209 tigated this phenomenon using a rat model of hypertrophy induced by thoracic aortic banding (TAB).

210 Using a rat model of cardiac hypertrophy induced by thoracic aortic banding, we found

211 Our data suggest that muscle hypertrophy, induced by myostatin inhibition, leads to l

212 HFD-induced liver macrovesicular steatosis, hypertrophy, inflammation, and collagen content.

213 riptional regulation by FoxO1 during cardiac hypertrophy, information that is essential for its thera

214 essure overload-induced pathological cardiac hypertrophy is a common predecessor of heart failure, th

215 Cardiac hypertrophy is a context-dependent phenomenon wherein a

216 Compensated hypertrophy is accompanied by an increase in I(Na,late)

217 We report that asymmetrical cardiac myocyte hypertrophy is modulated by SRF (serum response factor)

218 Although cardiomyocyte hypertrophy is often associated with these processes, wh

219 l-endothelial transition (MEndoT) in cardiac hypertrophy is unclear.

220 At the decompensated stage of hypertrophy, isolated hearts were perfused with (13)C LC

221 , transgenic (PLM(3SA)), ouabain-treated and hypertrophied Langendorff-perfused mouse hearts are stud

222 e overload, and progressive left ventricular hypertrophy, leading to elevated N-terminal probrain nat

223 ce were protected from systolic dysfunction, hypertrophy, lung congestion, and fibrosis induced by ch

224 edia thickness (cIMT), left ventricular (LV) hypertrophy, LV ejection fraction <50%, and peripheral a

225 Individuals with left ventricular hypertrophy (LVH) and elevated cardiac biomarkers in mid

226 Left ventricular hypertrophy (LVH) and late gadolinium enhancement (LGE)

227 baseline moderate or severe left ventricular hypertrophy (LVH) and paired measurements of LVMi at bas

228 information about high-risk left ventricular hypertrophy (LVH) embedded in CAC-CT.

229 A malignant subphenotype of left ventricular hypertrophy (LVH) has been described, in which minimal e

230 Left ventricular hypertrophy (LVH) was present in 60 subjects (67%) at ba

231 ith respect to diagnosis of left ventricular hypertrophy (LVH), eligibility for disease-specific ther

232 rs, 43% male, 24 [55%] with left ventricular hypertrophy [LVH]) and 27 healthy controls with multipar

233 hemidiaphragm paralysis causes muscle fibre hypertrophy, maintaining global oxygen supply, although

234 While hypertrophy/mass (LVM) can be objectively measured, fibr

235 stimulated chondrogenesis in OAC, it induced hypertrophy, mineralization, and MMP-13 in OA-MSC.

236 During compensatory and maladaptive hypertrophy, mitochondria become more active.

237 pplying this pipeline to our prior-knowledge hypertrophy network with context-specific data revealed

238 3% relative to baseline) and skeletal muscle hypertrophy occurred in all groups.

239 , CRF increased excitatory input and induced hypertrophy of BLA principal neurons.

240 PC recurrent axonal collateral formation and hypertrophy of GABAergic basket cell axonal processes, c

241 le for hepatic resection due to insufficient hypertrophy of the FLR.

242 reased following functional overload-induced hypertrophy of the plantaris muscle in mice and during d

243 In select carriers without left ventricular hypertrophy on echocardiogram, SCD occurred, myocyte dis

244 ertrophy on the myofiber level, we report no hypertrophy on the muscle level.

245 Despite massive hypertrophy on the myofiber level, we report no hypertro

246 during pathological remodeling (eg, cardiac hypertrophy or failure) forms an exciting target for fur

247 c structural abnormalities, left ventricular hypertrophy, or concentric geometry, were highest in tho

248 TG mice exhibited a physiologic-like cardiac hypertrophy phenotype at 8 wk evidenced by: 1) the absen

249 on, we recapitulated the anticipated cardiac hypertrophy phenotype.

250 thy, exhibiting less albuminuria, glomerular hypertrophy, podocyte injury, and interstitial fibrosis

251 r driving progression from pressure-overload hypertrophy (POH) to HFpEF is the activation and prolife

252 patients starting ERT (60% left ventricular hypertrophy-positive) were compared with 18 patients wit

253 e role of Myocilin (Myoc), a skeletal muscle hypertrophy-promoting protein that we showed is downregu

254 gical hypertrophy, which can be diagnosed if hypertrophy regresses.

255 r apoptosis, and elevated mRNA expression of hypertrophy-related and profibrotic marker genes, withou

256 h concentric LV remodeling and concentric LV hypertrophy, respectively.

257 cular systolic pressure, reduces right heart hypertrophy, restores the cardiac index, and reduces pul

258 RACs), vessel density, and right ventricular hypertrophy (RVH).

259 ulmonary vessel density, and right ventricle hypertrophy (RVH).Measurements and Main Results: Antenat

260 g hypochord undergoes rapid ossification and hypertrophy; second, thyroid hormone directly affects hy

261 n variants) and were associated with similar hypertrophy severity and adverse event rates as observed

262 re evenly dispersed throughout the gene, and hypertrophy severity and outcomes were not associated wi

263 phic signaling pathways, less is known about hypertrophy signaling as a whole network and how this ne

264 Pressure overload-induced cardiac hypertrophy, such as that caused by hypertension, is a k

265 and PDE4B is decreased in pressure overload hypertrophy, suggesting that increasing PDE4B in the hea

266 t change following the development of robust hypertrophy, suggesting there is no role for cardiomyocy

267 vidual mdx muscle fibers undergo progressive hypertrophy that continues through the lifespan.

268 al shortening associated with a mild cardiac hypertrophy that resorbed with age.

269 function remains constant during compensated hypertrophy then decreases in HF, when there is also an

270 Ca(2+) content increases during compensated hypertrophy then decreases in HF.

271 regulation of the HBP triggers decompensated hypertrophy through activation of mTOR while Gfat1 defic

272 e deacetylases (HDACs) repress cardiomyocyte hypertrophy through association with the prohypertrophic

273 ositively regulates physiologic-like cardiac hypertrophy through FIP3-mediated endosomal recycling of

274 e of endothelial leptin signaling in cardiac hypertrophy, transverse aortic constriction was used in

275 During anabolism and hypertrophy, UBR5 gene expression increased following ac

276 n promotes endothelial dysfunction, vascular hypertrophy, vascular inflammation, and end-organ damage

277 e chronic CAVB animals developed dilated and hypertrophied ventricles with preserved systolic functio

278 field indicates that mechanical loads induce hypertrophy via a mechanism that requires signaling thro

279 terminus is reported to contribute to muscle hypertrophy via the IGF-1 growth pathway.

280 mplete bundle branch block, left ventricular hypertrophy voltage criteria, long QTc, and T-wave inver

281 LV hypertrophy was an independent predictor of hard CHD eve

282 Phenylephrine-induced hypertrophy was associated with increased glucose consum

283 ificantly elevated and left ventricular (LV) hypertrophy was evident by a 50% increase in the LV weig

284 Left ventricular hypertrophy was present in 19 individuals (86%) at basel

285 Left ventricular (LV) hypertrophy was reported in 73% of male and 74% of femal

286 The loss of NQO1 during hypertrophy was rescued by ectopic expression of the dis

287 hing, a key event at middle-stage of cardiac hypertrophy, was successfully targeted by Dapagliflozin,

288 Similar molecular patterns of hypertrophy were also observed in human patient samples

289 creases in contractility and skeletal muscle hypertrophy were lost in beta-arrestin 1 knockout mice,

290 Indicators of hypertrophy were not mitigated in TGF-beta1 + KGN cultur

291 sis, mesangial matrix expansion, and tubular hypertrophy were observed in 0-copy and A71915-treated 2

292 s in Ca(2+) handling at baseline and myocyte hypertrophy were present throughout the left ventricle (

293 uring detraining (following training induced hypertrophy) when exercise was ceased and lean mass retu

294 DNA methylation) after human skeletal muscle hypertrophy, where its gene expression is positively cor

295 ed diagnostic test to identify physiological hypertrophy, which can be diagnosed if hypertrophy regre

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

297 We found that db/db mice developed cardiac hypertrophy with normal cardiac function at 6 weeks of a

298 ) myocardium collected from patients with RV hypertrophy with normal RV systolic function (RV fractio

299 mediated by hyperadrenergic drive in cardiac hypertrophy, with functional effects on the channel conf

300 tissue/min), increased inflammation, myocyte hypertrophy (WT, 19.8 mum; CatA-TG, 21.9 mum), cellular