ライフサイエンスコーパス: hypertrophic

1 gnalling pathway, thereby achieving its anti-hypertrophic action.

2 ase 2 (GRK2) pro-death activity and GRK5 pro-hypertrophic action.

3 ocytes with phenylephrine (PE), a well known hypertrophic agonist, suppresses autophagy and that acti

4 The compounds modulated the hypertrophic agonist-induced cardiac gene expression.

5 due to increased clenbuterol-stimulated pro-hypertrophic Akt signaling in the GRK2 KO skeletal muscl

6 of myofilament tension development predicts hypertrophic and dilated cardiomyopathies in mice associ

7 iously been associated with features of both hypertrophic and dilated cardiomyopathy in mice.

8 rring during pressure overload bridging both hypertrophic and hypoxia-stimulated paracrine signaling.

9 During pressure overload, both hypertrophic and hypoxic signals can stimulate angiogene

10 ression of S100A12 in the epidermis of human hypertrophic and keloid scar.

11 rray, and myocardial fibrosis and attenuates hypertrophic and profibrotic gene expression in mice har

12 tations, resulting in a mix of KO-equivalent hypertrophic and wild type-like phenotypes.

13 th biallelic mutations presented with severe hypertrophic and/or dilated cardiomyopathy in utero, at

14 sing chondrocytes expressed prehypertrophic, hypertrophic, and subsequently bone formation markers in

15 dated in human disease where myelin-positive hypertrophic astrocytes showed increased nuclear localiz

16 and pulmonary inflammation on soleus muscle hypertrophic capacities, we challenged male Wistar rats

17 l fatty acid oxidation initiates deleterious hypertrophic cardiac remodeling independent of fibrosis.

18 Dilated and hypertrophic cardiomyopathies are the most common; restr

19 me (31%), coronary artery disease (22%), and hypertrophic cardiomyopathy (14%).

20 ndromes (5), dilated cardiomyopathy (2), and hypertrophic cardiomyopathy (2).

21 diography was performed in 427 patients with hypertrophic cardiomyopathy (66% men, age 52+/-15 years)

22 Hypertrophic cardiomyopathy (9 [53%]) and respiratory in

23 We analyzed 531 patients with hypertrophic cardiomyopathy (age: 56+/-14 years, men 55%

24 ventricular cardiomyopathy (ARVC) (13%); and hypertrophic cardiomyopathy (HCM) (6%).

25 wall thickening, and apply the technique in hypertrophic cardiomyopathy (HCM) and DCM.

26 pathogenic mutations in the TNT1 region, six hypertrophic cardiomyopathy (HCM) and two dilated cardio

27 The 2 most commonly affected genes in hypertrophic cardiomyopathy (HCM) are MYH7 (beta-myosin

28 tein C) founder mutations account for 35% of hypertrophic cardiomyopathy (HCM) cases in the Netherlan

29 terations in autophagy have been reported in hypertrophic cardiomyopathy (HCM) caused by Danon diseas

30 The features of the hypertrophic cardiomyopathy (HCM) ECG make it a challeng

31 graphic data for automated discrimination of hypertrophic cardiomyopathy (HCM) from physiological hyp

32 Hypertrophic cardiomyopathy (HCM) is a clinically and ge

33 Hypertrophic cardiomyopathy (HCM) is a genetic disorder

34 RATIONALE: Hypertrophic cardiomyopathy (HCM) is a prototypic single

35 Hypertrophic cardiomyopathy (HCM) is a relatively common

36 Hypertrophic cardiomyopathy (HCM) is an inherited diseas

37 Hypertrophic cardiomyopathy (HCM) is caused by mutations

38 The natural history of hypertrophic cardiomyopathy (HCM) is complex and may inc

39 Yield of causative variants in hypertrophic cardiomyopathy (HCM) is increased in some p

40 Hypertrophic cardiomyopathy (HCM) is one of the most com

41 specific clinical red flags in patients with hypertrophic cardiomyopathy (HCM) older than 25 years.

42 A previously under-recognized subset of hypertrophic cardiomyopathy (HCM) patients with left ven

43 h genetic mutations that are associated with hypertrophic cardiomyopathy (HCM) remains challenging.

44 with severe heart failure due to obstructive hypertrophic cardiomyopathy (HCM) who are at unacceptabl

45 for treatment of long QT-3 syndrome (LQT-3), hypertrophic cardiomyopathy (HCM), and ventricular tachy

46 AF), the most common sustained arrhythmia in hypertrophic cardiomyopathy (HCM), is capable of produci

47 the time of greatest risk for patients with hypertrophic cardiomyopathy (HCM), largely because of th

48 omeric mutation, which is exhibited in human hypertrophic cardiomyopathy (HCM), to investigate the in

49 ns, such as dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM), which are often due t

50 ) hypertrophy (LVH) are cardinal features of hypertrophic cardiomyopathy (HCM).

51 young carriers of mutations associated with hypertrophic cardiomyopathy (HCM).

52 ute to arrhythmias and adverse remodeling in hypertrophic cardiomyopathy (HCM).

53 (cMyBP-C), are the two most common causes of hypertrophic cardiomyopathy (HCM).

54 in an important proportion of patients with hypertrophic cardiomyopathy (HCM).

55 veral mutations in hVELC are associated with hypertrophic cardiomyopathy (HCM).

56 ied filamin C (FLNC) as a candidate gene for hypertrophic cardiomyopathy (HCM).

57 ND One-hundred and ninety-five patients with hypertrophic cardiomyopathy (median age, 52.8+/-15.1 yea

58 ular cardiomyopathy (n = 111), DCM (n = 95), hypertrophic cardiomyopathy (n = 40) and peripartum card

59 2), occult myocardial infarction (n=13), and hypertrophic cardiomyopathy (n=9) were most frequent.

60 fficiency represents a target for therapy in hypertrophic cardiomyopathy although therapeutic benefit

61 ry hypertension in patients with obstructive hypertrophic cardiomyopathy and advanced heart failure.

62 ciated with adverse outcome in patients with hypertrophic cardiomyopathy and may help to optimize ris

63 tions reflect the complex pathophysiology of hypertrophic cardiomyopathy and may provide clues for th

64 tive athletes, two deaths were attributed to hypertrophic cardiomyopathy and none to arrhythmogenic r

65 conversions associated with fatal infantile hypertrophic cardiomyopathy and the neurological disorde

66 Double mutations in patients with hypertrophic cardiomyopathy are much less common than pr

67 gests that double mutations in patients with hypertrophic cardiomyopathy are not rare and are associa

68 r predicting adverse events in patients with hypertrophic cardiomyopathy are still limited.

69 sidase A gene variants are misinterpreted as hypertrophic cardiomyopathy because of the lack of extra

70 ure of cardiomyopathies, with an emphasis on hypertrophic cardiomyopathy caused by sarcomeric mutatio

71 ce in SHaRe most frequently occurred because hypertrophic cardiomyopathy centers had access to differ

72 Discordance in variant classification among hypertrophic cardiomyopathy centers is largely attributa

73 ment may be achieved by: 1) confining ASA to hypertrophic cardiomyopathy centers of excellence with h

74 rophic cardiomyopathy probands at 5 tertiary hypertrophic cardiomyopathy centers.

75 d >3 times and accounted for 78 of 185 (42%) hypertrophic cardiomyopathy families with a causal varia

76 ic cardiomyopathy who had undergone targeted hypertrophic cardiomyopathy genetic testing (either mult

77 more than a decade, risk stratification for hypertrophic cardiomyopathy has been enhanced by targete

78 t of drug-refractory symptoms of obstructive hypertrophic cardiomyopathy has long been debated and is

79 Infants with hypertrophic cardiomyopathy have a 2-year mortality of 3

80 lts, clinicians routinely assess the risk of hypertrophic cardiomyopathy in a patient's relatives and

81 rn pathological and clinical descriptions of hypertrophic cardiomyopathy in the 1950s, which focused

82 e of multiple rare variants in patients with hypertrophic cardiomyopathy in the setting of comprehens

83 atients followed at the Tufts Medical Center Hypertrophic Cardiomyopathy Institute for 4.8+/-3.4 year

84 Hypertrophic cardiomyopathy is a genetic disorder charac

85 Hypertrophic cardiomyopathy is a genetically heterogeneo

86 Hypertrophic cardiomyopathy is associated with sudden ca

87 g exercise recommendations for patients with hypertrophic cardiomyopathy is challenging because of co

88 tricular tachycardia (NSVT) in patients with hypertrophic cardiomyopathy is incompletely resolved.

89 Hypertrophic cardiomyopathy is the most common type of c

90 The most common single genetic cause of hypertrophic cardiomyopathy is the recurrent MYBPC3 (myo

91 sis light chain [AL] type), 40 patients with hypertrophic cardiomyopathy matched for demographics and

92 ated in hypertrophic hearts of patients with hypertrophic cardiomyopathy or aortic stenosis.

93 iameter, volume, and strain to risk stratify hypertrophic cardiomyopathy patients for new-onset atria

94 In end-stage, hypertrophic cardiomyopathy patients undergoing transpla

95 METHODS AND Clinical data of all hypertrophic cardiomyopathy patients with 2 rare genetic

96 onary hypertension was common in obstructive hypertrophic cardiomyopathy patients with advanced heart

97 of measured cardiopulmonary hemodynamics in hypertrophic cardiomyopathy patients with heart failure,

98 ith similar EF in 20 control subjects and 20 hypertrophic cardiomyopathy patients with increased wall

99 op of LA diameter to predict new-onset AF in hypertrophic cardiomyopathy patients with LA diameter <4

100 METHODS AND A total of 242 hypertrophic cardiomyopathy patients without AF history

101 me, and strain all relate to new-onset AF in hypertrophic cardiomyopathy patients.

102 g was performed on 358 consecutive genotyped hypertrophic cardiomyopathy probands at 5 tertiary hyper

103 METHODS AND Of 758 hypertrophic cardiomyopathy probands, we included 382 wi

104 Icelandic patients clinically diagnosed with hypertrophic cardiomyopathy resulted in identification o

105 thmias, supporting the importance of NSVT in hypertrophic cardiomyopathy risk stratification.

106 risk prediction model for SCD (HCM Risk-SCD [hypertrophic cardiomyopathy risk-SCD]).

107 markedly lower among centers specialized in hypertrophic cardiomyopathy than among clinical laborato

108 d clinical trial involving 136 patients with hypertrophic cardiomyopathy was conducted between April

109 genic (LP/P; >/=2) variants in patients with hypertrophic cardiomyopathy were described 10 years ago

110 ents from apparently unrelated families with hypertrophic cardiomyopathy were evaluated.

111 ferences between MYH7- and MYBPC3-associated hypertrophic cardiomyopathy when assessed by cardiac mag

112 METHODS AND Forty-one patients with hypertrophic cardiomyopathy who had undergone targeted h

113 10 (20%) heterozygous family members showed hypertrophic cardiomyopathy with an atypical distributio

114 cardiac magnetic resonance imaging revealed hypertrophic cardiomyopathy with left ventricular dysfun

115 ients undergoing septal alcohol ablation for hypertrophic cardiomyopathy, a human model of planned my

116 nder fasting conditions.Sirt5KO mice develop hypertrophic cardiomyopathy, as evident from the increas

117 importance of this finding in patients with hypertrophic cardiomyopathy, as well as the long-term sa

118 this case the two major clinical phenotypes (hypertrophic cardiomyopathy, HCM and dilated cardiomyopa

119 cardial strain are reported in patients with hypertrophic cardiomyopathy, ischemic heart disease, dia

120 is preliminary study involving patients with hypertrophic cardiomyopathy, moderate-intensity exercise

121 e underlying sarcomere hypercontractility of hypertrophic cardiomyopathy, one of the most prevalent h

122 ation (ASA) for the treatment of obstructive hypertrophic cardiomyopathy, the arrhythmogenicity of th

123 l fibrosis (MF) has clinical implications in hypertrophic cardiomyopathy, the extent, type, and distr

124 l hypertrophy, traditionally associated with hypertrophic cardiomyopathy, was the commonest pattern o

125 The hypertrophic cardiomyopathy-associated mutant D145E, in

126 bstitution in Sco1, which in humans causes a hypertrophic cardiomyopathy.

127 ostic value of GLS and LAVI in patients with hypertrophic cardiomyopathy.

128 nical management and genetic architecture of hypertrophic cardiomyopathy.

129 duced MEE at the early and advanced stage of hypertrophic cardiomyopathy.

130 ng improves exercise capacity in adults with hypertrophic cardiomyopathy.

131 achycardia, congenital long QT syndrome, and hypertrophic cardiomyopathy.

132 ficiency causes Danon's disease, an X-linked hypertrophic cardiomyopathy.

133 nt of Fabry disease mimicking nonobstructive hypertrophic cardiomyopathy.

134 gulated in dilated cardiomyopathy but not in hypertrophic cardiomyopathy.

135 er phenotypes, including 1,078 patients with hypertrophic cardiomyopathy.

136 ice developed a cardiac phenotype similar to hypertrophic cardiomyopathy.

137 tonia, optic atrophy, axonal neuropathy, and hypertrophic cardiomyopathy.

138 f cardiac disease, such as arrhythmogenic or hypertrophic cardiomyopathy.

139 MI), patients undergoing septal ablation for hypertrophic cardiomyopathy.

140 eta-adrenergic signaling, heart failure, and hypertrophic cardiomyopathy.

141 f MF in 30 transplanted hearts of end-stage, hypertrophic cardiomyopathy.

142 s support a cumulative variant hypothesis in hypertrophic cardiomyopathy.

143 red with suspicion of genetically determined hypertrophic cardiomyopathy.

144 t of routine evaluation of all patients with hypertrophic cardiomyopathy.

145 anxiety-like behavior in an animal model of hypertrophic cardiomyopathy.

146 in successfully prevented the development of hypertrophic cardiomyopathy.

147 ve feedback loop in response to a myocardial hypertrophic challenge in adulthood.

148 protein subunits produced minor atrophic and hypertrophic changes in muscle mass, respectively.

149 nically relevant murine model of nonischemic hypertrophic CHF, transverse aortic constriction (TAC).

150 lopment, whereas ablation of C-Raf decreases hypertrophic chondrocyte apoptosis and impairs vasculari

151 isoforms are required for phosphate-induced hypertrophic chondrocyte apoptosis, mice lacking all thr

152 Erk1/2 (Mapk3/1) phosphorylation, leading to hypertrophic chondrocyte apoptosis.

153 phospho-Erk1/2 immunoreactivity and impaired hypertrophic chondrocyte apoptosis.

154 Hypophosphatemia causes rickets by impairing hypertrophic chondrocyte apoptosis.

155 e mutant protein and subsequently disrupting hypertrophic chondrocyte differentiation.

156 educing the MCDS-associated abnormalities in hypertrophic chondrocyte differentiation.

157 eased phospho-ERK1/2 immunoreactivity in the hypertrophic chondrocyte layer and impaired vascular inv

158 tal death and a significant expansion of the hypertrophic chondrocyte layer of the growth plate, acco

159 atially-dependent phenotypic overlap between hypertrophic chondrocytes and osteoblasts at the chondro

160 e-induced ERK1/2 phosphorylation in cultured hypertrophic chondrocytes and perform essential, but par

161 nfluencing the osteogenic differentiation of hypertrophic chondrocytes and provided insight into the

162 for replacement of terminally differentiated hypertrophic chondrocytes by bone.

163 However, cultured hypertrophic chondrocytes from these mice did not exhibi

164 levated and sustained SOX9 in SHP2-deficient hypertrophic chondrocytes impaired their differentiation

165 Hypertrophic chondrocytes in the TZ activate expression

166 Transdifferentiation of hypertrophic chondrocytes into bone-forming osteoblasts

167 nduction of MEK1/2-ERK1/2 phosphorylation in hypertrophic chondrocytes is required for phosphate-medi

168 owever, VEGF (Vegfa) immunoreactivity in the hypertrophic chondrocytes of c-Raf(f/f);ColII-Cre(+) mic

169 stromal cells, osteoblasts, osteocytes, and hypertrophic chondrocytes secrete a C-type lectin domain

170 liferating immature chondrocytes into mature hypertrophic chondrocytes to become osteoblasts at the e

171 chondral bone formation postulates that most hypertrophic chondrocytes undergo programmed cell death

172 gh there was no up-regulation of markers for hypertrophic chondrocytes, a TUNEL assay showed a marked

173 pecialized cells, also including osteocytes, hypertrophic chondrocytes, and odontoblasts.

174 -Raf is the predominant isoform expressed in hypertrophic chondrocytes, chondrocyte-specific c-Raf kn

175 ssing cells, predominantly proliferating and hypertrophic chondrocytes, using "Cre-loxP"-mediated gen

176 y expressed within prehypertrophic and early hypertrophic chondrocytes.

177 on-contraction coupling in health as well as hypertrophic compensatory adaptation and represent a str

178 translation in response to developmental and hypertrophic cues.

179 accelerated the transition of progenitors to hypertrophic (differentiating) chondrocytes as revealed

180 eased chondrocyte proliferation, accelerated hypertrophic differentiation and cell death with reduced

181 ctivation is responsible for the accelerated hypertrophic differentiation and kyphosis, whereas the o

182 sociated with reduced proliferation and poor hypertrophic differentiation and the improved bone growt

183 disease in patients and families, including hypertrophic, dilated, and arrhythmogenic cardiomyopathi

184 he diverse molecules and pathways that cause hypertrophic, dilated, restrictive, and arrhythmogenic c

185 in-sensitive mTOR only partially blocked the hypertrophic effects of chronic RE.

186 proinflammatory cytokines (e.g., TNFalpha), hypertrophic factors (e.g., ANP), and profibrotic factor

187 deling and activate spatially segregated pro-hypertrophic factors.

188 d from the sarcolemma to the myofilaments in hypertrophic failing rabbit myocytes.

189 ted with downregulation of caveolin-3 in the hypertrophic failing rabbit myocytes.

190 it is critically important to determine how hypertrophic fat tissue alters T cell balance to drive i

191 sistent with their combined action promoting hypertrophic gene expression.

192 m cell-derived CMs, decreasing expression of hypertrophic genes and regulating hypertrophic pathways.

193 or overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6

194 Cardiac hypertrophic growth in response to pathological cues is

195 omyocytes undergo a critical hyperplastic-to-hypertrophic growth transition at early postnatal age, w

196 nd is likely associated with hyperplastic-to-hypertrophic growth transition.

197 portant functions in cardiac hyperplastic-to-hypertrophic growth transition.

198 n signalling pathways required for postnatal hypertrophic growth were also observed in skeletal muscl

199 Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific

200 3A is present in resting, proliferating, and hypertrophic growth-plate cartilage and assembles into a

201 agy suppression and subsequent initiation of hypertrophic growth.

202 metabolism are the key mediators of cardiac hypertrophic growth.

203 can facilitate the promotion of compensatory hypertrophic growth.

204 ctor (Srf) is needed for optimal SC-mediated hypertrophic growth.

205 Cardiac beta-myosin variants cause hypertrophic (HCM) or dilated (DCM) cardiomyopathy by di

206 cardiomyopathy that mimics hypertensive and hypertrophic heart disease and often goes undiagnosed.

207 tein expression levels were downregulated in hypertrophic hearts from mice.

208 ein kinase (AMPK) in aged and Ang II-induced hypertrophic hearts in vivo as well as in cardiomyocytes

209 uman, DPF3a is significantly up-regulated in hypertrophic hearts of patients with hypertrophic cardio

210 al-time images compare to static images from hypertrophic hearts reported in the literature): 1) Inse

211 In human hypertrophic hearts, BRG1 and FOXM1 expression is also a

212 This study demonstrates profibrosis and hypertrophic inward remodelling within the largest cereb

213 af in chondrocytes leads to expansion of the hypertrophic layer of the growth plate, with decreased p

214 n human gingiva and skin and in gingival and hypertrophic-like scar-forming skin wound healing in a p

215 cumulated over time and persisted in forming hypertrophic-like scars, whereas few CD26-positive cells

216 sisting TRAS in Pten(-/-) mice and abrogated hypertrophic liver growth.

217 n association of PTEN with TRAS turnover and hypertrophic liver growth.

218 s the burning of TRAS-derived lipids to fuel hypertrophic liver regeneration.

219 The aggregation of hypertrophic macrophages constitutes the basis of all gr

220 d1 protein levels lead to elevated levels of hypertrophic markers in cultured rat cardiomyocytes.

221 formed in the discs and expressed cartilage hypertrophic markers Runx2 and ColX.

222 Hypertrophic microglia were found to enclose or engulf c

223 c hypertrophy via elevated expression of pro-hypertrophic miR-208a, myocardial damage, and suppressio

224 ymethylome in embryonic, neonatal, adult and hypertrophic mouse cardiomyocytes, showing that dynamic

225 kground (Mtn(-/-)/Errgamma(Tg/+)) results in hypertrophic muscle with a high oxidative capacity thus

226 essure overload-induced HF mice and isolated hypertrophic myocardial cells, fatty acid beta-oxidation

227 s via FGF receptor (FGFR) 4 thereby inducing hypertrophic myocyte growth and the development of left

228 als and its requirement to achieve efficient hypertrophic myofiber growth.

229 tions in human beta-cardiac myosin using the hypertrophic myopathy mutation R453C.

230 ve (MV) surgery are unknown in patients with hypertrophic obstructive cardiomyopathy (HOCM) undergoin

231 sitive/phenotype negative), 10 patients with hypertrophic obstructive cardiomyopathy (HOCM), 10 patie

232 Hypertrophic obstructive cardiomyopathy is an inherited

233 n myonuclear accretion and activation of pro-hypertrophic pathways.

234 ression of hypertrophic genes and regulating hypertrophic pathways.

235 absence of Herpud1 generates a pathological hypertrophic phenotype by regulating IP3R protein levels

236 ar hypertrophy but there is an important pre-hypertrophic phenotype with features including crypts, a

237 ctRIIB- and ActRIIA-deficient mice display a hypertrophic phenotype.

238 and electrophysiological changes during the hypertrophic process are still largely unknown.

239 ion in the transition of chondrocytes to the hypertrophic program.

240 nsive, vasodilatory, anti-fibrotic, and anti-hypertrophic properties of BNP are well established in m

241 y for common disorders like appendicitis and hypertrophic pyloric stenosis are all supported by good

242 In hypertrophic rabbit myocytes, selectively enhanced beta2

243 -) mice shortly after induction of knockout, hypertrophic regeneration was accelerated and led to hep

244 yte cell cycle progression while promoting a hypertrophic regenerative response, without increasing a

245 owing a switch in the basal compartment to a hypertrophic regimen with thyroxine, the cartilage discs

246 intact spinal cords formed CTs with proximal hypertrophic regions and distal non-hypertrophic regions

247 proximal hypertrophic regions and distal non-hypertrophic regions, whereas removal of spinal cords re

248 rteries, including the occurrence of outward hypertrophic remodeling and increased stiffness.

249 Hypertrophic remodeling of white adipose tissues is asso

250 miR-1 in heart development and cardiomyocyte hypertrophic remodeling, we additionally found that MCU

251 at is susceptible to loss of function during hypertrophic remodeling.

252 hysiological versus pathological patterns of hypertrophic remodeling.

253 ogical blockade of microRNA-146a blunted the hypertrophic response and attenuated cardiac dysfunction

254 d in mice lacking SRC-2 induces an abrogated hypertrophic response and decreases sustained cardiac fu

255 Anti-miR-182 treatment inhibits the hypertrophic response and prevents the Akt/mTORC1 activa

256 ther miRNAs contribute to the development of hypertrophic response associated with myocardial angioge

257 is thought to act as an initiator of cardiac hypertrophic response at the level of the sarcolemma, bu

258 elated protein 2 (sFRP2), which inhibits the hypertrophic response in neighbouring cardiomyocytes.

259 on of Bcat2, Foxo3 and Adcy6 to regulate the hypertrophic response in PlGF mice.

260 ) that was designed to detect an exaggerated hypertrophic response to hypertension and tested its pot

261 1/2, but not Smad2/3, attenuated the cardiac hypertrophic response to pressure overload stimulation.

262 and specifically in fibroblasts, reduces the hypertrophic response to pressure overload; however, kno

263 This blunted hypertrophic response was associated with a reduction in

264 This hypertrophic response was comparable to that of 4 weeks'

265 ulator of cardiac fibrosis but may delay the hypertrophic response.

266 matching blood supply, it may also promote a hypertrophic response.

267 n important role in the angiogenesis induced-hypertrophic response.

268 Ageing is associated with impaired hypertrophic responses to resistance exercise training (

269 Hypertrophic responses to RET with age are diminished co

270 In response to 6 weeks RET, we found blunted hypertrophic responses with age are underpinned by chron

271 ly cytoskeleton, force transmission disease; hypertrophic-restrictive cardiomyopathies as sarcomeric,

272 Hypertrophic scar (HTS) formation is a frequent postoper

273 cal delivery of S100A12 resulted in a marked hypertrophic scar formation in a validated rabbit hypert

274 trophic scar formation in a validated rabbit hypertrophic scar model compared with saline control.

275 rmabrasion, wound healing, safety, scarring, hypertrophic scar, and keloid.

276 ion of wound healing to attenuate or prevent hypertrophic scarring, well-designed trials to confirm t

277 e and surgery to minimise the development of hypertrophic scarring.

278 Hypertrophic scars (HTS), frequently seen after traumati

279 Preventing the formation of hypertrophic scars, especially those that are a result o

280 p-regulated in skin wounds and in normal and hypertrophic scars.

281 Unlike humans, rats do not develop hypertrophic scars.

282 hment of committed progenitors, formation of hypertrophic sebaceous glands, and increased epidermal d

283 under hypoxia was lethal, suggesting that a hypertrophic signal in the presence of insufficient oxyg

284 ssion further enhances calcineurin-dependent hypertrophic signal transduction, and its knockdown repr

285 contribute to cardiac remodeling by inducing hypertrophic signaling, apoptosis, and necrosis.

286 binds calcineurin, a phosphatase controlling hypertrophic signaling, we examined the effects of CEFIP

287 The processes that selectively induce these hypertrophic states are poorly understood.

288 keletal muscle, are activated in response to hypertrophic stimuli and give rise to myogenic progenito

289 ases substantially in response to stress and hypertrophic stimuli through largely obscure mechanisms.

290 Upon hypertrophic stimuli, casein kinase 2 phosphorylates DPF

291 transgenic (Sike-TG) mice are protected from hypertrophic stimuli.

292 and optimal muscle remodeling in response to hypertrophic stimuli.

293 gesting that the non-response of muscle to a hypertrophic stimulus could be modulated by epigenetic m

294 crease size and DNA content in response to a hypertrophic stimulus, thus providing a physiological mo

295 ble in vitro and in vivo upon removal of the hypertrophic stimulus.

296 parameters in differentiating CA from other hypertrophic substrates, especially in the gray zone of

297 nd the brain natriuretic peptide (Bnp) whose hypertrophic upregulation is mediated by both class I an

298 nism that controls PASMC survival to promote hypertrophic vascular remodeling and PAH.-

299 but how this translates into the spectrum of hypertrophic versus dilated cardiomyopathy is unknown.

300 CDS-associated expansion of the growth plate hypertrophic zone, attenuated enhanced expression of ER