ライフサイエンスコーパス: hypertrophic

1 h categories ranging from "oligotrophic" to "hypertrophic".

2 ory phenotype, which is pro-fibrotic and pro-hypertrophic.

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 low-up and divided into categories: dilated, hypertrophic, alcohol/drug-induced, and other.

6 wledge of which and how TNNT2 variants cause hypertrophic and dilated cardiomyopathies could improve

7 Pathogenic TNNT2 variants are a cause of hypertrophic and dilated cardiomyopathies, which promote

8 beta-cardiac myosin gene are associated with hypertrophic and dilated cardiomyopathy, respectively.

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

10 nd in isolated cardiomyocytes in response to hypertrophic and inflammatory stimuli.

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

12 are-fibre diode laser significantly improved hypertrophic and keloid scars based on both subjective a

13 Hypertrophic and keloid scars result from abnormal wound

14 al fibre delivery device in the treatment of hypertrophic and keloid scars.

15 Impaired relaxation is a hallmark of hypertrophic and restrictive cardiomyopathies (HCM and R

16 hich 2631 (59%) were dilated, 673 (15%) were hypertrophic, and 480 (11%) were alcohol/drug-induced.

17 y in cardiomyocytes, but allowed response to hypertrophic as well as proliferative stimuli.

18 AAV9-M7.8L RNAi suppressed the expression of hypertrophic biomarkers, reduced heart weight, and atten

19 ice (Mcoln1 (-/-) ) induces a hyperdistended/hypertrophic bladder phenotype.

20 By this minimal invasive method, hypertrophic bleb complication of XEN gel implant has be

21 e objective and subjective changes in mature hypertrophic burn scars treated with a fractional ablati

22 Subjects aged 11 years or older with hypertrophic burn scars were recruited.

23 hickness, appearance, and symptoms of mature hypertrophic burn scars.

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

25 tating heart conditions, notably dilated and hypertrophic cardiomyopathies (CMs), are associated with

26 Dilated and hypertrophic cardiomyopathies are the most common; restr

27 y, phenotype-positive patients with isolated hypertrophic cardiomyopathy <18 years of age at diagnosi

28 The global estimates for hypertrophic cardiomyopathy (1/500 individuals), dilated

29 disease (8%), congenital heart disease (2%), hypertrophic cardiomyopathy (2%), and others (5%).

30 ses: long QT syndrome (LQTS) (n = 48 [42%]), hypertrophic cardiomyopathy (HCM) (n = 28 [24%]), Brugad

31 Hypertrophic cardiomyopathy (HCM) affects 1 in 500 peopl

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

33 ferential strain) in a genotyped cohort with hypertrophic cardiomyopathy (HCM) and to explore correla

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

35 Although the genetic causes of hypertrophic cardiomyopathy (HCM) are widely recognized,

36 tests and a case cohort of individuals with hypertrophic cardiomyopathy (HCM) based on comprehensive

37 etic screening of relatives of patients with hypertrophic cardiomyopathy (HCM) caused by sarcomere pr

38 End-stage (ES) hypertrophic cardiomyopathy (HCM) has been considered a

39 Hypertrophic cardiomyopathy (HCM) has been considered a

40 Over the last 50 years, the epidemiology of hypertrophic cardiomyopathy (HCM) has changed because of

41 he impact of sex on phenotypic expression in hypertrophic cardiomyopathy (HCM) has not been well char

42 amine the contribution of MYBPC3(Delta25) to hypertrophic cardiomyopathy (HCM) in a large patient coh

43 To assess the genetic architecture of hypertrophic cardiomyopathy (HCM) in patients of predomi

44 Hypertrophic cardiomyopathy (HCM) is a common genetic di

45 Hypertrophic cardiomyopathy (HCM) is a genetic cardiovas

46 Hypertrophic cardiomyopathy (HCM) is a genetic disease t

47 Hypertrophic cardiomyopathy (HCM) is a heritable myocard

48 Hypertrophic cardiomyopathy (HCM) is a prevalent and com

49 Hypertrophic cardiomyopathy (HCM) is a worldwide genetic

50 Hypertrophic cardiomyopathy (HCM) is an inherited diseas

51 Hypertrophic cardiomyopathy (HCM) is an uncommon but imp

52 Myocardial ischemia in hypertrophic cardiomyopathy (HCM) is associated with poo

53 Hypertrophic cardiomyopathy (HCM) is caused by pathogeni

54 Hypertrophic cardiomyopathy (HCM) is considered a leadin

55 Hypertrophic cardiomyopathy (HCM) is frequently caused b

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

57 Hypertrophic cardiomyopathy (HCM) is the most common her

58 Hypertrophic cardiomyopathy (HCM) is the most common inh

59 Genetic testing is helpful for diagnosis of hypertrophic cardiomyopathy (HCM) mimics.

60 Hypertrophic cardiomyopathy (HCM) occurs as a spontaneou

61 Genetic testing for families with hypertrophic cardiomyopathy (HCM) provides a significant

62 prospective registry of 2,755 patients with hypertrophic cardiomyopathy (HCM) recruited from 44 site

63 eric gene mutation carriers with early-stage hypertrophic cardiomyopathy (HCM) to test whether valsar

64 e term "end stage" has been used to describe hypertrophic cardiomyopathy (HCM) with left ventricular

65 hickness such as cardiac amyloidosis, septal hypertrophic cardiomyopathy (HCM), and apical HCM exhibi

66 ures in noncompaction cardiomyopathy (NCCM), hypertrophic cardiomyopathy (HCM), and dilated cardiomyo

67 e autosomal dominant phenocopy of sarcomeric hypertrophic cardiomyopathy (HCM), characterized by vent

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

69 e linked to dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM), respectively.

70 Although hypertrophic cardiomyopathy (HCM), the most common inher

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

72 heavy chain 7) represent a leading cause of hypertrophic cardiomyopathy (HCM).

73 n unmet need for treatments that can prevent hypertrophic cardiomyopathy (HCM).

74 MYBPC3 splicing errors are a common cause of hypertrophic cardiomyopathy (HCM).

75 of RAF1 present with severe and often lethal hypertrophic cardiomyopathy (HCM).

76 ay is a likely focus for fatal arrhythmia in hypertrophic cardiomyopathy (HCM).

77 ventricular arrhythmias among patients with hypertrophic cardiomyopathy (HCM).

78 tral valve is often structurally abnormal in hypertrophic cardiomyopathy (HCM).

79 rker for outcome prediction in patients with hypertrophic cardiomyopathy (HCM); however, its clinical

80 Patients with nonobstructive hypertrophic cardiomyopathy (nHCM) often experience a hi

81 Obstructive hypertrophic cardiomyopathy (oHCM) is characterized by u

82 g biomechanical abnormalities in obstructive hypertrophic cardiomyopathy (oHCM).

83 expression was also modestly associated with hypertrophic cardiomyopathy (p = 6.3e-04).

84 educed in CA compared with both controls and hypertrophic cardiomyopathy (P<0.001).

85 FD had T2 elevation (FD 58.2+/-5.0 ms versus hypertrophic cardiomyopathy 55.6+/-4.3 ms, chronic myoca

86 n in Adults With Symptomatic Non-Obstructive Hypertrophic Cardiomyopathy [MAVERICK-HCM]; NCT03442764)

87 ted with shortened survival in patients with hypertrophic cardiomyopathy across all three cohorts, an

88 One hundred eighty-three patients with hypertrophic cardiomyopathy and a low- or intermediate 5

89 LGE presence and its extent in patients with hypertrophic cardiomyopathy and a low-intermediate 5-yea

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

91 t (LGE) is an important prognostic marker in hypertrophic cardiomyopathy and an extent >15% it is ass

92 n I (TNNI3) gene mutations account for 3% of hypertrophic cardiomyopathy and carriers have a heteroge

93 larified the prognostic usefulness of MRI in hypertrophic cardiomyopathy and Fabry disease.

94 re also observed in human patient samples of hypertrophic cardiomyopathy and heart failure.

95 n Mendelian forms of these diseases, such as hypertrophic cardiomyopathy and long-QT syndrome, uncove

96 Patients with hypertrophic cardiomyopathy and MYBPC3 variants were ide

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

98 sults showed the animal suffered from feline hypertrophic cardiomyopathy and severe pulmonary edema a

99 d Gaa(c.1826dupA) murine model recapitulates hypertrophic cardiomyopathy and skeletal muscle weakness

100 Available pharmacological options for hypertrophic cardiomyopathy are inadequate or poorly tol

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

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

103 autosomal recessive form of NS with massive hypertrophic cardiomyopathy as clinically the most preva

104 ion to accelerated aging, these mice develop hypertrophic cardiomyopathy at ~13 months of age, presum

105 This executive summary of the hypertrophic cardiomyopathy clinical practice guideline

106 Aim This executive summary of the hypertrophic cardiomyopathy clinical practice guideline

107 BPC3 variants and relatively small genotyped hypertrophic cardiomyopathy cohorts have precluded detai

108 We sequenced 29 families with hypertrophic cardiomyopathy enriched for pediatric-onset

109 es on mortality in patients with obstructive hypertrophic cardiomyopathy following myectomy.

110 Consecutive patients treated with ASA for hypertrophic cardiomyopathy from 2003 to 2019 at a terti

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

112 ucture Many recommendations from the earlier hypertrophic cardiomyopathy guidelines have been updated

113 Many recommendations from the earlier hypertrophic cardiomyopathy guidelines have been updated

114 We report the early onset of severe hypertrophic cardiomyopathy in a novel murine IOPD model

115 rithms for clinicians to diagnose and manage hypertrophic cardiomyopathy in adult and pediatric patie

116 rithms for clinicians to diagnose and manage hypertrophic cardiomyopathy in adult and pediatric patie

117 Among 4756 genotyped patients with hypertrophic cardiomyopathy in Sarcomeric Human Cardiomy

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

119 Hypertrophic cardiomyopathy is the leading cause of sudd

120 scle, suggesting that MYL2 mutated models of hypertrophic cardiomyopathy may be useful research tools

121 We generated maps of regulatory elements on hypertrophic cardiomyopathy patients (ChIP-seq N=14 and

122 rentially active regulatory elements between hypertrophic cardiomyopathy patients and controls can of

123 rs of genes differentially regulated between hypertrophic cardiomyopathy patients and controls showed

124 ating differentially expressed genes between hypertrophic cardiomyopathy patients and controls.

125 outcomes of medically refractory obstructive hypertrophic cardiomyopathy patients undergoing alcohol

126 The study cohort comprises 217 consecutive hypertrophic cardiomyopathy patients with primary preven

127 C mutant, we sought to determine whether the hypertrophic cardiomyopathy phenotype observed in papill

128 ogenic mechanisms that drive severe clinical hypertrophic cardiomyopathy phenotypes and for identifyi

129 Conclusion In the hypertrophic cardiomyopathy population, a three-dimensio

130 Patients with obstructive hypertrophic cardiomyopathy referred for either ASA or S

131 Hypertrophic cardiomyopathy registries have revealed dis

132 The HCMR (Hypertrophic Cardiomyopathy Registry) is a National Hear

133 ype of this unique mutation in patients with hypertrophic cardiomyopathy remains unknown.

134 naire-Clinical Summary Score (KCCQ-CSS), and Hypertrophic Cardiomyopathy Symptom Questionnaire Shortn

135 ate a SCD risk prediction model in pediatric hypertrophic cardiomyopathy to guide SCD prevention stra

136 explain the responsiveness of patients with hypertrophic cardiomyopathy to verapamil in managing lef

137 dically refractory patients with obstructive hypertrophic cardiomyopathy treated according to the Ame

138 microvasculature's role in diseases such as hypertrophic cardiomyopathy where misalignment of cardio

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

140 outcomes of 2,482 patients with obstructive hypertrophic cardiomyopathy who underwent transaortic se

141 cular centres in 13 countries, patients with hypertrophic cardiomyopathy with an LVOT gradient of 50

142 effect in South Lebanon and causes malignant hypertrophic cardiomyopathy with early SCD even in the a

143 n in Adults With Symptomatic Non-Obstructive Hypertrophic Cardiomyopathy) explored the safety and eff

144 uating Disease Evolution in Early Sarcomeric Hypertrophic Cardiomyopathy) targeted young sarcomeric g

145 or pulmonary arterial hypertension, 0.91 for hypertrophic cardiomyopathy, 0.86 for cardiac amyloid, a

146 Additionally, 28 patients with hypertrophic cardiomyopathy, 30 with chronic myocardial

147 agnosed with dilated cardiomyopathy, 246 had hypertrophic cardiomyopathy, 61 had alcohol/drug-induced

148 In hypertrophic cardiomyopathy, after a primary prevention

149 cardiomyopathy, 1.09 (95% CI, 1.06-1.12) for hypertrophic cardiomyopathy, and 1.10 (1.06-1.13) for al

150 rformed at diastole and systole in 20 CA, 11 hypertrophic cardiomyopathy, and 10 control subjects wit

151 ith aortic stenosis and associated secondary hypertrophic cardiomyopathy, and 15 controls) in identic

152 y is a key pathophysiological abnormality in hypertrophic cardiomyopathy, and a major determinant of

153 function not only in participants with overt hypertrophic cardiomyopathy, but also in carriers of sar

154 e following septal myectomy in patients with hypertrophic cardiomyopathy, but their incidence and eff

155 nd disease (pulmonary arterial hypertension, hypertrophic cardiomyopathy, cardiac amyloid, and mitral

156 ed from surgical explants from patients with hypertrophic cardiomyopathy, from a transaortic-constric

157 e show several pathophysiological insults in hypertrophic cardiomyopathy, including the R403Q myosin

158 In hypertrophic cardiomyopathy, multimodality imaging is cr

159 thic pulmonary fibrosis, systemic sclerosis, hypertrophic cardiomyopathy, or myelofibrosis from Stanf

160 nding protein C ( MYBPC3) gene, which causes hypertrophic cardiomyopathy, recapitulated seminal disea

161 inding for the sarcomere variants that cause hypertrophic cardiomyopathy, the titin and sarcomere var

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

163 ently affected with typical manifestation of hypertrophic cardiomyopathy, which can progress to heart

164 Hypertrophic cardiomyopathy-associated TNNT2 variants ca

165 Our study found that hypertrophic cardiomyopathy-associated TNNT2 variants in

166 The hypertrophic cardiomyopathy-causing cardiac troponin T (

167 The alpha-cardiac actin M305L hypertrophic cardiomyopathy-causing mutation lies near r

168 in C), are the most common cause of familial hypertrophic cardiomyopathy.

169 for preventing sudden death in patients with hypertrophic cardiomyopathy.

170 displaying skeletal myopathy with late-onset hypertrophic cardiomyopathy.

171 mechanism of a mutation that causes familial hypertrophic cardiomyopathy.

172 myosin inhibitor, in symptomatic obstructive hypertrophic cardiomyopathy.

173 meric genes and with phenotypic overlap with hypertrophic cardiomyopathy.

174 iomyopathy, and 2 were found to be end-stage hypertrophic cardiomyopathy.

175 aluated its prognostic role in patients with hypertrophic cardiomyopathy.

176 nt of Fabry disease mimicking nonobstructive hypertrophic cardiomyopathy.

177 s support a cumulative variant hypothesis in hypertrophic cardiomyopathy.

178 anisotropy effectively discriminate CA from hypertrophic cardiomyopathy.

179 es risk factors that are unique to pediatric hypertrophic cardiomyopathy.

180 mpaction, and 2 fourth-degree relatives with hypertrophic cardiomyopathy.

181 therapeutic strategy to treat NS-associated hypertrophic cardiomyopathy.

182 d health status in patients with obstructive hypertrophic cardiomyopathy.

183 issense variants in JPH2 have been linked to hypertrophic cardiomyopathy; however, pathogenic "loss o

184 -2) yr(-1), corresponding to "eutrophic" to "hypertrophic" categories.

185 levels in the cytosol of chondroblastic and hypertrophic cells.

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

187 e mutant protein and subsequently disrupting hypertrophic chondrocyte differentiation.

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

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

190 Compression elevated the transcription of hypertrophic chondrocyte marker MMP13 and pre-osterix tr

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

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

193 Atomic force microscopy showed that hypertrophic chondrocytes are the least mechanically sti

194 suggest that SOC has evolved to protect the hypertrophic chondrocytes from the high mechanical stres

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

196 A mutator mice displayed elevated numbers of hypertrophic chondrocytes in articular calcified cartila

197 ncentric lamellae, which were present around hypertrophic chondrocytes in the ACC are described for t

198 The lamellae were associated with hypertrophic chondrocytes throughout the ACC.Novel micro

199 periments revealed the high vulnerability of hypertrophic chondrocytes to mechanical stress and showe

200 ma of endochondral bone ossification is that hypertrophic chondrocytes undergo apoptosis, while invad

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

202 Panx3 was phosphorylated in prehypertrophic, hypertrophic chondrocytes, and bone areas of the newborn

203 tissues, with cells staining for markers of hypertrophic chondrocytes, including collagen X and runt

204 t cartilage was enriched for homeostatic and hypertrophic chondrocytes, while damaged cartilage was e

205 r fetal-like markers, transiently arose from hypertrophic crypts known to facilitate regeneration.

206 racellular matrix remodeling and chondrocyte hypertrophic differentiation in vitro, in a kinase-indep

207 MEndoT showed significantly upregulated anti-hypertrophic factors and downregulated pro-hypertrophic

208 i-hypertrophic factors and downregulated pro-hypertrophic factors.

209 NAs is altered this affects chondrogenic and hypertrophic gene expression.

210 ated protein kinase signaling hyperactivity, hypertrophic gene response and cellular hypertrophy.

211 nted myocyte apoptosis, and up-regulation of hypertrophic genes were also not significantly different

212 However, its contribution to cardiac hypertrophic growth and heart failure remains incomplete

213 and its downstream mediator in cardiomyocyte hypertrophic growth and metabolic remodeling.

214 n significantly blunts phenylephrine-induced hypertrophic growth in cultured cardiomyocytes.

215 Thus, inhibition of myofiber hypertrophic growth is a consistent feature of pediatric

216 Cardiac hypertrophic growth is mediated by robust changes in gen

217 ivo, pressure overload-induced cardiomyocyte hypertrophic growth is prevented with FoxO1 knockdown or

218 ploidy is a prerequisite or a consequence of hypertrophic growth is unclear.

219 ated, and if so, what its function is during hypertrophic growth of cardiac myocytes.

220 ights into the link between hyperplastic and hypertrophic growth of cardiomyocytes.

221 isms of how preservation of FAO prevents the hypertrophic growth of cardiomyocytes.

222 , and the FoxO1-Dio2 axis governs TH-induced hypertrophic growth of neonatal cardiomyocytes in vitro

223 Increasing Pck2 was sufficient to promote hypertrophic growth similar to that caused by increasing

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

225 data suggest that FoxO1 may mediate cardiac hypertrophic growth via regulation of pol II de novo rec

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

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

228 tterning and a reduction in binucleation and hypertrophic growth with increased fetal troponin (Tropo

229 Lin28a attenuated pressure overload-induced hypertrophic growth, cardiac dysfunction, and alteration

230 rdiac muscle transitions from hyperplasic to hypertrophic growth, the extracellular matrix (ECM) unde

231 es in FoxO1 chromatin binding during cardiac hypertrophic growth, which positively correlate with ext

232 3A is present in resting, proliferating, and hypertrophic growth-plate cartilage and assembles into a

233 responses, impacting both muscle repair and hypertrophic growth.

234 least in part, the role of Lin28a in cardiac hypertrophic growth.

235 agy suppression and subsequent initiation of hypertrophic growth.

236 metabolism are the key mediators of cardiac hypertrophic growth.

237 the HBP is induced in cardiomyocytes during hypertrophic growth.

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

239 TAC, prevented the reduced LCFA oxidation in hypertrophic hearts and normalized energy state (phospho

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

241 vance of an Orai1 inhibition strategy during hypertrophic insult.

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

243 yzed Regnase-3-deficient mice, which develop hypertrophic lymph nodes.

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

245 , sacubitril/valsartan and valsartan reduced hypertrophic markers, but only sacubitril/valsartan redu

246 ice showed the typical chronic posttraumatic hypertrophic morphology.

247 n of Mettl21e was strikingly up-regulated in hypertrophic muscles and during myogenic differentiation

248 ssed in human adipose cells and increased in hypertrophic obesity.

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

250 These translated to 4 genes/1 ncRNA in hypertrophic obstructive cardiomyopathy, 131 genes/17 nc

251 ique differentially methylated regions: 5 in hypertrophic obstructive cardiomyopathy, 151 in dilated

252 le HF patients encompassing causes including hypertrophic obstructive cardiomyopathy, ischemic cardio

253 Hypertrophic olivary degeneration (HOD) is a unique neur

254 Hypertrophic olivary degeneration is an infrequent neuro

255 events) and nutrient loading (eutrophic vs. hypertrophic) on total phytoplankton chlorophyll-a and c

256 ell-derived cardiomyocytes recapitulated the hypertrophic phenotype and uncovered a so-far-not-descri

257 Expression of hypertrophic phenotype was also limited in the coculture

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

259 ats) repair and demonstrated a rescue of the hypertrophic phenotype.

260 which, in turn, facilitates regenerative and hypertrophic processes that restore structure to injured

261 Infantile hypertrophic pyloric stenosis (IHPS) is a disorder of yo

262 t functional upregulation of SK2 channels in hypertrophic rat ventricular cardiomyocytes is driven by

263 hy revealed increased LV dilatation, altered hypertrophic remodeling and exacerbated contractile dysf

264 the early degenerative changes and possible hypertrophic remodeling at cardiac left ventricular tiss

265 actility, but impaired relaxation and evoked hypertrophic remodeling with increased energetic stress.

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

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

268 lating the pressure overload induced cardiac hypertrophic response and in controlling the expression

269 he presence of gene changes that limited the hypertrophic response and promoted cardiomyocyte surviva

270 scription factor ATF6beta in regulating this hypertrophic response are not well-understood.

271 rophic stimuli and is necessary for a normal hypertrophic response in cardiomyocytes.

272 Hypertrophic response to pathological stimuli is a compl

273 These molecular changes translated to a mild hypertrophic response to TAC with decreased maladaptive

274 ar translocation and effectively blocked the hypertrophic response, demonstrating the utility of this

275 rate of protein synthesis and the subsequent hypertrophic response.

276 NORD96A resulted in changes in chondrogenic, hypertrophic, rRNA and osteoarthritis related gene expre

277 A hypertrophic scar (HS) is a cutaneous condition characte

278 Similar to the hypertrophic scar and keloids, the efficacy of glucortic

279 tic to prevent formation of a fibrotic scar (hypertrophic scar or keloid) or to prevent cutaneous fib

280 sential for normal healing and prevention of hypertrophic scarring.

281 udy was performed involving 21 patients with hypertrophic scars (HS) (n = 9) and keloids (n = 12) res

282 zation have all been proposed to encode this hypertrophic signal.

283 e in mediating both contractile function and hypertrophic signaling in ventricular cardiomyocytes.

284 Although numerous studies have investigated hypertrophic signaling pathways, less is known about hyp

285 -trisphosphate receptors (IP(3)Rs), engaging hypertrophic signaling pathways.

286 as a plausible mechanism for IP(3)-dependent hypertrophic signaling via Ca(2+)-sensitive transcriptio

287 o normalize the pressure overload-stimulated hypertrophic signals by activating G protein-coupled rec

288 and CaN-Gbetagamma interactions in mediating hypertrophic signals in ISO-specific context and reveale

289 found a significant increase in response to hypertrophic stimulation, suggesting a potential role fo

290 modification that is enhanced in response to hypertrophic stimuli and is necessary for a normal hyper

291 anscription factor that is also regulated by hypertrophic stimuli in the heart.

292 ntake by 40% to slow growth reduced podocyte hypertrophic stress and "froze" all elements of the prog

293 that glomerular enlargement drives podocyte hypertrophic stress leading to accelerated podocyte deta

294 for maintaining contractility reserve after hypertrophic stress.

295 The mutant anthers display swollen, hypertrophic tapetal cells and pollen grains, suggesting

296 nd polyhaline (PH) salinity zones, and from "hypertrophic" to "eutrophic" for the mesohaline (MH) sal

297 myocardial infarction border zone and in the hypertrophic ventricle, involving regulatory sequences p

298 eft ventricular cardiac dysfunction and were hypertrophic, with a thicker left ventricular posterior

299 At the edge of the hypertrophic zone, chondrocytes re-enter the cell cycle

300 Geo reporter in chondrocytes, but not in the hypertrophic zone.