ライフサイエンスコーパス: aortic constriction

1 c hypertrophy (pressure overload by thoracic aortic constriction).

2 ed Galpha(q)(*) and pressure overload due to aortic constriction).

3 hem to mechanical stress in vivo (transverse aortic constriction).

4 and circulating H2S levels after transverse aortic constriction.

5 ablished cardiac remodeling after transverse aortic constriction.

6 progression of hypertrophy after transverse aortic constriction.

7 4,5)P3 and IP3-R(2) are caused by transverse aortic constriction.

8 Nox4 knockout mice 2 weeks after transverse aortic constriction.

9 ypertrophy, and improves following relief of aortic constriction.

10 cardiac hypertrophy and HF after transverse aortic constriction.

11 ompared with wild-type mice after transverse aortic constriction.

12 ic cardiac changes that occur in response to aortic constriction.

13 stolic dysfunction in response to transverse aortic constriction.

14 eletion of GRK5 were subjected to transverse aortic constriction.

15 ns of angiotensin-II infusion or transversal aortic constriction.

16 ned ventricular tachycardia after transverse aortic constriction.

17 s mice from early mortality after transverse aortic constriction.

18 diac myocyte apoptosis induced by transverse aortic constriction.

19 ation is disrupted in response to transverse aortic constriction.

20 cantly upregulated in response to transverse aortic constriction.

21 ac insufficiency at 2 weeks after transverse aortic constriction.

22 nd IL10 knockout (IL10KO) mice by transverse aortic constriction.

23 r inducing cardiac hypertrophy by transverse aortic constriction.

24 pertrophy/fibrosis from sustained transverse aortic constriction.

25 e to pressure overload induced by transverse aortic constriction.

26 demonstrate dysregulation after exposure and aortic constriction.

27 ardiac hypertrophy in response to transverse aortic constriction.

28 subjected to pressure overload by transverse aortic constriction.

29 kload for 5 min with dobutamine infusion and aortic constriction.

30 all hLpL0 mice died within 48 h of abdominal aortic constriction.

31 severely to dilated cardiomyopathy following aortic constriction.

32 onic pressure overload induced by transverse aortic constriction.

33 hic gene induction in response to transverse aortic constriction.

34 s decreased in gp91phox-deficient mice after aortic constriction.

35 the increase in myocyte cell size induced by aortic constriction.

36 that have subsequently undergone transverse aortic constriction.

37 ic inhibitor of mTOR, to mice with ascending aortic constriction.

38 ontrols underwent chronic Ang II infusion or aortic constriction.

39 model of heart failure created by ascending aortic constriction.

40 and after acute mechanical stress induced by aortic constriction.

41 onic pressure overload induced by transverse aortic constriction.

42 ollowing induction of cardiac hypertrophy by aortic constriction.

43 rabbits by combined aortic insufficiency and aortic constriction.

44 termate controls both prior to and following aortic constriction.

45 was achieved following 7 days of transverse aortic constriction.

46 neutral promoter to one that is activated by aortic constriction.

47 issue from hypertrophied hearts subjected to aortic constriction.

48 e transcriptional activation of this gene by aortic constriction.

49 starting 3 weeks before surgical transverse aortic constriction.

50 ngs were seen in HFpEF induced by transverse aortic constriction.

51 delayed dilation after 28 days of transverse aortic constriction.

52 e were studied for 12 weeks after transverse aortic constriction.

53 f failing hearts after reversible transverse aortic constriction.

54 and contractile dysfunction after transverse aortic constriction.

55 ptive cardiac phenotype following transverse aortic constriction.

56 AT transcriptional activity after transverse aortic constriction.

57 either by isoproterenol administration or by aortic constriction.

58 ssion to heart failure seen after transverse aortic constriction.

59 re derived from bone marrow after transverse aortic constriction.

60 diac structure and function after transverse aortic constriction.

61 NGFR was not significantly altered following aortic constriction (44 +/- 5 nl/min vs. 47 +/- 5 nl/min

62 rtality from cardiac stress after transverse aortic constriction, 5) abnormal mitochondrial function

63 s; however, after 7 to 28 days of transverse aortic constriction, a subset of cardiomyocytes in fibro

64 t) for 4 weeks, following which an abdominal aortic constriction (AAC) was produced.

65 ressure-overload as a result of an abdominal aortic constriction (AAC).

66 hronic pressure overload caused by ascending aortic constriction (AAC).

67 rsisted after pressure overload by ascending aortic constriction (AAC).

68 Transverse aortic constriction activated FYN in the left ventricle

69 nd pathology in mice subjected to transverse aortic constriction after the consumption of a fish oil

70 ids were observed after 1 week of transverse aortic constriction and 5 days after MI.

71 rdiac transcriptional response to transverse aortic constriction and altered DNA methylation.

72 Transverse aortic constriction and angiotensin-II (Ang-II) infusion

73 hypertrophy in mice subjected to transverse aortic constriction and improved cardiac function.

74 inal myofiber shortening that was induced by aortic constriction and improved following relief of the

75 Longer duration of transverse aortic constriction and MI led to a decrease in purines,

76 Both transverse aortic constriction and MI were associated with profound

77 pertrophic stimulation, including transverse aortic constriction and phenylephrine treatment.

78 Mice underwent transverse aortic constriction and serially followed up with echoca

79 T1 measurements, was elevated by transverse aortic constriction and showed direct linear correlation

80 ere both activated in response to transverse aortic constriction and the kinetics of LV T-cell infilt

81 ressed gene in mouse hearts after transverse aortic constriction and was normalized after removal of

82 In mice with LV hypertrophy (aortic constriction) and normal mice, the actual LV mass

83 n is impaired with heart failure (induced by aortic constriction); and 3) if inhibiting [Ca2+]m efflu

84 unction than wild-type mice after transverse aortic constriction, and cardiac-specific CSE transgenic

85 was induced in aortic SMCs after transverse aortic constriction, and Foxe3 deficiency increased SMC

86 diomyocytes, pressure overload by transverse aortic constriction, and myocardial infarction.

87 Mice underwent transverse aortic constriction, and the characteristics of cardiac

88 ed in CycD2(-/-) myocardium after transverse aortic constriction, and there is no dissociation of TBP

89 tensin II or pressure overload by transverse aortic constriction as measured by echocardiography.

90 Following chronic transverse aortic constriction, both SUR1-tg and Kir6.2 KO mice dev

91 cardiac hypertrophic responses to transverse aortic constriction but unchanged cardiac function, wher

92 Four weeks after transverse aortic constriction, Carabin-deficient (Carabin(-/-)) mi

93 LV ejection fraction (61+/-2% in transverse aortic constriction cardiac Nix KO versus 36+/-6% in tra

94 Aortic constriction caused an exaggerated increase in p2

95 in Akt-nuc transgenic mice after transverse aortic constriction coincident with higher ANP expressio

96 sed in mouse hearts after chronic transverse aortic constriction, coincident with the onset of ventri

97 scribe a novel guinea pig HF/SCD model using aortic constriction combined with daily beta-adrenergic

98 perivascular fibrotic areas after transverse aortic constriction compared with sham-treated control s

99 otected from HF development after transverse aortic constriction compared with wild-type littermates.

100 e overload at 5 and 9 weeks after transverse aortic constriction compared with wild-type-transverse a

101 failure associated with long-term transverse aortic constriction, conferring a survival benefit.

102 icular vasculature in response to transverse aortic constriction, corresponding to decreased expressi

103 2.5-Cre) Nix KO mice subjected to transverse aortic constriction developed significantly less LV dila

104 total of 10 sheep were banded with variable aortic constriction devices, progressively inflated to i

105 Aortic constriction did not change thioredoxin expressio

106 Likewise, transverse aortic constriction-elicited increases in hypertrophic m

107 ckout mice exposed to PO induced by thoracic aortic constriction exhibit a normal hypertrophic respon

108 Following abdominal aortic constriction expression levels of genes regulatin

109 In alpha1ABKO hearts, aortic constriction failed to activate ERK, and in alpha

110 on (2.5 microg/kg for 14 days) or transverse aortic constriction for 28 days to provoke cardiac remod

111 C57/Bl6 mice underwent transverse aortic constriction for 4 weeks, increasing cardiac mass

112 re subjected to pressure overload (ascending aortic constriction) for 1 week, echocardiography was pe

113 Within 48 h following aortic constriction, fulminant biventricular congestive

114 In a mouse model of transverse aortic constriction, galectin-3 expression was markedly

115 olic and diastolic dysfunction in transverse aortic constriction groups as expected.

116 The Cav-3 OE mice subjected to transverse aortic constriction had increased survival, reduced card

117 rior to any functional decline in transverse aortic constriction hearts.

118 ained preserved even in untreated transverse aortic constriction hearts.

119 or descending artery ligation and transverse aortic constriction HF mouse models after 4 and 8 weeks

120 e left ventricular myocardium in response to aortic constriction, however, was preserved in IGF-1(m/m

121 /kg/day), initiated 4 weeks after transverse aortic constriction, improved survival and cardiac funct

122 ed by pressure overload induced by ascending aortic constriction in a mouse model.

123 lt) rat aorta, of SMCs proximal to abdominal aortic constriction in adult rats, and of SMCs in the ne

124 an explain the failure to activate ERK after aortic constriction in alpha1ABKO mice and can contribut

125 p91phox isoform, Nox4, was upregulated after aortic constriction in gp91phox-/- mice.

126 rdiac pressure overload resulting from trans-aortic constriction in mice leads to cardiac fibrosis an

127 n nonischemic forms of HF such as transverse aortic constriction in mice.

128 heart failure obtained by creating ascending aortic constriction in rats.

129 cently developed a model of gradual proximal aortic constriction in the adult canine that mimicked th

130 trast, all 3 MAPK pathways were activated by aortic constriction in the TG betaARKct hearts, suggesti

131 imposed on the left ventricle by transverse aortic constriction in the wild-type and in mice lacking

132 st-specific loss of beta-catenin after trans-aortic constriction in vivo.

133 ism in male C57BL/6 mice model of transverse aortic constriction in which left ventricular hypertroph

134 aluated the induction of MAPK activity after aortic constriction in wild-type and in 2 types of cardi

135 Following thoracic aortic constriction in young mice, we observed enhanced

136 KO mice had decreased FOXO1 after transverse aortic constriction, in agreement with the reports that

137 with myocardial hypertrophy after transverse aortic constriction, in pigs with chronic myocardial isc

138 In heart tissue, transverse aortic constriction increased active transforming growth

139 However, aortic constriction increased cardiac NADPH oxidase acti

140 Aortic constriction increased the heart weight-to-body w

141 Although transverse aortic constriction induced a similar increase in hypert

142 ha1-adrenergic receptor (alpha1-AR) binding, aortic constriction induced apoptosis, dilated cardiomyo

143 In addition, transverse aortic constriction induced puma expression in a partial

144 In control mice, 4 weeks of transverse aortic constriction induced significant cardiac dysfunct

145 tenuated hypertrophic response to transverse aortic constriction-induced (TAC-induced) pressure overl

146 ce (IL10KO chimeric mice) reduced transverse aortic constriction-induced BM-FPC mobilization compared

147 mentation with fish oil prevented transverse aortic constriction-induced cardiac dysfunction and card

148 antation in IL10KO mice inhibited transverse aortic constriction-induced cardiac fibrosis and improve

149 378 levels significantly attenuated thoracic aortic constriction-induced cardiac hypertrophy and impr

150 vector encoding Carabin prevented transverse aortic constriction-induced cardiac hypertrophy with pre

151 Parkin knockout mice exposed to aortic constriction-induced cardiac pressure-overload or

152 Transverse aortic constriction-induced HF results in increased extr

153 ve response of IL-10 was found in transverse aortic constriction-induced hypertrophy and heart failur

154 ersisting through day 7 (0.29+/-0.14), after aortic constriction-induced hypertrophy in a mouse model

155 survival in the chronic phase of transverse aortic constriction-induced hypertrophy.

156 w altered S427 phosphorylation in transverse aortic constriction-induced hypertrophy.

157 were inhibited in gp91phox-/- mice, whereas aortic constriction-induced increases in cardiac mass an

158 as control mice manifested robust transverse aortic constriction-induced increases in cardiac mass, P

159 wild-type mice were subjected to transverse aortic constriction-induced pressure overload.

160 ficiency also exacerbated chronic transverse aortic constriction-induced ventricular hypertrophy and

161 to myocardial stresses including transverse aortic constriction, ischemia/reperfusion injury, and my

162 ivalent haemodynamic loads, within 30 min of aortic constriction, Kir6.2-KO showed an aberrant prolon

163 m of SERCA (SERCA2a) 8 weeks after ascending aortic constriction (left ventricular hypertrophy (LVH))

164 We further stressed transverse aortic constriction mice by feeding a high fructose diet

165 ht ventricular insertion point of transverse aortic constriction mice concordant with the foci of fib

166 Transverse aortic constriction mice displayed compensated hypertens

167 Moreover, CMs isolated from transverse aortic constriction mice treated with MR-409 showed impr

168 Compared with transverse aortic constriction mice, transverse aortic constriction

169 striction compared with wild-type-transverse aortic constriction mice.

170 sus 27.6+/-1.4% in wild type plus transverse aortic constriction mice; P<0.0001).

171 ersus 25.9+/-2.6% in control plus transverse aortic constriction mice; P<0.0001).

172 te heart failure was studied in an abdominal aortic constriction model of murine cardiac hypertrophy

173 cardiac remodeling in a long-term transverse aortic constriction mouse model.

174 Twelve weeks post transverse aortic constriction, myocardial tissues were collected t

175 underwent either sham procedures (n = 8) or aortic constriction (n = 12) with a customized pre-shape

176 Transverse aortic constriction-operated mice showed significantly i

177 mice demonstrated protection from transverse aortic constriction or Ang-II-induced pathological hyper

178 response to pressure overload resulting from aortic constriction or constitutive cardiac activation o

179 c tissue from mice in response to transverse aortic constriction or expression of activated calcineur

180 hy as WT controls when subjected to thoracic aortic constriction or isoproterenol infusion.

181 miR-212/132 was upregulated after transverse aortic constriction or on activation of alpha1- and beta

182 e C57BL/6J mice were subjected to transverse aortic constriction or permanent coronary occlusion (myo

183 yAB/HSPB2 genes were subjected to transverse aortic constriction or sham surgery.

184 Mice were subjected to transverse aortic constriction or sham surgery.

185 d was either increased (pressure overload by aortic constriction) or decreased (mechanical unloading

186 beta-MHC) promoter was increased 3.0-fold by aortic constriction (P<.005), an increment similar to th

187 compared with sham controls after transverse aortic constriction (P<0.01).

188 odel of cardiac hypertrophy after transverse aortic constriction, PDE3 effects were not affected, whe

189 ild-type mice, angiotensin II and transverse aortic constriction perturbations caused left-ventricula

190 nsverse aortic constriction mice, transverse aortic constriction plus deoxycorticosterone acetate mic

191 inhibition of Meg3 in vivo after transverse aortic constriction prevented cardiac MMP-2 induction, l

192 depletion in wild-type mice after transverse aortic constriction prevented HF.

193 Most die within 1 h of transverse aortic constriction, probably due to arrhythmia.

194 Even at 12 weeks after transverse aortic constriction, Puma(-/-) mice displayed only sligh

195 compared with cells isolated from control or aortic constriction rat hearts.

196 Transverse aortic constriction rats progressively developed "concen

197 s or from mice with HF induced by transverse aortic constriction revealed enhanced adhesion to activa

198 deficient mice to cardiac stress by thoracic aortic constriction revealed that antifibrotic effects w

199 After transverse aortic constriction, S2814A mice did not exhibit pulmona

200 ficient mouse hearts 1 week after transverse aortic constriction showed comparable increases in fibro

201 amic loading imposed by 7 days of transverse aortic constriction showed that the beta1 integrin knock

202 on of rapamycin before exposure to ascending aortic constriction significantly attenuated the load-in

203 function in cardiac fibroblasts after trans-aortic constriction significantly preserves cardiac func

204 tation of the GATA motif markedly attenuated aortic constriction-stimulated transcription (1.6-fold,

205 33-bp beta-MHC promoter, it had no effect on aortic constriction-stimulated transcription (3.5-fold i

206 Basal and aortic constriction-stimulated transcription of the beta

207 ere measured in sham-operated and transverse aortic constriction (studied 2 weeks later) mice without

208 itase activity was decreased with transverse aortic constriction, suggesting that G6PD deficiency inc

209 were subjected to either sham or transverse aortic constriction surgery to induce HF.

210 Eight weeks after transverse aortic constriction surgery, mice were divided into hear

211 sudden arrhythmogenic death after transverse aortic constriction surgery.

212 hmias versus wild-type mice after transverse aortic constriction surgery.

213 In response to transverse aortic constriction, T cell-deficient mice (T-cell recep

214 se as a control for in vivo PO by transverse aortic constriction (TAC) and for cultured cardiomyocyte

215 AND miR-133a is downregulated in transverse aortic constriction (TAC) and isoproterenol-induced hype

216 phy and early heart failure after transverse aortic constriction (TAC) because of GRK5 nuclear accumu

217 C57BL/6 mice subjected to transverse aortic constriction (TAC) developed cardiac hypertrophy

218 Male C57/Bl6 mice underwent transverse aortic constriction (TAC) for 1 week followed by FTY-720

219 Mice were subjected to transverse aortic constriction (TAC) for 1 week, after which the co

220 on of betaARKct peptide underwent transverse aortic constriction (TAC) for 12 weeks.

221 Mice were subjected to transverse aortic constriction (TAC) for 3 weeks to establish hyper

222 SPARC-null mice underwent either transverse aortic constriction (TAC) for 4 weeks or served as nonop

223 rly, pressure overload induced by transverse aortic constriction (TAC) for 6 weeks caused greater lef

224 We performed transverse aortic constriction (TAC) in dopamine beta-hydroxylase k

225 rtrophy was induced using 4 wk of transverse aortic constriction (TAC) in mice overexpressing the hum

226 In WT and KO mice, transverse aortic constriction (TAC) induced comparable increases i

227 in the progression to HF using a transverse aortic constriction (TAC) model.

228 art tissues of wild type (WT) and transverse aortic constriction (TAC) mouse models were analyzed.

229 thological development induced by transverse aortic constriction (TAC) or isoproterenol infusion.

230 experimental pressure overload by transverse aortic constriction (TAC) or myocardial infarction (MI).

231 ced cardiac hypertrophy following transverse aortic constriction (TAC) or phenylephrine/Ang II infusi

232 e induced pressure overload by transthoracic aortic constriction (TAC) or volume overload by aortocav

233 In wild-type mice, chronic transverse aortic constriction (TAC) resulted in myocardial iNOS ex

234 pressure-overload-induced HF with transverse aortic constriction (TAC) surgery and compared among 4 s

235 Mice underwent transverse aortic constriction (TAC) surgery and deoxycorticosteron

236 o inflammation and fibrosis after transverse aortic constriction (TAC) surgery, a pressure-volume ove

237 lation and increased survival after thoracic aortic constriction (TAC) surgery-induced HF.

238 eart muscle hypertrophy caused by transverse aortic constriction (TAC) to determine SIRT5's role in c

239 -type (WT) mice were subjected to transverse aortic constriction (TAC) to increase left ventricle loa

240 and control (CON) mice underwent transverse aortic constriction (TAC) to induce pressure overload.

241 In the reverse direction, we used transverse aortic constriction (TAC) to induce pressure overload.

242 ertrophy, we subjected animals to transverse aortic constriction (TAC) to induce pressure overload.

243 othesis, we used a mouse model of transverse aortic constriction (TAC) together with PET and assessed

244 evelopment of heart failure after transverse aortic constriction (TAC) using global and T-cell-specif

245 Transverse aortic constriction (TAC) was applied to MAFbx knockout

246 Transverse aortic constriction (TAC) was performed in CD1 mice to i

247 After 4 weeks of aortic banding (transverse aortic constriction (TAC)), increases in left ventricula

248 8 weeks of pressure overload via transverse aortic constriction (TAC), ACC2H-/- mice exhibited a sub

249 ricle of male C57BL/6J mice after transverse aortic constriction (TAC), and the fraction of cells exp

250 After transverse aortic constriction (TAC), G4D mice developed overt hear

251 remodeling events in response to transverse aortic constriction (TAC), including temporal changes in

252 on is observed transiently during transverse aortic constriction (TAC), its mechanism of inactivation

253 At 2 weeks after transverse aortic constriction (TAC), KO mouse survival was only 60

254 Following pressure overload by transverse aortic constriction (TAC), ST2(-/-) mice had more left v

255 7beta-estradiol (E2), followed by transverse aortic constriction (TAC), to induce pressure overload.

256 compared with control mice after transverse aortic constriction (TAC), which was largely blocked by

257 normal donors and from mice after transverse aortic constriction (TAC)-induced CHF.

258 the global proteomics changes in transverse aortic constriction (TAC)-induced heart failure and the

259 of nonischemic hypertrophic CHF, transverse aortic constriction (TAC).

260 infusion (400 ng/kg/min, 28 d) or transverse aortic constriction (TAC).

261 ion (MI) or pressure overload via transverse aortic constriction (TAC).

262 e (WT) controls were subjected to transverse aortic constriction (TAC).

263 d to pressure overload induced by transverse aortic constriction (TAC).

264 d to pressure overload induced by transverse aortic constriction (TAC).

265 overload-induced LVH, produced by transverse aortic constriction (TAC).

266 th increased pressure load due to transverse aortic constriction (TAC).

267 e molecule (Bmx knockout mice) to transverse aortic constriction (TAC).

268 t [KO]) mice and A(1)R KO mice to transverse aortic constriction (TAC).

269 stress, such as that generated by transverse aortic constriction (TAC).

270 ability of the heart to adapt to transverse aortic constriction (TAC).

271 or their nontransgenic littermates underwent aortic constriction (TAC).

272 ately 13 000 mRNAs in response to transverse aortic constriction (TAC).

273 s of pressure overload induced by transverse aortic constriction (TAC).

274 ute hemodynamic stress imposed by transverse aortic constriction (TAC); 4) cardiac dysfunction by 6 w

275 Chronic transverse aortic constriction (TAC; for 3 and 9 weeks) in control

276 l (aging) and pathophysiological (transverse aortic constriction [TAC]) mouse model.

277 perated (SHAM) and hypertrophied (transverse aortic constriction [TAC]) rat hearts.

278 l-established mouse model of LVH (transverse aortic constriction [TAC]).

279 ssure overload hypertrophy model (transverse aortic constriction; TAC).

280 express Txnip develop less hypertrophy after aortic constriction than control cells in the same anima

281 On aortic constriction, the hypercontractile cardiac functi

282 With aortic constriction, the knockout mice survived but had

283 By 6 weeks transverse aortic constriction, the metabolic profile reversed with

284 pression and collagen deposition after trans-aortic constriction.Understanding the mechanisms causing

285 ensitivity in response to 2 weeks transverse aortic constriction versus sham, linked to enhanced insu

286 sulted in cardioprotection during transverse aortic constriction via upregulation of the vascular end

287 ypertrophic growth in response to transverse aortic constriction was attenuated in CycD2-null compare

288 Transverse aortic constriction was performed in wild-type, CSE knoc

289 deleted (DCM-2TgxIP3-R(2)-/-) and transverse aortic constriction was performed on IP3-R(2)-/- mice.

290 response to pressure overload by transverse aortic constriction were exaggerated in ANP-null mice co

291 on of perivascular fibrosis after transverse aortic constriction, when compared with mock- or dominan

292 lted in aggravated fibrosis after transverse aortic constriction, when compared with wild-type contro

293 rtality was 61% in the ACi group <4 weeks of aortic constriction, whereas the death rate in the ACi p

294 t animals, hypertrophy induced by transverse aortic constriction, which causes translocation of HDACs

295 n early cardiac hypertrophy after transverse aortic constriction, which was in sharp contrast to well

296 cardiac Nix KO versus 36+/-6% in transverse aortic constriction wild-type mice; P=0.003) at 9 weeks,

297 Adult mice were subjected to ascending aortic constriction, with and without subsequent reversa

298 iRs to miR-29b induced excess fibrosis after aortic constriction without overt deterioration in cardi