ライフサイエンスコーパス: aortic constriction

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

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

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

4 mutation were subjected to chronic ascending aortic constriction.

5 f failing hearts after reversible transverse aortic constriction.

6 and contractile dysfunction after transverse aortic constriction.

7 ptive cardiac phenotype following transverse aortic constriction.

8 AT transcriptional activity after transverse aortic constriction.

9 either by isoproterenol administration or by aortic constriction.

10 ssion to heart failure seen after transverse aortic constriction.

11 diac structure and function after transverse aortic constriction.

12 and circulating H2S levels after transverse aortic constriction.

13 ablished cardiac remodeling after transverse aortic constriction.

14 progression of hypertrophy after transverse aortic constriction.

15 ptosis and fibrotic remodeling in transverse aortic constriction.

16 4,5)P3 and IP3-R(2) are caused by transverse aortic constriction.

17 Nox4 knockout mice 2 weeks after transverse aortic constriction.

18 ypertrophy, and improves following relief of aortic constriction.

19 cardiac hypertrophy and HF after transverse aortic constriction.

20 eeks infusion of isoproterenol or transverse aortic constriction.

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

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

23 stolic dysfunction in response to transverse aortic constriction.

24 eletion of GRK5 were subjected to transverse aortic constriction.

25 ned ventricular tachycardia after transverse aortic constriction.

26 s mice from early mortality after transverse aortic constriction.

27 diac myocyte apoptosis induced by transverse aortic constriction.

28 ation is disrupted in response to transverse aortic constriction.

29 cantly upregulated in response to transverse aortic constriction.

30 ac insufficiency at 2 weeks after transverse aortic constriction.

31 wth to ATF6 cKO mice subjected to transverse aortic constriction.

32 r inducing cardiac hypertrophy by transverse aortic constriction.

33 pertrophy/fibrosis from sustained transverse aortic constriction.

34 e to pressure overload induced by transverse aortic constriction.

35 ardiac hypertrophy in response to transverse aortic constriction.

36 subjected to pressure overload by transverse aortic constriction.

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

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

39 severely to dilated cardiomyopathy following aortic constriction.

40 onic pressure overload induced by transverse aortic constriction.

41 hic gene induction in response to transverse aortic constriction.

42 -in mice were subjected to chronic ascending aortic constriction.

43 heart failure was established by transverse aortic constriction.

44 either by raising left atrial pressure or by aortic constriction.

45 173 mg; P<0.0001) 20 weeks after transverse aortic constriction.

46 ressure overload, induced through transverse aortic constriction.

47 ejection fraction after 7 days of transverse aortic constriction.

48 d genes at baseline and 91% after transverse aortic constriction.

49 re derived from bone marrow after transverse aortic constriction.

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

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

52 demonstrate dysregulation after exposure and aortic constriction.

53 that have subsequently undergone transverse aortic constriction.

54 starting 3 weeks before surgical transverse aortic constriction.

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

56 delayed dilation after 28 days of transverse aortic constriction.

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

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

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

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

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

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

63 Transverse aortic constriction activated FYN in the left ventricle

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

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

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

67 f LA RNA sequencing datasets from transverse aortic constriction and angiotensin II-treated mice show

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

69 Both transverse aortic constriction and exercise upregulated RHEB, activ

70 O [conditional knockout]) blunted transverse aortic constriction and exercise-induced cardiac myocyte

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

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

73 Here we used transverse aortic constriction and in vitro cardiac hypertrophy mod

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

75 Both transverse aortic constriction and MI were associated with profound

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

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

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

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

80 ibroblasts from mice subjected to transverse aortic constriction and treated with the small molecule

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

82 rload model of myocardial stress (transverse aortic constriction) and cardiomyocyte-specific knockout

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

84 ion had increased mortality after transverse aortic constriction, and A61603 did not rescue cardiac f

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

86 tf6b were subjected to 2 weeks of transverse aortic constriction, and each showed a significant reduc

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

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

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

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

91 50% reduction) in isoproterenol-, transverse aortic constriction-, and myocardial infarction (MI)-ind

92 Utilizing transverse aortic constriction as a model of hemodynamic stress in

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

94 els of cardiac pressure overload, transverse aortic constriction banding and angiotensin II infusion,

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

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

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

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

99 Aortic constriction caused an exaggerated increase in p2

100 In wild-type mice, ascending aortic constriction caused myocyte apoptosis, LV dilatio

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

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

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

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

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

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

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

108 2.5-Cre) Nix KO mice subjected to transverse aortic constriction developed significantly less LV dila

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

110 Aortic constriction did not change thioredoxin expressio

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

112 58% increase in heart function in ascending aortic constriction ensuing heart failure, a 38% reducti

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

114 Following abdominal aortic constriction expression levels of genes regulatin

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

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

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

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

119 Within 48 h following aortic constriction, fulminant biventricular congestive

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

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

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

123 tecture remains broadly stable in transverse aortic constriction hearts, whereas Ctcf knockout result

124 ained preserved even in untreated transverse aortic constriction hearts.

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

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

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

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

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

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

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

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

133 study calcineurin signaling after transverse aortic constriction in vivo.

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

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

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

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

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

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

140 Although transverse aortic constriction induced a similar increase in hypert

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

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

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

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

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

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

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

148 378 levels significantly attenuated thoracic aortic constriction-induced cardiac hypertrophy and impr

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

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

151 ed in left ventricle of mice with transverse aortic constriction-induced fibrotic cardiac remodeling

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

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

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

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

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

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

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

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

163 r dysfunction and remodeling post-transverse aortic constriction/MI (left ventricular ejection fracti

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

171 sus 27.6+/-1.4% in wild type 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 models were used for the studies: transverse aortic constriction/myocardial infarction (MI) in mice a

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

177 hyperactive TGFbeta signaling in transverse aortic constriction-operated Lrg1-deficient mice (mean d

178 romosomal coordinates of sham- or transverse aortic constriction-operated mouse hearts.

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

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

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

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

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

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

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

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

187 ce subjected to an acute model of transverse aortic constriction, or to free-wheel exercise, both of

188 injections (3 mg.kg(-1).mg(-1)), transverse aortic constriction, or vehicle injection/sham surgery.

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

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

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

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

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

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

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

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

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

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

199 ophy in C57BL/6J mice produced by suprarenal aortic constriction (SAC).

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

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

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

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

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

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

206 sudden arrhythmogenic death after transverse aortic constriction surgery.

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

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

209 Methods: C57Bl6/N mice underwent transverse aortic constriction (TAC) (n = 22), sham surgery (n = 12

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

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

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

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

214 Adult mice subjected to transverse aortic constriction (TAC) developed cardiac hypertrophy

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

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

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

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

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

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

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

222 activate AMPK transiently before transverse aortic constriction (TAC) in wild-type and cardiomyocyte

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

224 Transverse aortic constriction (TAC) is a well-established model of

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

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

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

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

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

230 pathological pressure overload by transverse aortic constriction (TAC) prior to MU by heterotopic hea

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

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

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

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

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

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

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

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

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

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

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

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

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

244 metastasis colonization, we used transverse aortic constriction (TAC), a model for pressure overload

245 8 weeks of pressure overload via transverse aortic constriction (TAC), ACC2H-/- mice exhibited a sub

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

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

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

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

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

251 7beta-estradiol (E2), followed by transverse aortic constriction (TAC), to induce pressure overload.

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

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

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

255 Transverse aortic constriction (TAC)-to increase wall stress in the

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

257 dysfunction in mice subjected to transverse aortic constriction (TAC).

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

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

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

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

262 swim exercise protocol as well as 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 e molecule (Bmx knockout mice) to transverse aortic constriction (TAC).

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

268 +/) (flox) mice were subjected to transverse aortic constriction (TAC).

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

270 onic pressure overload induced by transverse aortic constriction (TAC).

271 city under pathological stress of transverse aortic constriction (TAC).

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

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

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

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

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

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

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

279 l-established mouse model of LVH (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 signaling in cardiac hypertrophy, transverse aortic constriction was used in mice with inducible endo

291 rapamycin) phosphorylation after transverse aortic constriction were blunted in End.LepR-KO hearts.

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

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

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

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

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

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

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

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

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