ライフサイエンスコーパス: transverse aortic constriction

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

2 in a maladaptive cardiac phenotype following transverse aortic constriction.

3 bit less NFAT transcriptional activity after transverse aortic constriction.

4 arly progression to heart failure seen after transverse aortic constriction.

5 ntained cardiac structure and function after transverse aortic constriction.

6 myocardial and circulating H2S levels after transverse aortic constriction.

7 versing established cardiac remodeling after transverse aortic constriction.

8 evented apoptosis and fibrotic remodeling in transverse aortic constriction.

9 t alter the progression of hypertrophy after transverse aortic constriction.

10 s in Ins(1,4,5)P3 and IP3-R(2) are caused by transverse aortic constriction.

11 ac-specific Nox4 knockout mice 2 weeks after transverse aortic constriction.

12 athological cardiac hypertrophy and HF after transverse aortic constriction.

13 uced by 2 weeks infusion of isoproterenol or transverse aortic constriction.

14 ) loading compared with wild-type mice after transverse aortic constriction.

15 sis, and systolic dysfunction in response to transverse aortic constriction.

16 th global deletion of GRK5 were subjected to transverse aortic constriction.

17 oped sustained ventricular tachycardia after transverse aortic constriction.

18 vivo rescues mice from early mortality after transverse aortic constriction.

19 cardiac growth to ATF6 cKO mice subjected to transverse aortic constriction.

20 hibited cardiac myocyte apoptosis induced by transverse aortic constriction.

21 this association is disrupted in response to transverse aortic constriction.

22 was significantly upregulated in response to transverse aortic constriction.

23 loped cardiac insufficiency at 2 weeks after transverse aortic constriction.

24 ly and after inducing cardiac hypertrophy by transverse aortic constriction.

25 worsened hypertrophy/fibrosis from sustained transverse aortic constriction.

26 nal response to pressure overload induced by transverse aortic constriction.

27 d form of cardiac hypertrophy in response to transverse aortic constriction.

28 mice were subjected to pressure overload by transverse aortic constriction.

29 osed to chronic pressure overload induced by transverse aortic constriction.

30 d hypertrophic gene induction in response to transverse aortic constriction.

31 odel of chronic pressure overload induced by transverse aortic constriction.

32 n the mouse was achieved following 7 days of transverse aortic constriction.

33 d in both human heart failure and mice after transverse aortic constriction.

34 ially improved cardiac function after severe transverse aortic constriction.

35 ximately 50% reduction in the LVH induced by transverse aortic constriction.

36 lerated diastolic dysfunction in response to transverse aortic constriction.

37 were observed in wild-type mice after severe transverse aortic constriction.

38 ell infiltration and fibrosis in response to transverse aortic constriction.

39 ac-expressed genes at baseline and 91% after transverse aortic constriction.

40 oad-induced heart failure was established by transverse aortic constriction.

41 (133 versus 173 mg; P<0.0001) 20 weeks after transverse aortic constriction.

42 f cardiac pressure overload, induced through transverse aortic constriction.

43 duction in ejection fraction after 7 days of transverse aortic constriction.

44 roblasts were derived from bone marrow after transverse aortic constriction.

45 type (WT) and IL10 knockout (IL10KO) mice by transverse aortic constriction.

46 n utero and that have subsequently undergone transverse aortic constriction.

47 MAO (0.12%) starting 3 weeks before surgical transverse aortic constriction.

48 milar findings were seen in HFpEF induced by transverse aortic constriction.

49 ckouts had delayed dilation after 28 days of transverse aortic constriction.

50 Mice were studied for 12 weeks after transverse aortic constriction.

51 recovery of failing hearts after reversible transverse aortic constriction.

52 fibrosis, and contractile dysfunction after transverse aortic constriction.

53 ncreased mortality from cardiac stress after transverse aortic constriction, 5) abnormal mitochondria

54 ofibroblasts; however, after 7 to 28 days of transverse aortic constriction, a subset of cardiomyocyt

55 Transverse aortic constriction activated FYN in the left

56 fibrosis and pathology in mice subjected to transverse aortic constriction after the consumption of

57 in amino acids were observed after 1 week of transverse aortic constriction and 5 days after MI.

58 altered cardiac transcriptional response to transverse aortic constriction and altered DNA methylati

59 analysis of LA RNA sequencing datasets from transverse aortic constriction and angiotensin II-treate

60 Transverse aortic constriction and angiotensin-II (Ang-I

61 Adult male C57BL/6J mice were subjected to transverse aortic constriction and developed significant

62 Both transverse aortic constriction and exercise upregulated

63 f6 (ATF6 cKO [conditional knockout]) blunted transverse aortic constriction and exercise-induced card

64 ted cardiac hypertrophy in mice subjected to transverse aortic constriction and improved cardiac func

65 Here we used transverse aortic constriction and in vitro cardiac hype

66 P2 proteolysis by calpain and in response to transverse aortic constriction and isoproterenol was blo

67 ency preserved cardiac function in mice with transverse aortic constriction and led to improved recov

68 Longer duration of transverse aortic constriction and MI led to a decrease

69 Both transverse aortic constriction and MI were associated wi

70 nd after hypertrophic stimulation, including transverse aortic constriction and phenylephrine treatme

71 Mice underwent transverse aortic constriction and serially followed up

72 ostcontrast T1 measurements, was elevated by transverse aortic constriction and showed direct linear

73 dothelium were both activated in response to transverse aortic constriction and the kinetics of LV T-

74 f cardiac fibroblasts from mice subjected to transverse aortic constriction and treated with the smal

75 ersibly repressed gene in mouse hearts after transverse aortic constriction and was normalized after

76 ressure-overload model of myocardial stress (transverse aortic constriction) and cardiomyocyte-specif

77 1A KI mutation had increased mortality after transverse aortic constriction, and A61603 did not rescu

78 on and dysfunction than wild-type mice after transverse aortic constriction, and cardiac-specific CSE

79 r Atf6 or Atf6b were subjected to 2 weeks of transverse aortic constriction, and each showed a signif

80 expression was induced in aortic SMCs after transverse aortic constriction, and Foxe3 deficiency inc

81 ultured cardiomyocytes, pressure overload by transverse aortic constriction, and myocardial infarctio

82 cal cardiac hypertrophy in mice subjected to transverse aortic constriction, and that VIMP knockdown

83 Mice underwent transverse aortic constriction, and the characteristics

84 is unchanged in CycD2(-/-) myocardium after transverse aortic constriction, and there is no dissocia

85 fibrosis (~50% reduction) in isoproterenol-, transverse aortic constriction-, and myocardial infarcti

86 Utilizing transverse aortic constriction as a model of hemodynamic

87 with angiotensin II or pressure overload by transverse aortic constriction as measured by echocardio

88 murine models of cardiac pressure overload, transverse aortic constriction banding and angiotensin I

89 After 1 week of transverse aortic constriction, both carabin and STK24 a

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

91 attenuated cardiac hypertrophic responses to transverse aortic constriction but unchanged cardiac fun

92 Four weeks after transverse aortic constriction, Carabin-deficient (Carab

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

94 Following transverse aortic constriction, CCL24 deficiency amelior

95 remodeling in Akt-nuc transgenic mice after transverse aortic constriction coincident with higher AN

96 ntly increased in mouse hearts after chronic transverse aortic constriction, coincident with the onse

97 in wild-type and JP2(CR) mice 5 weeks after transverse aortic constriction compared with sham surger

98 tively, in perivascular fibrotic areas after transverse aortic constriction compared with sham-treate

99 latively protected from HF development after transverse aortic constriction compared with wild-type l

100 to pressure overload at 5 and 9 weeks after transverse aortic constriction compared with wild-type-t

101 t of heart failure associated with long-term transverse aortic constriction, conferring a survival be

102 left ventricular vasculature in response to transverse aortic constriction, corresponding to decreas

103 ecific (Nkx2.5-Cre) Nix KO mice subjected to transverse aortic constriction developed significantly l

104 Following transverse aortic constriction, dysferlin protein expres

105 Likewise, transverse aortic constriction-elicited increases in hyp

106 n II infusion (2.5 microg/kg for 14 days) or transverse aortic constriction for 28 days to provoke ca

107 C57/Bl6 mice underwent transverse aortic constriction for 4 weeks, increasing c

108 In a mouse model of transverse aortic constriction, galectin-3 expression wa

109 ng and systolic and diastolic dysfunction in transverse aortic constriction groups as expected.

110 The Cav-3 OE mice subjected to transverse aortic constriction had increased survival, r

111 matin architecture remains broadly stable in transverse aortic constriction hearts, whereas Ctcf knoc

112 ctivity remained preserved even in untreated transverse aortic constriction hearts.

113 occurred prior to any functional decline in transverse aortic constriction hearts.

114 left anterior descending artery ligation and transverse aortic constriction HF mouse models after 4 a

115 ment (10 mg/kg/day), initiated 4 weeks after transverse aortic constriction, improved survival and ca

116 velopment in nonischemic forms of HF such as transverse aortic constriction in mice.

117 verload was imposed on the left ventricle by transverse aortic constriction in the wild-type and in m

118 re used to study calcineurin signaling after transverse aortic constriction in vivo.

119 mic metabolism in male C57BL/6 mice model of transverse aortic constriction in which left ventricular

120 and Kir6.2 KO mice had decreased FOXO1 after transverse aortic constriction, in agreement with the re

121 In mice with myocardial hypertrophy after transverse aortic constriction, in pigs with chronic myo

122 In heart tissue, transverse aortic constriction increased active transfor

123 Although transverse aortic constriction induced a similar increas

124 In mice, transverse aortic constriction induced progressive systo

125 In addition, transverse aortic constriction induced puma expression i

126 In control mice, 4 weeks of transverse aortic constriction induced significant cardi

127 ed in an attenuated hypertrophic response to transverse aortic constriction-induced (TAC-induced) pre

128 d IL10KO mice (IL10KO chimeric mice) reduced transverse aortic constriction-induced BM-FPC mobilizati

129 tary supplementation with fish oil prevented transverse aortic constriction-induced cardiac dysfuncti

130 th their cognate antigen were protected from transverse aortic constriction-induced cardiac dysfuncti

131 row transplantation in IL10KO mice inhibited transverse aortic constriction-induced cardiac fibrosis

132 ated viral vector encoding Carabin prevented transverse aortic constriction-induced cardiac hypertrop

133 ly suppressed in left ventricle of mice with transverse aortic constriction-induced fibrotic cardiac

134 Transverse aortic constriction-induced HF results in inc

135 dioprotective response of IL-10 was found in transverse aortic constriction-induced hypertrophy and h

136 lly, we show altered S427 phosphorylation in transverse aortic constriction-induced hypertrophy.

137 unction and survival in the chronic phase of transverse aortic constriction-induced hypertrophy.

138 weight and completely protected against the transverse aortic constriction-induced impairments in le

139 reticulum calcium ATPase 2a, by attenuating transverse aortic constriction-induced increases in calp

140 Whereas control mice manifested robust transverse aortic constriction-induced increases in card

141 In mice, transverse aortic constriction-induced left ventricular

142 ox2KO), and wild-type mice were subjected to transverse aortic constriction-induced pressure overload

143 pha gene deficiency also exacerbated chronic transverse aortic constriction-induced ventricular hyper

144 intracoronary injection at d0 (percutaneous transverse aortic constriction induction) and d28.

145 in response to myocardial stresses including transverse aortic constriction, ischemia/reperfusion inj

146 Both at baseline and after transverse aortic constriction, knockout hearts exhibite

147 ventricular dysfunction and remodeling post-transverse aortic constriction/MI (left ventricular ejec

148 We further stressed transverse aortic constriction mice by feeding a high fr

149 nferior right ventricular insertion point of transverse aortic constriction mice concordant with the

150 Transverse aortic constriction mice displayed compensate

151 Moreover, CMs isolated from transverse aortic constriction mice treated with MR-409

152 Compared with transverse aortic constriction mice, transverse aortic c

153 aortic constriction compared with wild-type-transverse aortic constriction mice.

154 +/-1.6% versus 27.6+/-1.4% in wild type plus transverse aortic constriction mice; P<0.0001).

155 .9+/-1.2% versus 25.9+/-2.6% in control plus transverse aortic constriction mice; P<0.0001).

156 By studying a tool compound in a transverse aortic constriction mouse model, we were able

157 ression of cardiac remodeling in a long-term transverse aortic constriction mouse model.

158 Twelve weeks post transverse aortic constriction, myocardial tissues were

159 rt failure models were used for the studies: transverse aortic constriction/myocardial infarction (MI

160 ction), and hyperactive TGFbeta signaling in transverse aortic constriction-operated Lrg1-deficient m

161 Transverse aortic constriction-operated mice showed sign

162 ross the chromosomal coordinates of sham- or transverse aortic constriction-operated mouse hearts.

163 expressing mice demonstrated protection from transverse aortic constriction or Ang-II-induced patholo

164 d in cardiac tissue from mice in response to transverse aortic constriction or expression of activate

165 15 or ISGylation is upregulated in mice with transverse aortic constriction or infused with angiotens

166 he cluster miR-212/132 was upregulated after transverse aortic constriction or on activation of alpha

167 Male C57BL/6J mice were subjected to transverse aortic constriction or permanent coronary occ

168 In Tie2-Gfp mice subjected to transverse aortic constriction or sham surgery, we perfo

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

170 n of the CryAB/HSPB2 genes were subjected to transverse aortic constriction or sham surgery.

171 duced in mice subjected to an acute model of transverse aortic constriction, or to free-wheel exercis

172 oproterenol injections (3 mg.kg(-1).mg(-1)), transverse aortic constriction, or vehicle injection/sha

173 d 3.5-fold compared with sham controls after transverse aortic constriction (P<0.01).

174 In a mild model of cardiac hypertrophy after transverse aortic constriction, PDE3 effects were not af

175 In wild-type mice, angiotensin II and transverse aortic constriction perturbations caused left

176 ed with transverse aortic constriction mice, transverse aortic constriction plus deoxycorticosterone

177 ic PDE9 inhibition with CRD-733 in the mouse transverse aortic constriction pressure overload HF mode

178 After undergoing transverse aortic constriction pressure overload or sham

179 nsistently, inhibition of Meg3 in vivo after transverse aortic constriction prevented cardiac MMP-2 i

180 re, T-cell depletion in wild-type mice after transverse aortic constriction prevented HF.

181 Most die within 1 h of transverse aortic constriction, probably due to arrhythm

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

183 Transverse aortic constriction rats progressively develo

184 HF patients or from mice with HF induced by transverse aortic constriction revealed enhanced adhesio

185 After transverse aortic constriction, S2814A mice did not exhi

186 TRPC6-deficient mouse hearts 1 week after transverse aortic constriction showed comparable increas

187 Hemodynamic loading imposed by 7 days of transverse aortic constriction showed that the beta1 int

188 yed structural remodeling following chronic (transverse aortic constriction) stress.

189 scription were measured in sham-operated and transverse aortic constriction (studied 2 weeks later) m

190 on and aconitase activity was decreased with transverse aortic constriction, suggesting that G6PD def

191 kout (BCAT2(-)(/-)) mice underwent a sham or transverse aortic constriction surgery to induce heart f

192 57Bl/6 mice were subjected to either sham or transverse aortic constriction surgery to induce HF.

193 Eight weeks after transverse aortic constriction surgery, mice were divide

194 osition to sudden arrhythmogenic death after transverse aortic constriction surgery.

195 uced arrhythmias versus wild-type mice after transverse aortic constriction surgery.

196 subjected to ischemia-reperfusion injury or transverse aortic constriction surgery.

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

198 Methods: C57Bl6/N mice underwent transverse aortic constriction (TAC) (n = 22), sham surg

199 ld-type mouse as a control for in vivo PO by transverse aortic constriction (TAC) and for cultured ca

200 METHODS AND miR-133a is downregulated in transverse aortic constriction (TAC) and isoproterenol-i

201 ed hypertrophy and early heart failure after transverse aortic constriction (TAC) because of GRK5 nuc

202 C57BL/6 mice subjected to transverse aortic constriction (TAC) developed cardiac h

203 Adult mice subjected to transverse aortic constriction (TAC) developed cardiac h

204 Male C57/Bl6 mice underwent transverse aortic constriction (TAC) for 1 week followed

205 Mice were subjected to transverse aortic constriction (TAC) for 1 week, after w

206 ic expression of betaARKct peptide underwent transverse aortic constriction (TAC) for 12 weeks.

207 Mice were subjected to transverse aortic constriction (TAC) for 3 weeks to esta

208 pe (WT) and SPARC-null mice underwent either transverse aortic constriction (TAC) for 4 weeks or serv

209 Similarly, pressure overload induced by transverse aortic constriction (TAC) for 6 weeks caused

210 We performed transverse aortic constriction (TAC) in dopamine beta-hy

211 ardiac hypertrophy was induced using 4 wk of transverse aortic constriction (TAC) in mice overexpress

212 rdiac function/structure were analyzed after Transverse Aortic Constriction (TAC) in mice undergone v

213 (AICAR) to activate AMPK transiently before transverse aortic constriction (TAC) in wild-type and ca

214 In WT and KO mice, transverse aortic constriction (TAC) induced comparable

215 Transverse aortic constriction (TAC) is a well-establish

216 of T cells in the progression to HF using a transverse aortic constriction (TAC) model.

217 ins from heart tissues of wild type (WT) and transverse aortic constriction (TAC) mouse models were a

218 tion and pathological development induced by transverse aortic constriction (TAC) or isoproterenol in

219 underwent experimental pressure overload by transverse aortic constriction (TAC) or myocardial infar

220 ls and reduced cardiac hypertrophy following transverse aortic constriction (TAC) or phenylephrine/An

221 Mice were subjected to afterload stress via transverse aortic constriction (TAC) or sham surgery (sh

222 andardized pathological pressure overload by transverse aortic constriction (TAC) prior to MU by hete

223 a 48 h cold (16 degrees C) in mice following transverse aortic constriction (TAC) reduced cardiac gen

224 In wild-type mice, chronic transverse aortic constriction (TAC) resulted in myocard

225 e model of pressure-overload-induced HF with transverse aortic constriction (TAC) surgery and compare

226 Mice underwent transverse aortic constriction (TAC) surgery and deoxyco

227 es linked to inflammation and fibrosis after transverse aortic constriction (TAC) surgery, a pressure

228 d-induced heart muscle hypertrophy caused by transverse aortic constriction (TAC) to determine SIRT5'

229 )) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) to increase left ve

230 AC6-KO and control (CON) mice underwent transverse aortic constriction (TAC) to induce pressure

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

232 during hypertrophy, we subjected animals to transverse aortic constriction (TAC) to induce pressure

233 Mice underwent transverse aortic constriction (TAC) to model pressure o

234 st this hypothesis, we used a mouse model of transverse aortic constriction (TAC) together with PET a

235 3) on the development of heart failure after transverse aortic constriction (TAC) using global and T-

236 Transverse aortic constriction (TAC) was applied to MAFb

237 Transverse aortic constriction (TAC) was performed in CD

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

239 growth and metastasis colonization, we used transverse aortic constriction (TAC), a model for pressu

240 After 8 weeks of pressure overload via transverse aortic constriction (TAC), ACC2H-/- mice exhi

241 e left ventricle of male C57BL/6J mice after transverse aortic constriction (TAC), and the fraction o

242 After transverse aortic constriction (TAC), G4D mice developed

243 ute cardiac remodeling events in response to transverse aortic constriction (TAC), including temporal

244 30 activation is observed transiently during transverse aortic constriction (TAC), its mechanism of i

245 At 2 weeks after transverse aortic constriction (TAC), KO mouse survival

246 Following pressure overload by transverse aortic constriction (TAC), ST2(-/-) mice had

247 lacebo or 17beta-estradiol (E2), followed by transverse aortic constriction (TAC), to induce pressure

248 hypertrophy compared with control mice after transverse aortic constriction (TAC), which was largely

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

250 to evaluate the global proteomics changes in transverse aortic constriction (TAC)-induced heart failu

251 Transverse aortic constriction (TAC)-to increase wall st

252 intensive swim exercise protocol as well as transverse aortic constriction (TAC).

253 r conditions of pressure overload induced by transverse aortic constriction (TAC).

254 by Ang II infusion (400 ng/kg/min, 28 d) or transverse aortic constriction (TAC).

255 ial infarction (MI) or pressure overload via transverse aortic constriction (TAC).

256 and wildtype (WT) controls were subjected to transverse aortic constriction (TAC).

257 nd subjected to pressure overload induced by transverse aortic constriction (TAC).

258 re subjected to pressure overload induced by transverse aortic constriction (TAC).

259 f pressure overload-induced LVH, produced by transverse aortic constriction (TAC).

260 cient in the molecule (Bmx knockout mice) to transverse aortic constriction (TAC).

261 3)R knockout [KO]) mice and A(1)R KO mice to transverse aortic constriction (TAC).

262 ) and Yap (+/) (flox) mice were subjected to transverse aortic constriction (TAC).

263 of cardiac stress, such as that generated by transverse aortic constriction (TAC).

264 2-week chronic pressure overload induced by transverse aortic constriction (TAC).

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

266 activated in the mouse heart in response to transverse aortic constriction (TAC).

267 es lipotoxicity under pathological stress of transverse aortic constriction (TAC).

268 urine model of nonischemic hypertrophic CHF, transverse aortic constriction (TAC).

269 in mice with increased pressure load due to transverse aortic constriction (TAC).

270 ng approximately 13 000 mRNAs in response to transverse aortic constriction (TAC).

271 nd systolic dysfunction in mice subjected to transverse aortic constriction (TAC).

272 ollowing acute hemodynamic stress imposed by transverse aortic constriction (TAC); 4) cardiac dysfunc

273 Chronic transverse aortic constriction (TAC; for 3 and 9 weeks)

274 ophy and dysfunction were induced in rats by transverse-aortic constriction (TAC).

275 hysiological (aging) and pathophysiological (transverse aortic constriction [TAC]) mouse model.

276 n in sham-operated (SHAM) and hypertrophied (transverse aortic constriction [TAC]) rat hearts.

277 used a well-established mouse model of LVH (transverse aortic constriction [TAC]).

278 s and a pressure overload hypertrophy model (transverse aortic constriction; TAC).

279 By 6 weeks transverse aortic constriction, the metabolic profile re

280 on in an experimental model of HF induced by transverse aortic constriction, through the regulation o

281 ll-CSE overexpressing mice were subjected to transverse aortic constriction to induce heart failure w

282 nducted at 7 weeks RESULTS: After 7 weeks of transverse aortic constriction, vehicle mice had marked

283 d insulin sensitivity in response to 2 weeks transverse aortic constriction versus sham, linked to en

284 SG-1002 resulted in cardioprotection during transverse aortic constriction via upregulation of the v

285 Hypertrophic growth in response to transverse aortic constriction was attenuated in CycD2-n

286 Transverse aortic constriction was performed in wild-typ

287 ) had been deleted (DCM-2TgxIP3-R(2)-/-) and transverse aortic constriction was performed on IP3-R(2)

288 ial leptin signaling in cardiac hypertrophy, transverse aortic constriction was used in mice with ind

289 After transverse aortic constriction, we compared the hypertro

290 n target of rapamycin) phosphorylation after transverse aortic constriction were blunted in End.LepR-

291 ECs from EC-STING(-/-) mice subjected to transverse aortic constriction were enriched in gene set

292 roblasts in response to pressure overload by transverse aortic constriction were exaggerated in ANP-n

293 Male mice subjected to transverse aortic constriction were treated with oxamate

294 50% reduction of perivascular fibrosis after transverse aortic constriction, when compared with mock-

295 mice) resulted in aggravated fibrosis after transverse aortic constriction, when compared with wild-

296 In adult animals, hypertrophy induced by transverse aortic constriction, which causes translocati

297 signaling in early cardiac hypertrophy after transverse aortic constriction, which was in sharp contr

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

299 in wild-type left-ventricular myocytes after transverse aortic constriction with robust proliferation

300 In response to transverse aortic constriction, WT mice developed reduce