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1 subjected them to mechanical stress in vivo (transverse aortic constriction).
2 athological cardiac hypertrophy and HF after transverse aortic constriction.
3 ) loading compared with wild-type mice after transverse aortic constriction.
4 sis, and systolic dysfunction in response to transverse aortic constriction.
5 th global deletion of GRK5 were subjected to transverse aortic constriction.
6 oped sustained ventricular tachycardia after transverse aortic constriction.
7 vivo rescues mice from early mortality after transverse aortic constriction.
8 type (WT) and IL10 knockout (IL10KO) mice by transverse aortic constriction.
9 hibited cardiac myocyte apoptosis induced by transverse aortic constriction.
10 this association is disrupted in response to transverse aortic constriction.
11 was significantly upregulated in response to transverse aortic constriction.
12 loped cardiac insufficiency at 2 weeks after transverse aortic constriction.
13 n utero and that have subsequently undergone transverse aortic constriction.
14 ly and after inducing cardiac hypertrophy by transverse aortic constriction.
15 worsened hypertrophy/fibrosis from sustained transverse aortic constriction.
16 nal response to pressure overload induced by transverse aortic constriction.
17 d form of cardiac hypertrophy in response to transverse aortic constriction.
18 mice were subjected to pressure overload by transverse aortic constriction.
19 osed to chronic pressure overload induced by transverse aortic constriction.
20 d hypertrophic gene induction in response to transverse aortic constriction.
21 odel of chronic pressure overload induced by transverse aortic constriction.
22 MAO (0.12%) starting 3 weeks before surgical transverse aortic constriction.
23 n the mouse was achieved following 7 days of transverse aortic constriction.
24 milar findings were seen in HFpEF induced by transverse aortic constriction.
25 ckouts had delayed dilation after 28 days of transverse aortic constriction.
26 Mice were studied for 12 weeks after transverse aortic constriction.
27 recovery of failing hearts after reversible transverse aortic constriction.
28 fibrosis, and contractile dysfunction after transverse aortic constriction.
29 in a maladaptive cardiac phenotype following transverse aortic constriction.
30 bit less NFAT transcriptional activity after transverse aortic constriction.
31 roblasts were derived from bone marrow after transverse aortic constriction.
32 arly progression to heart failure seen after transverse aortic constriction.
33 ntained cardiac structure and function after transverse aortic constriction.
34 myocardial and circulating H2S levels after transverse aortic constriction.
35 versing established cardiac remodeling after transverse aortic constriction.
36 t alter the progression of hypertrophy after transverse aortic constriction.
37 s in Ins(1,4,5)P3 and IP3-R(2) are caused by transverse aortic constriction.
38 ac-specific Nox4 knockout mice 2 weeks after transverse aortic constriction.
39 ncreased mortality from cardiac stress after transverse aortic constriction, 5) abnormal mitochondria
40 ofibroblasts; however, after 7 to 28 days of transverse aortic constriction, a subset of cardiomyocyt
42 fibrosis and pathology in mice subjected to transverse aortic constriction after the consumption of
44 altered cardiac transcriptional response to transverse aortic constriction and altered DNA methylati
46 ted cardiac hypertrophy in mice subjected to transverse aortic constriction and improved cardiac func
49 nd after hypertrophic stimulation, including transverse aortic constriction and phenylephrine treatme
51 ostcontrast T1 measurements, was elevated by transverse aortic constriction and showed direct linear
52 dothelium were both activated in response to transverse aortic constriction and the kinetics of LV T-
53 ersibly repressed gene in mouse hearts after transverse aortic constriction and was normalized after
54 on and dysfunction than wild-type mice after transverse aortic constriction, and cardiac-specific CSE
55 expression was induced in aortic SMCs after transverse aortic constriction, and Foxe3 deficiency inc
56 ultured cardiomyocytes, pressure overload by transverse aortic constriction, and myocardial infarctio
58 is unchanged in CycD2(-/-) myocardium after transverse aortic constriction, and there is no dissocia
59 with angiotensin II or pressure overload by transverse aortic constriction as measured by echocardio
61 attenuated cardiac hypertrophic responses to transverse aortic constriction but unchanged cardiac fun
63 d preserved LV ejection fraction (61+/-2% in transverse aortic constriction cardiac Nix KO versus 36+
64 remodeling in Akt-nuc transgenic mice after transverse aortic constriction coincident with higher AN
65 ntly increased in mouse hearts after chronic transverse aortic constriction, coincident with the onse
66 tively, in perivascular fibrotic areas after transverse aortic constriction compared with sham-treate
67 latively protected from HF development after transverse aortic constriction compared with wild-type l
68 to pressure overload at 5 and 9 weeks after transverse aortic constriction compared with wild-type-t
69 t of heart failure associated with long-term transverse aortic constriction, conferring a survival be
70 left ventricular vasculature in response to transverse aortic constriction, corresponding to decreas
71 ecific (Nkx2.5-Cre) Nix KO mice subjected to transverse aortic constriction developed significantly l
73 n II infusion (2.5 microg/kg for 14 days) or transverse aortic constriction for 28 days to provoke ca
80 left anterior descending artery ligation and transverse aortic constriction HF mouse models after 4 a
81 ment (10 mg/kg/day), initiated 4 weeks after transverse aortic constriction, improved survival and ca
83 verload was imposed on the left ventricle by transverse aortic constriction in the wild-type and in m
84 mic metabolism in male C57BL/6 mice model of transverse aortic constriction in which left ventricular
85 and Kir6.2 KO mice had decreased FOXO1 after transverse aortic constriction, in agreement with the re
86 In mice with myocardial hypertrophy after transverse aortic constriction, in pigs with chronic myo
91 ed in an attenuated hypertrophic response to transverse aortic constriction-induced (TAC-induced) pre
92 d IL10KO mice (IL10KO chimeric mice) reduced transverse aortic constriction-induced BM-FPC mobilizati
93 tary supplementation with fish oil prevented transverse aortic constriction-induced cardiac dysfuncti
94 row transplantation in IL10KO mice inhibited transverse aortic constriction-induced cardiac fibrosis
95 ated viral vector encoding Carabin prevented transverse aortic constriction-induced cardiac hypertrop
97 dioprotective response of IL-10 was found in transverse aortic constriction-induced hypertrophy and h
101 ox2KO), and wild-type mice were subjected to transverse aortic constriction-induced pressure overload
102 pha gene deficiency also exacerbated chronic transverse aortic constriction-induced ventricular hyper
103 in response to myocardial stresses including transverse aortic constriction, ischemia/reperfusion inj
105 nferior right ventricular insertion point of transverse aortic constriction mice concordant with the
115 expressing mice demonstrated protection from transverse aortic constriction or Ang-II-induced patholo
116 d in cardiac tissue from mice in response to transverse aortic constriction or expression of activate
117 he cluster miR-212/132 was upregulated after transverse aortic constriction or on activation of alpha
122 In a mild model of cardiac hypertrophy after transverse aortic constriction, PDE3 effects were not af
124 ed with transverse aortic constriction mice, transverse aortic constriction plus deoxycorticosterone
125 nsistently, inhibition of Meg3 in vivo after transverse aortic constriction prevented cardiac MMP-2 i
130 HF patients or from mice with HF induced by transverse aortic constriction revealed enhanced adhesio
132 TRPC6-deficient mouse hearts 1 week after transverse aortic constriction showed comparable increas
133 Hemodynamic loading imposed by 7 days of transverse aortic constriction showed that the beta1 int
134 scription were measured in sham-operated and transverse aortic constriction (studied 2 weeks later) m
135 on and aconitase activity was decreased with transverse aortic constriction, suggesting that G6PD def
136 57Bl/6 mice were subjected to either sham or transverse aortic constriction surgery to induce HF.
141 ld-type mouse as a control for in vivo PO by transverse aortic constriction (TAC) and for cultured ca
142 METHODS AND miR-133a is downregulated in transverse aortic constriction (TAC) and isoproterenol-i
143 ed hypertrophy and early heart failure after transverse aortic constriction (TAC) because of GRK5 nuc
149 pe (WT) and SPARC-null mice underwent either transverse aortic constriction (TAC) for 4 weeks or serv
152 ardiac hypertrophy was induced using 4 wk of transverse aortic constriction (TAC) in mice overexpress
155 ins from heart tissues of wild type (WT) and transverse aortic constriction (TAC) mouse models were a
156 tion and pathological development induced by transverse aortic constriction (TAC) or isoproterenol in
157 underwent experimental pressure overload by transverse aortic constriction (TAC) or myocardial infar
158 ls and reduced cardiac hypertrophy following transverse aortic constriction (TAC) or phenylephrine/An
160 e model of pressure-overload-induced HF with transverse aortic constriction (TAC) surgery and compare
162 es linked to inflammation and fibrosis after transverse aortic constriction (TAC) surgery, a pressure
163 d-induced heart muscle hypertrophy caused by transverse aortic constriction (TAC) to determine SIRT5'
164 )) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) to increase left ve
167 during hypertrophy, we subjected animals to transverse aortic constriction (TAC) to induce pressure
168 st this hypothesis, we used a mouse model of transverse aortic constriction (TAC) together with PET a
169 3) on the development of heart failure after transverse aortic constriction (TAC) using global and T-
174 e left ventricle of male C57BL/6J mice after transverse aortic constriction (TAC), and the fraction o
176 ute cardiac remodeling events in response to transverse aortic constriction (TAC), including temporal
177 30 activation is observed transiently during transverse aortic constriction (TAC), its mechanism of i
180 lacebo or 17beta-estradiol (E2), followed by transverse aortic constriction (TAC), to induce pressure
181 hypertrophy compared with control mice after transverse aortic constriction (TAC), which was largely
183 to evaluate the global proteomics changes in transverse aortic constriction (TAC)-induced heart failu
198 ollowing acute hemodynamic stress imposed by transverse aortic constriction (TAC); 4) cardiac dysfunc
205 d insulin sensitivity in response to 2 weeks transverse aortic constriction versus sham, linked to en
206 SG-1002 resulted in cardioprotection during transverse aortic constriction via upregulation of the v
209 ) had been deleted (DCM-2TgxIP3-R(2)-/-) and transverse aortic constriction was performed on IP3-R(2)
210 roblasts in response to pressure overload by transverse aortic constriction were exaggerated in ANP-n
211 50% reduction of perivascular fibrosis after transverse aortic constriction, when compared with mock-
212 mice) resulted in aggravated fibrosis after transverse aortic constriction, when compared with wild-
213 In adult animals, hypertrophy induced by transverse aortic constriction, which causes translocati
214 signaling in early cardiac hypertrophy after transverse aortic constriction, which was in sharp contr
215 onstriction cardiac Nix KO versus 36+/-6% in transverse aortic constriction wild-type mice; P=0.003)
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