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1 line HFpEF model induced by slow-progressive pressure overload.
2 of TNC in cardiac hypertrophy in response to pressure overload.
3 , genetically altered mice were subjected to pressure overload.
4 icular HF was induced by combined volume and pressure overload.
5 ve remodeling and arrhythmias in response to pressure overload.
6  of ST2 exacerbated cardiac hypertrophy with pressure overload.
7   Both cardiac phenotypes were aggravated on pressure overload.
8 pertrophy in the hearts of mice subjected to pressure overload.
9 y and fibrosis in a disease model of cardiac pressure overload.
10 s develop an aggravated phenotype induced by pressure overload.
11 uring HF induced by myocardial infarction or pressure overload.
12 /-) gain-of-function mutation in response to pressure overload.
13  maladaptive autophagy in a model of cardiac pressure overload.
14 (HF) forms of cardiac hypertrophy because of pressure overload.
15 ided significantly protective benefits after pressure overload.
16 ling occurs in a model of volume rather than pressure overload.
17 blast lineages also remained unchanged after pressure overload.
18 ead to improved cardiac remodeling following pressure overload.
19  for cardiac phenotyping in a mouse model of pressure overload.
20 ed redox stress in response to infarction or pressure overload.
21 hypertrophy in response to phenylephrine and pressure overload.
22 ate the left ventricular response to chronic pressure overload.
23 2+) handling, and hypertrophy in response to pressure overload.
24 nflammation, hypertrophy, and dysfunction on pressure overload.
25 ion, hypertrophy, and failure in response to pressure overload.
26 en during the earliest stages of exposure to pressure overload.
27  can track myocardial tissue remodeling from pressure overload.
28 ed to transverse aortic constriction-induced pressure overload.
29 bservation was confirmed in a mouse model of pressure overload.
30 lpha) is critical to the heart's response to pressure overload.
31 , which produces both high shear and cardiac pressure overload.
32 c damage or aggravating cardiomyopathy after pressure overload.
33 ight ventricular (RV) failure (RVF) after RV pressure overload.
34 nst excessive remodeling in response to mild pressure overload.
35 ular dilation after long-term stimulation by pressure overload.
36 ted to transverse aorta constriction-induced pressure overload.
37   Subsequently, HF was induced by volume and pressure overload.
38 t failure and cardiac dilation after 2 wk of pressure overload.
39 thways (ERK1/2 and Akt) on exposure to acute pressure overload.
40  cardiac Fstl1 in the remodeling response to pressure overload.
41 the heart from hemodynamic stresses, such as pressure overload.
42 ge subset into the myocardium in response to pressure overload.
43 4 after adrenergic stimulation or myocardial pressure overload.
44 esponse for pyruvate dehydrogenase kinase to pressure overload.
45 ult mouse hearts expressing ssTnI to chronic pressure overload.
46 tch and from sera of mice undergoing cardiac pressure overload.
47 of MeCP2 target genes remained stable during pressure overload.
48 nversation regulates the heart's response to pressure overload.
49 itochondrial respiration despite elevated RV pressure-overload.
50 ysfunction, partially independent of chronic pressure-overload.
51 es of isoprenaline stress under baseline and pressure-overload.
52 rt failure, and accelerates maladaptation to pressure overloading.
53 ure and exacerbated cardiac remodeling after pressure overloading.
54 inhibition of NF-kappaB at the time of acute pressure overload accelerates the progression of left ve
55 tion of CTGF levels in the heart with aging, pressure overload, agonist infusion, or TGF-beta overexp
56 ed cardiac hypertrophy, and following severe pressure overload all Erbin(-/-) mice died from heart fa
57 ally, ANGPTL2-knockdown in mice subjected to pressure overload ameliorates cardiac dysfunction.
58          However, after the establishment of pressure overload, an increase in leptin levels has prot
59 n important regulator of NCX1 in response to pressure overload and aimed to identify molecular mechan
60                              On pathological pressure overload and beta-adrenergic stimulation, DKO m
61 he concentric myocyte hypertrophy induced by pressure overload and catecholamine infusion.
62 rtant for the cardiac hypertrophy induced by pressure overload and catecholamine toxicity.
63 TORC1 is necessary for cardiac adaptation to pressure overload and development of compensatory hypert
64 iling heart from the perspectives of chronic pressure overload and diabetes mellitus.
65 her impaired cardiac function in response to pressure overload and exacerbated fibrosis by enhancing
66 ed in myocardial phospholipids after chronic pressure overload and explored plausible links between t
67 d fatty acid redistribution in rat models of pressure overload and hypertensive heart disease and sig
68         Hence, we investigated the impact of pressure overload and infarction on myocardial metabolis
69 sis in a clinically relevant animal model of pressure overload and is sensitive to pharmacological re
70 in vivo blunts pathological remodeling after pressure overload and preserves cardiac function.
71 rdiac function and mortality after long-term pressure overload and prevented disease progression in c
72 d its functional significance during cardiac pressure overload and unloading.
73 role in the myocardial response to ischemia, pressure overload, and heart failure.
74 ECM in the setting of myocardial infarction, pressure overload, and volume overload.
75 s of exercise training followed by 1 week of pressure overload (aortic-banding) to induce pathologica
76 the remodeling responses of the RV and LV to pressure overload are largely similar, there are several
77 ning in 57% of FGR, which supports increased pressure overload as a mechanism for cardiovascular prog
78 ubjected to cardiac hypertrophy secondary to pressure-overload as a result of an abdominal aortic con
79 K-TG) led to exaggerated cardiac response to pressure overload, as manifested by markedly exacerbated
80 worsened systolic dysfunction in response to pressure overload at 5 and 9 weeks after transverse aort
81                                       During pressure overload, both hypertrophic and hypoxic signals
82 wo major angiogenic stimuli occurring during pressure overload bridging both hypertrophic and hypoxia
83  myocardial remodeling and dysfunction after pressure overload but not after volume overload.
84 ic responses to phenylephrine and to chronic pressure overload, but it affected neither antiapoptotic
85 orts hypertrophy and cardiac function during pressure overload by affecting endothelial cells and fib
86 ontrol, influences the metabolic response to pressure overload by direct regulation of the catalytic
87 pled receptor, confers resistance to chronic pressure overload by markedly reducing myocardial hypert
88                       Mice were subjected to pressure overload by means of angiotensin-II infusion or
89  in the adaptation of the heart and aorta to pressure overload by negatively regulating TGF-beta sign
90  in an in vivo model of cardiac hypertrophy (pressure overload by thoracic aortic constriction).
91 elief of the right ventricular volume and/or pressure overload by TPVR will have a beneficial effect
92       Starting 1 week after the induction of pressure overload by transaortic constriction, mice were
93                                   We induced pressure overload by transthoracic aortic constriction (
94 ontrol mice and in mice subjected to chronic pressure-overload by transverse aorta constriction (TAC)
95 ontrol mice and in mice subjected to chronic pressure-overload by transverse aorta constriction.
96 ure after myocardial infarction or long-term pressure overload, by preventing cardiac cell death and
97 tophagic mitochondrial DNA degradation after pressure overload can activate Toll-like receptor-9 medi
98  Pathological conditions such as ischemia or pressure overload can induce a release of extracellular
99 tect against hypertrophy or dysfunction from pressure overload, combined deletion was protective, sup
100                               Under a severe pressure-overload condition induced by 2 weeks of transv
101                               Under a milder pressure-overload condition, CPT1b(+/-) mice exhibited e
102 a heterogeneous population of fibroblasts on pressure overload could suggest that common signaling me
103                                          The pressure overload data sets were also compared with the
104                                              Pressure overload depresses NO/heme-dependent sGC activa
105 n basal conditions, knockout mice exposed to pressure overload developed less hypertrophy and showed
106                                           LV pressure overload did not upregulate miR-182.
107 ion (hypoxia) and fuel starvation, ischemia, pressure overload, dilated cardiomyopathy, hypertrophy,
108 ase-specific, because angiotensin II-induced pressure overload does not trigger significant EPDC fibr
109                                              Pressure overload enhanced BM-FPC mobilization and homin
110  knockdown preserved capillary density after pressure overload, enhancing BMP7, a regulator of the en
111 yocytes or activated fibroblasts exacerbates pressure overload-evoked fibrosis.
112 ial triglyceride (TG) turnover is reduced in pressure-overloaded, failing hearts, limiting the availa
113  labels fibroblasts, we found that following pressure overload, fibroblasts were not derived from hem
114 rmalization of left ventricular geometry and pressure overload following AVR, therefore we aimed to i
115               In the ACi group 4 weeks after pressure overload, fractional shortening and the rate of
116                  In a mouse model of cardiac pressure overload, global genetic deletion of miR-29 or
117 ur lab has shown that, following ventricular pressure overload, GRK5, a primary cardiac GRK, facilita
118                        Preclinical models of pressure overload have shown that phosphodiesterase type
119 s caused by arsenic-induced liver insult and pressure overload heart injury.
120 ischemia due to peripheral arterial disease, pressure-overload heart failure, wound healing, and chro
121 athophysiology of ischemic heart disease and pressure-overload heart failure.
122 ocardium against excessive remodeling of the pressure-overloaded heart.
123 brosis, and cardiomyocyte hypertrophy in the pressure-overloaded heart.
124 In a model of aortic banding-induced chronic pressure overload, heart function was similarly depresse
125                Echocardiographic analysis of pressure overloaded hearts revealed that all LV paramete
126     Estrogen and sildenafil had no impact on pressure-overloaded hearts from animals expressing dysfu
127 diac P2X4R overexpression in postinfarct and pressure overload HF as did eNOS knockout.
128                            In a rat model of pressure overload HF, BNIP3 knockdown significantly decr
129 rct or transverse aorta constriction-induced pressure overload HF.
130 ion, and were protected from postinfarct and pressure overload HF.
131 moting an intolerance to in vivo ventricular pressure overload; however, its endogenous requirement i
132 blasts, reduces the hypertrophic response to pressure overload; however, knocking out Pmca4 specifica
133  activation improved the cardiac function in pressure overloaded Hras null hearts in vivo.
134 r NKA-alpha2 were generated and subjected to pressure overload hypertrophic stimulation.
135 creasing PGC-1alpha levels in the context of pressure overload hypertrophy (POH) would preserve mitoc
136  not contribute to the progression of DCM or pressure overload hypertrophy, despite increased express
137 d miR-378 targets in mouse hearts undergoing pressure overload hypertrophy.
138 ively the former set of genes and ameliorate pressure overload hypertrophy.
139 on (TAC) was performed in CD1 mice to induce pressure overload hypertrophy.
140 e models of dilated cardiomyopathy (DCM) and pressure overload hypertrophy.
141 ight have an adaptive role in the setting of pressure-overload hypertrophy.
142 ession of diffuse cardiac fibrosis in murine pressure-overload hypertrophy.
143 en shown to be detrimental in the setting of pressure-overload hypertrophy.
144 ion and energetics during the development of pressure-overload hypertrophy.
145 en shown to be detrimental in the setting of pressure-overload hypertrophy.
146 ressed by transaortic constriction to induce pressure overload-hypertrophy.
147  hypertrophy was induced by slow progressive pressure overload in adult cats.
148 g compensatory left ventricular hypertrophy, pressure overload in cardiomyocyte NF-kappaB-deficient m
149                         Induction of cardiac pressure overload in Chip-/- mice resulted in robust hyp
150 ficantly decreased cardiac hypertrophy after pressure overload in mice at 2, 10, and 16 weeks of stim
151 xcessive collagen deposition during aging or pressure overload in mice due to enhanced fibroblast act
152                                              Pressure overload in mice lacking SRC-2 induces an abrog
153  and reverses cardiac hypertrophy induced by pressure overload in mice.
154 tor 2 (BMPR2) gene on right ventricular (RV) pressure overload in patients with pulmonary arterial hy
155 e factors (RhoGEFs) activated during cardiac pressure overload in vivo and show that RhoGEF12 is a ce
156 ST protein levels significantly decreased on pressure overload in wild-type mice, paralleling a decre
157  progression of heart failure in response to pressure overload independently of autoantibodies.
158 lls, develop normally, but when subjected to pressure overload induced by transaortic constriction (T
159                                We found that pressure overload induced by transaortic constriction in
160                               In response to pressure overload induced by transaortic constriction, c
161 earts were characterized under conditions of pressure overload induced by transverse aortic constrict
162                                   Similarly, pressure overload induced by transverse aortic constrict
163 ur in vivo studies further demonstrated that pressure overload induced decreases in peroxisome prolif
164 regulation, however HDAC5 knockout prevented pressure overload induced Ncx1 upregulation.
165 erimental model of cardiac fibrosis, cardiac pressure overload induced NETosis and significant platel
166                                 Furthermore, pressure overload induced systemic circulating IL-33 as
167 otent antiinflammatory cytokine, exacerbates pressure overload-induced adverse cardiac remodeling and
168 apeutic approach to limit the progression of pressure overload-induced adverse cardiac remodeling.
169 nd Nox2-deficient hearts were protected from pressure overload-induced adverse myocardial and intrace
170 fter the operation, puma deletion attenuated pressure overload-induced apoptosis and fibrosis; howeve
171                            Here, we examined pressure overload-induced cardiac fibrosis in fibroblast
172 to an epigenetic-miRNA regulatory pathway in pressure overload-induced cardiac fibrosis.
173 row fibroblast progenitor cells (BM-FPCs) in pressure overload-induced cardiac fibrosis.
174  shown that interleukin-10 (IL10) suppresses pressure overload-induced cardiac fibrosis; however, the
175 CaV1.2 calcium channels has been reported in pressure overload-induced cardiac hypertrophy and heart
176 ed ischemia/reperfusion injury and prevented pressure overload-induced cardiac hypertrophy.
177 ignaling mechanisms in pharmacologically and pressure overload-induced cardiac hypertrophy.
178 adverse structural remodeling in response to pressure overload-induced cardiac hypertrophy.
179  in protection against pharmacologically and pressure overload-induced cardiac hypertrophy.
180 trimeric G proteins is centrally involved in pressure overload-induced cardiac remodeling and plays a
181  to study the role of the G(12/13) family in pressure overload-induced cardiac remodeling.
182                                              Pressure overload-induced cardiac stress induces left ve
183 r Smad3, but not Smad2, markedly reduced the pressure overload-induced fibrotic response as well as f
184 ated that deletion of TRPC6 had no impact on pressure overload-induced heart failure despite inhibiti
185                                              Pressure overload-induced heart failure is more severe i
186 l profiles in the heart were determined in a pressure overload-induced heart failure model.
187  and exogenous H2S therapy in the setting of pressure overload-induced heart failure.
188 or therapeutic intervention in patients with pressure overload-induced heart failure.
189 le-strand break (SSB) in the pathogenesis of pressure overload-induced heart failure.
190 del, RBFox1 deficiency in the heart promoted pressure overload-induced heart failure.
191                                              Pressure overload-induced heart hypertrophy and failure
192 se proteins, we used an established model of pressure overload-induced heart muscle hypertrophy cause
193 s that occur during the early development of pressure overload-induced HF involve both transcriptiona
194                                           In pressure overload-induced HF mice and isolated hypertrop
195           We hypothesized that IL10 inhibits pressure overload-induced homing of BM-FPCs to the heart
196 ically overexpressed Fstl1 were resistant to pressure overload-induced hypertrophy and cardiac failur
197  basal heart function but protects mice from pressure overload-induced hypertrophy and fibrosis as ef
198 that IF1 is upregulated in mouse hearts with pressure overload-induced hypertrophy and in human heart
199  Stim1 silencing prevents the development of pressure overload-induced hypertrophy but also reverses
200 lt cardiac myocytes following development of pressure overload-induced hypertrophy.
201 cumulation of platelets and T lymphocytes in pressure overload-induced inflammation.
202 umbers of cardiac fibroblasts in response to pressure overload-induced injury; therefore, these proce
203 tential canonical 3 (TRPC3) channel mediates pressure overload-induced maladaptive cardiac fibrosis b
204 n cardiomyocytes, and specifically regulates pressure overload-induced maladaptive cardiac remodeling
205  that HDACs play a role in the regulation of pressure overload-induced miR-133a downregulation.
206  examined in the hearts of mice subjected to pressure overload-induced pathological cardiac hypertrop
207 NA-Seq data obtained from mouse hearts after pressure-overload-induced by transaortic constriction.
208 +) waves and correlated local contraction in pressure-overload-induced cardiomyopathy.
209  using small hairpin RNA (shRNA) accelerated pressure-overload-induced deterioration of cardiac funct
210  signaling pathways significantly changed in pressure-overload-induced heart failure.
211 n, and improves survival in a mouse model of pressure-overload-induced heart failure.
212 en the detrimental phenotype associated with pressure-overload-induced HF and identified physiologica
213                  We created a mouse model of pressure-overload-induced HF with transverse aortic cons
214 g blunts cardiac stress responses, including pressure-overload-induced hypertrophy.
215 ch developmental subset of fibroblasts after pressure overload injury.
216  IL-33 is crucial for translating myocardial pressure overload into a selective systemic inflammatory
217  expression of NKA-alpha2 on the heart after pressure overload is due to more efficient Ca2+ clearanc
218            RV hypertrophy (RVH) triggered by pressure overload is initially compensatory but often le
219 Chronic systemic hypertension causes cardiac pressure overload leading to increased myocardial O(2) c
220  drive extracellular matrix remodeling after pressure overload, leading to fibrosis and diastolic dys
221 ng of the left ventricle (LV) in response to pressure overload leads to the re-expression of the feta
222 otype, increased biomechanical stress due to pressure overload led to accelerated cardiac hypertrophy
223                                              Pressure overload led to severe heart failure in cMLCK k
224 e onset of severe contractile dysfunction in pressure-overload left ventricular hypertrophy in vivo.
225                         In mice subjected to pressure overload, LNA-antimiR-34 improved systolic func
226  overload LVH (VOH) is less profibrotic than pressure overload LVH (POH).
227                             Three days after pressure overload, macrophages and T lymphocytes accumul
228                                              Pressure overload-mediated changes in overall cardiac RN
229  we show that HKL blocks agonist-induced and pressure overload-mediated, cardiac hypertrophic respons
230 ogical hearts from Galphaq-overexpressing or pressure-overloaded mice after ovary removal; however, e
231 nhibitor, gallein, in a clinically relevant, pressure-overload model of HF.
232 d contractile performance in postinfarct and pressure overload models of HF by in vivo echocardiograp
233 ly, induction of RBFox1 expression in murine pressure overload models substantially attenuated cardia
234 ted in whole heart tissue in multiple murine pressure overload models.
235  of miR-1 as treatment with beta-blockers in pressure-overloaded mouse hearts prevented its down-regu
236  interrogate microRNA and mRNA regulation in pressure-overloaded mouse hearts, and performed a genome
237 ance to Rho-mediated maladaptive fibrosis in pressure-overloaded mouse hearts.
238 elopment and exercise) and pathologic (i.e., pressure overload) myocardial hypertrophy.
239 d that galectin-3 may be up-regulated in the pressure-overloaded myocardium and regulate hypertrophy
240 nd transdifferentiation to myofibroblasts in pressure-overloaded myocardium.
241  expression was markedly up-regulated in the pressure-overloaded myocardium.
242 N(G)-nitroarginine methyl ester (L-NAME) and pressure overload (n=11) from transaortic constriction (
243 tive beta1 integrin in adult CM; (5) in vivo pressure overload of the wild-type heart results in incr
244 gitation (AR) imposes significant volume and pressure overload on the left ventricle (LV), but such p
245                                 In addition, pressure overload or CTCF depletion remodeled long-range
246                                              Pressure overload or CTCF depletion selectively altered
247 arts with impaired contractility, induced by pressure overload or doxorubicin treatment, contractile
248 uded wild-type mice subjected to ventricular pressure overload or fasting, as well as patients diagno
249 adverse heart remodeling following sustained pressure overload or Gq agonist stimulation.
250          During the hypertrophic response to pressure overload or neurohormonal stimuli, miR-133a dow
251 posed to aortic constriction-induced cardiac pressure-overload or in response to systemic tunicamycin
252          The imposition of cardiac stress by pressure overload, or muscle stress by myotonia, did not
253                               During chronic pressure overload, overactivation of the sympathetic ner
254 knockout mice (n=31) died in the 16 weeks of pressure overload (P=0.02).
255 modeling response to a left ventricular (LV) pressure overload (PO) stimulus.
256 ss of ventricular performance in response to pressure overload, possibly through a mechanism involvin
257 hanisms by which the heart adapts to chronic pressure overload, producing compensated hypertrophy and
258                                     Instead, pressure overload promoted comparable proliferation and
259 ngenital alteration of SR Ca(2+) release and pressure overload promoted eccentric remodeling and HF d
260 s have found that an increase in Nox4 during pressure overload protects the heart against failure.
261                                    Sustained pressure overload rapidly led to greater chamber dilatio
262                                      Cardiac pressure overload resulted in a modest increase in c-kit
263                Furthermore, we observed that pressure overload resulted in LV segmental dyssynchrony
264                                              Pressure overload resulting from aortic stenosis causes
265                                      Cardiac pressure overload resulting from trans-aortic constricti
266 gulatory events occurring exclusively during pressure overload revealed signaling networks that may b
267 in murine models of primary and secondary RV pressure overload (RVPO) and further explore biventricul
268 structure and function but when subjected to pressure overload showed blunted hypertrophy, less fibro
269 he overall cardiac response to TGF-beta when pressure overload stimulation was applied.
270    However, alpha1C(-)/(+) mice subjected to pressure overload stimulation, isoproterenol infusion, a
271 rt decreases the hypertrophic response after pressure overload stimulation, reduces the degree of pat
272 enuated the cardiac hypertrophic response to pressure overload stimulation.
273                                        Under pressure overload stress, KO mice were prone to death an
274 ks related to homeostasis are disturbed upon pressure overload stress.
275 hypertrophy and heart failure in response to pressure overload stress.
276 at the sGC response to NO also declines with pressure-overload stress and assessed the role of heme-o
277 al responses to neurohormones, and sustained pressure-overload stress.
278 logic (e.g., exercise) and pathologic (e.g., pressure overload) stresses.
279 he heart before, but not after, the onset of pressure overload substantially attenuates cardiac hyper
280 ating the adaptive responses of the heart to pressure overload, suggesting its important role in myoc
281 athological cardiac growth after ventricular pressure overload, supporting its role as an endogenous
282 iac dysfunction with aging or in response to pressure overload that was characterized by reduced myoc
283 PPARalpha to DR1 was enhanced in response to pressure overload, that of RXRalpha was attenuated.
284 n2, we show that under conditions of in vivo pressure overload the cellular source of the exocytosis
285                                        After pressure overload, the TF genes in Module 1 were up-regu
286 pidly died of heart failure within 1 week of pressure overload, they showed an inability to upregulat
287 intaining cardiac oxidative metabolism under pressure overload to ensure survival.
288 ncRNA expression in murine CFs after chronic pressure overload to identify CF-enriched lncRNAs and in
289 Ras gene knockout mice and subjected them to pressure overload to induce cardiac hypertrophy and dysf
290 3, and ZO-1 was significantly perturbed upon pressure overload, underscored by disorganization of the
291 unction due to myocardial infarction (MI) or pressure overload via transverse aortic constriction (TA
292                             After 8 weeks of pressure overload via transverse aortic constriction (TA
293        The reduction in cMLCK protein during pressure overload was attenuated by inhibition of ubiqui
294                                              Pressure overload was induced in TNC knockout and wild-t
295                                              Pressure overload was induced in wild-type (WT) and IL10
296            Using a surgical model of cardiac pressure overload, we found that although calcineurin-de
297  binding, although antifibrotic effects with pressure overload were observed.
298 elerated cardiac hypertrophy after 7 days of pressure overload, whereas female galectin-3 knockouts h
299       Hypertension or aortic stenosis causes pressure overload, which evokes hypertrophic myocardial
300  to modulate TGF-beta in hearts subjected to pressure overload, with noncanonical pathways predominan

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