コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
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
59 n important regulator of NCX1 in response to pressure overload and aimed to identify molecular mechan
63 TORC1 is necessary for cardiac adaptation to pressure overload and development of compensatory hypert
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
69 sis in a clinically relevant animal model of pressure overload and is sensitive to pharmacological re
71 rdiac function and mortality after long-term pressure overload and prevented disease progression in c
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
82 wo major angiogenic stimuli occurring during pressure overload bridging both hypertrophic and hypoxia
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
89 in the adaptation of the heart and aorta to pressure overload by negatively regulating TGF-beta sign
91 elief of the right ventricular volume and/or pressure overload by TPVR will have a beneficial effect
94 ontrol mice and in mice subjected to chronic pressure-overload by transverse aorta constriction (TAC)
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
102 a heterogeneous population of fibroblasts on pressure overload could suggest that common signaling me
105 n basal conditions, knockout mice exposed to pressure overload developed less hypertrophy and showed
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
110 knockdown preserved capillary density after pressure overload, enhancing BMP7, a regulator of the en
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
117 ur lab has shown that, following ventricular pressure overload, GRK5, a primary cardiac GRK, facilita
120 ischemia due to peripheral arterial disease, pressure-overload heart failure, wound healing, and chro
124 In a model of aortic banding-induced chronic pressure overload, heart function was similarly depresse
126 Estrogen and sildenafil had no impact on pressure-overloaded hearts from animals expressing dysfu
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
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
148 g compensatory left ventricular hypertrophy, pressure overload in cardiomyocyte NF-kappaB-deficient m
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
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
158 lls, develop normally, but when subjected to pressure overload induced by transaortic constriction (T
161 earts were characterized under conditions of pressure overload induced by transverse aortic constrict
163 ur in vivo studies further demonstrated that pressure overload induced decreases in peroxisome prolif
165 erimental model of cardiac fibrosis, cardiac pressure overload induced NETosis and significant platel
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
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
180 trimeric G proteins is centrally involved in pressure overload-induced cardiac remodeling and plays a
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
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
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
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
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.
209 using small hairpin RNA (shRNA) accelerated pressure-overload-induced deterioration of cardiac funct
212 en the detrimental phenotype associated with pressure-overload-induced HF and identified physiologica
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
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
224 e onset of severe contractile dysfunction in pressure-overload left ventricular hypertrophy in vivo.
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
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
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
239 d that galectin-3 may be up-regulated in the pressure-overloaded myocardium and regulate hypertrophy
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
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
251 posed to aortic constriction-induced cardiac pressure-overload or in response to systemic tunicamycin
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
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.
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
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
276 at the sGC response to NO also declines with pressure-overload stress and assessed the role of heme-o
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
286 pidly died of heart failure within 1 week of pressure overload, they showed an inability to upregulat
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
298 elerated cardiac hypertrophy after 7 days of pressure overload, whereas female galectin-3 knockouts h
300 to modulate TGF-beta in hearts subjected to pressure overload, with noncanonical pathways predominan
WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。