ライフサイエンスコーパス: pressure overload

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