ライフサイエンスコーパス: pressure overload

1 n caused by transaortic constriction-induced pressure overload.

2 of TNC in cardiac hypertrophy in response to pressure overload.

3 thological cardiac remodeling in response to pressure overload.

4 nst excessive remodeling in response to mild pressure overload.

5 o identify the diffuse local inflammation in pressure overload.

6 inflammatory leukocyte infiltration early in pressure overload.

7 ge subset into the myocardium in response to pressure overload.

8 4 after adrenergic stimulation or myocardial pressure overload.

9 esponse for pyruvate dehydrogenase kinase to pressure overload.

10 ult mouse hearts expressing ssTnI to chronic pressure overload.

11 tch and from sera of mice undergoing cardiac pressure overload.

12 of MeCP2 target genes remained stable during pressure overload.

13 nversation regulates the heart's response to pressure overload.

14 ing in pathological LV remodelling following pressure overload.

15 , genetically altered mice were subjected to pressure overload.

16 icular HF was induced by combined volume and pressure overload.

17 ve remodeling and arrhythmias in response to pressure overload.

18 of ST2 exacerbated cardiac hypertrophy with pressure overload.

19 Both cardiac phenotypes were aggravated on pressure overload.

20 pertrophy in the hearts of mice subjected to pressure overload.

21 y and fibrosis in a disease model of cardiac pressure overload.

22 s develop an aggravated phenotype induced by pressure overload.

23 uring HF induced by myocardial infarction or pressure overload.

24 /-) gain-of-function mutation in response to pressure overload.

25 maladaptive autophagy in a model of cardiac pressure overload.

26 (HF) forms of cardiac hypertrophy because of pressure overload.

27 ided significantly protective benefits after pressure overload.

28 ling occurs in a model of volume rather than pressure overload.

29 blast lineages also remained unchanged after pressure overload.

30 ead to improved cardiac remodeling following pressure overload.

31 for cardiac phenotyping in a mouse model of pressure overload.

32 ed redox stress in response to infarction or pressure overload.

33 hypertrophy in response to phenylephrine and pressure overload.

34 ansaortic constriction as a model of cardiac pressure overload.

35 rtrophy and improved systolic function after pressure overload.

36 ed by VCP under the cardiac stress caused by pressure overload.

37 on on the translational level in response to pressure overload.

38 al cardiac remodeling in response to chronic pressure overload.

39 USP20 phosphorylation in cardiac response to pressure overload.

40 of FoxO1-bound, pol II-regulated genes after pressure overload.

41 for PKG1-mediated cardiac protection against pressure overload.

42 tial fibrosis in mice subjected to sustained pressure overload.

43 alpha or ATF6beta on the cardiac response to pressure overload.

44 Mice were subjected to chronic pressure overload.

45 nsition to heart failure (HF) in response to pressure overload.

46 line HFpEF model induced by slow-progressive pressure overload.

47 es of isoprenaline stress under baseline and pressure-overload.

48 itochondrial respiration despite elevated RV pressure-overload.

49 ysfunction, partially independent of chronic pressure-overload.

50 Myocardial YKL-40 increased in experimental pressure overload (6-fold in decompensated versus sham m

51 inhibition of NF-kappaB at the time of acute pressure overload accelerates the progression of left ve

52 al gene program and disrupts the response to pressure overload, accompanied by prominent effects on m

53 tion of CTGF levels in the heart with aging, pressure overload, agonist infusion, or TGF-beta overexp

54 ed cardiac hypertrophy, and following severe pressure overload all Erbin(-/-) mice died from heart fa

55 ally, ANGPTL2-knockdown in mice subjected to pressure overload ameliorates cardiac dysfunction.

56 However, after the establishment of pressure overload, an increase in leptin levels has prot

57 n important regulator of NCX1 in response to pressure overload and aimed to identify molecular mechan

58 On pathological pressure overload and beta-adrenergic stimulation, DKO m

59 rtant for the cardiac hypertrophy induced by pressure overload and catecholamine toxicity.

60 TORC1 is necessary for cardiac adaptation to pressure overload and development of compensatory hypert

61 iling heart from the perspectives of chronic pressure overload and diabetes mellitus.

62 her impaired cardiac function in response to pressure overload and exacerbated fibrosis by enhancing

63 ed in myocardial phospholipids after chronic pressure overload and explored plausible links between t

64 d fatty acid redistribution in rat models of pressure overload and hypertensive heart disease and sig

65 Hence, we investigated the impact of pressure overload and infarction on myocardial metabolis

66 sis in a clinically relevant animal model of pressure overload and is sensitive to pharmacological re

67 ut mice, Wnt-signaling-modulated hearts, and pressure overload and myocardial ischemia models were ap

68 rdiac function and mortality after long-term pressure overload and prevented disease progression in c

69 OA) results in chronic left ventricular (LV) pressure overload and subsequently leads to LV diastolic

70 d its functional significance during cardiac pressure overload and unloading.

71 ECM in the setting of myocardial infarction, pressure overload, and volume overload.

72 pathological and physiological responses to pressure overload are incompletely understood and genera

73 the remodeling responses of the RV and LV to pressure overload are largely similar, there are several

74 that drive atrial remodeling during cardiac pressure overload are poorly defined.

75 Animal models of pressure overload are valuable for understanding hyperte

76 ning in 57% of FGR, which supports increased pressure overload as a mechanism for cardiovascular prog

77 However, with long-term pressure overload both Atf6 and Atf6b null mice showed e

78 During pressure overload, both hypertrophic and hypoxic signals

79 wo major angiogenic stimuli occurring during pressure overload bridging both hypertrophic and hypoxia

80 myocardial remodeling and dysfunction after pressure overload but not after volume overload.

81 ic responses to phenylephrine and to chronic pressure overload, but it affected neither antiapoptotic

82 ontrol, influences the metabolic response to pressure overload by direct regulation of the catalytic

83 Mice were subjected to pressure overload by means of angiotensin-II infusion or

84 in an in vivo model of cardiac hypertrophy (pressure overload by thoracic aortic constriction).

85 elief of the right ventricular volume and/or pressure overload by TPVR will have a beneficial effect

86 Starting 1 week after the induction of pressure overload by transaortic constriction, mice were

87 We induced pressure overload by transthoracic aortic constriction (

88 earts subjected to standardized pathological pressure overload by transverse aortic constriction (TAC

89 ontrol mice and in mice subjected to chronic pressure-overload by transverse aorta constriction (TAC)

90 ontrol mice and in mice subjected to chronic pressure-overload by transverse aorta constriction.

91 ure after myocardial infarction or long-term pressure overload, by preventing cardiac cell death and

92 Pathological conditions such as ischemia or pressure overload can induce a release of extracellular

93 cated in the pathogenesis of several chronic pressure overload cardiac diseases.

94 tect against hypertrophy or dysfunction from pressure overload, combined deletion was protective, sup

95 A prolonged state of left ventricular pressure overload, commonly caused by hypertension and a

96 V1 is downregulated in the LA during cardiac pressure overload, contributing to both electrical and s

97 a heterogeneous population of fibroblasts on pressure overload could suggest that common signaling me

98 ults We used a mouse model of left ventricle pressure overload coupled to in vitro studies in primary

99 The pressure overload data sets were also compared with the

100 LV pressure overload did not upregulate miR-182.

101 ase-specific, because angiotensin II-induced pressure overload does not trigger significant EPDC fibr

102 Pressure overload enhanced BM-FPC mobilization and homin

103 bited accelerated systolic dysfunction after pressure overload, evidenced by an early 40% reduction i

104 Results: Pressure overload evoked rapid left ventricular dilation

105 yocytes or activated fibroblasts exacerbates pressure overload-evoked fibrosis.

106 ial triglyceride (TG) turnover is reduced in pressure-overloaded, failing hearts, limiting the availa

107 labels fibroblasts, we found that following pressure overload, fibroblasts were not derived from hem

108 In the ACi group 4 weeks after pressure overload, fractional shortening and the rate of

109 Accelerated systolic dysfunction in pressure-overloaded FS3KO mice was associated with accen

110 tor attenuated early systolic dysfunction in pressure-overloaded FS3KO mice, suggesting that the prot

111 In a mouse model of cardiac pressure overload, global genetic deletion of miR-29 or

112 ur lab has shown that, following ventricular pressure overload, GRK5, a primary cardiac GRK, facilita

113 s caused by arsenic-induced liver insult and pressure overload heart injury.

114 position in the standard murine nonischemic, pressure-overload heart failure model.

115 ischemia due to peripheral arterial disease, pressure-overload heart failure, wound healing, and chro

116 athophysiology of ischemic heart disease and pressure-overload heart failure.

117 technique can isolate diffuse leukocytes in pressure-overload heart failure.

118 Mice lacking PPP1R3A are protected against pressure-overload heart failure.

119 LUM attenuates collagen cross-linking in the pressure-overloaded heart, leading to increased mortalit

120 ocardium against excessive remodeling of the pressure-overloaded heart.

121 brosis, and cardiomyocyte hypertrophy in the pressure-overloaded heart.

122 In a model of aortic banding-induced chronic pressure overload, heart function was similarly depresse

123 Echocardiographic analysis of pressure overloaded hearts revealed that all LV paramete

124 Estrogen and sildenafil had no impact on pressure-overloaded hearts from animals expressing dysfu

125 diac P2X4R overexpression in postinfarct and pressure overload HF as did eNOS knockout.

126 In a rat model of pressure overload HF, BNIP3 knockdown significantly decr

127 rct or transverse aorta constriction-induced pressure overload HF.

128 ion, and were protected from postinfarct and pressure overload HF.

129 blasts, reduces the hypertrophic response to pressure overload; however, knocking out Pmca4 specifica

130 activation improved the cardiac function in pressure overloaded Hras null hearts in vivo.

131 r NKA-alpha2 were generated and subjected to pressure overload hypertrophic stimulation.

132 creasing PGC-1alpha levels in the context of pressure overload hypertrophy (POH) would preserve mitoc

133 al Ca(2+) handling and PDE4B is decreased in pressure overload hypertrophy, suggesting that increasin

134 d miR-378 targets in mouse hearts undergoing pressure overload hypertrophy.

135 ively the former set of genes and ameliorate pressure overload hypertrophy.

136 on (TAC) was performed in CD1 mice to induce pressure overload hypertrophy.

137 e models of dilated cardiomyopathy (DCM) and pressure overload hypertrophy.

138 els, a major factor driving progression from pressure-overload hypertrophy (POH) to HFpEF is the acti

139 ight have an adaptive role in the setting of pressure-overload hypertrophy.

140 ession of diffuse cardiac fibrosis in murine pressure-overload hypertrophy.

141 en shown to be detrimental in the setting of pressure-overload hypertrophy.

142 Upon induction of pressure overload, immune activation occurs across the e

143 hypertrophy was induced by slow progressive pressure overload in adult cats.

144 g compensatory left ventricular hypertrophy, pressure overload in cardiomyocyte NF-kappaB-deficient m

145 t 1) signaling axis in the LA during cardiac pressure overload in humans and mouse models and explore

146 ficantly decreased cardiac hypertrophy after pressure overload in mice at 2, 10, and 16 weeks of stim

147 Pressure overload in mice lacking SRC-2 induces an abrog

148 and reverses cardiac hypertrophy induced by pressure overload in mice.

149 tor 2 (BMPR2) gene on right ventricular (RV) pressure overload in patients with pulmonary arterial hy

150 ST protein levels significantly decreased on pressure overload in wild-type mice, paralleling a decre

151 progression of heart failure in response to pressure overload independently of autoantibodies.

152 taline + shunt-induced PAH, and rats with RV pressure overload induced by pulmonary artery banding we

153 earts were characterized under conditions of pressure overload induced by transverse aortic constrict

154 Similarly, pressure overload induced by transverse aortic constrict

155 catecholamine infusion and a 2-week chronic pressure overload induced by transverse aortic constrict

156 for ATF6alpha and ATF6beta in regulating the pressure overload induced cardiac hypertrophic response

157 To examine the role of LUM in pressure overload induced cardiac remodeling, we subject

158 ur in vivo studies further demonstrated that pressure overload induced decreases in peroxisome prolif

159 regulation, however HDAC5 knockout prevented pressure overload induced Ncx1 upregulation.

160 erimental model of cardiac fibrosis, cardiac pressure overload induced NETosis and significant platel

161 Furthermore, pressure overload induced systemic circulating IL-33 as

162 yofibroblasts using a mouse model of cardiac pressure overload, induced through transverse aortic con

163 nd Nox2-deficient hearts were protected from pressure overload-induced adverse myocardial and intrace

164 SAC/VAL significantly ameliorated pressure overload-induced cardiac fibrosis by blocking C

165 Here, we examined pressure overload-induced cardiac fibrosis in fibroblast

166 row fibroblast progenitor cells (BM-FPCs) in pressure overload-induced cardiac fibrosis.

167 to an epigenetic-miRNA regulatory pathway in pressure overload-induced cardiac fibrosis.

168 shown that interleukin-10 (IL10) suppresses pressure overload-induced cardiac fibrosis; however, the

169 riction (TAC) is a well-established model of pressure overload-induced cardiac hypertrophy and failur

170 CaV1.2 calcium channels has been reported in pressure overload-induced cardiac hypertrophy and heart

171 t different stages during the progression of pressure overload-induced cardiac hypertrophy in a mouse

172 enylephrine-stimulated cardiomyocytes and in pressure overload-induced cardiac hypertrophy in vivo.

173 verse aortic constriction (TAC), a model for pressure overload-induced cardiac hypertrophy, and follo

174 specific overexpression of Gfat1 exacerbates pressure overload-induced cardiac hypertrophy, fibrosis,

175 Pressure overload-induced cardiac hypertrophy, such as t

176 adverse structural remodeling in response to pressure overload-induced cardiac hypertrophy.

177 in protection against pharmacologically and pressure overload-induced cardiac hypertrophy.

178 ed ischemia/reperfusion injury and prevented pressure overload-induced cardiac hypertrophy.

179 ignaling mechanisms in pharmacologically and pressure overload-induced cardiac hypertrophy.

180 Pressure overload-induced cardiac stress induces left ve

181 In vitro, endothelin-1- and, in vivo, pressure overload-induced cardiomyocyte hypertrophic gro

182 r Smad3, but not Smad2, markedly reduced the pressure overload-induced fibrotic response as well as f

183 ated that deletion of TRPC6 had no impact on pressure overload-induced heart failure despite inhibiti

184 Pressure overload-induced heart failure is more severe i

185 Pressure overload-induced heart failure was established

186 le-strand break (SSB) in the pathogenesis of pressure overload-induced heart failure.

187 del, RBFox1 deficiency in the heart promoted pressure overload-induced heart failure.

188 Pressure overload-induced heart hypertrophy and failure

189 se proteins, we used an established model of pressure overload-induced heart muscle hypertrophy cause

190 s that occur during the early development of pressure overload-induced HF involve both transcriptiona

191 In pressure overload-induced HF mice and isolated hypertrop

192 We hypothesized that IL10 inhibits pressure overload-induced homing of BM-FPCs to the heart

193 rdiac-specific deletion of Lin28a attenuated pressure overload-induced hypertrophic growth, cardiac d

194 that IF1 is upregulated in mouse hearts with pressure overload-induced hypertrophy and in human heart

195 tive cardiac fibrosis and dysfunction during pressure overload-induced hypertrophy and suggests that

196 Stim1 silencing prevents the development of pressure overload-induced hypertrophy but also reverses

197 We characterised a surgical model of pressure overload-induced hypertrophy in C57BL/6J mice p

198 lt cardiac myocytes following development of pressure overload-induced hypertrophy.

199 umbers of cardiac fibroblasts in response to pressure overload-induced injury; therefore, these proce

200 tential canonical 3 (TRPC3) channel mediates pressure overload-induced maladaptive cardiac fibrosis b

201 n cardiomyocytes, and specifically regulates pressure overload-induced maladaptive cardiac remodeling

202 that HDACs play a role in the regulation of pressure overload-induced miR-133a downregulation.

203 Often, pressure overload-induced myocardial remodeling does not

204 icant mediator of cardiac protection against pressure overload-induced pathological cardiac hypertrop

205 examined in the hearts of mice subjected to pressure overload-induced pathological cardiac hypertrop

206 Pressure overload-induced pathological cardiac hypertrop

207 ecific CIP4 gene deletion in mice attenuated pressure overload-induced pathological cardiac remodelin

208 he progression of myocardial infarction- and pressure overload-induced pathological remodeling.

209 +) waves and correlated local contraction in pressure-overload-induced cardiomyopathy.

210 an be serially imaged in the early stages of pressure-overload-induced heart failure and to compare t

211 en the detrimental phenotype associated with pressure-overload-induced HF and identified physiologica

212 We created a mouse model of pressure-overload-induced HF with transverse aortic cons

213 ch developmental subset of fibroblasts after pressure overload injury.

214 IL-33 is crucial for translating myocardial pressure overload into a selective systemic inflammatory

215 expression of NKA-alpha2 on the heart after pressure overload is due to more efficient Ca2+ clearanc

216 RV hypertrophy (RVH) triggered by pressure overload is initially compensatory but often le

217 drive extracellular matrix remodeling after pressure overload, leading to fibrosis and diastolic dys

218 Sustained pressure overload leads to dilative remodeling and systo

219 ng of the left ventricle (LV) in response to pressure overload leads to the re-expression of the feta

220 otype, increased biomechanical stress due to pressure overload led to accelerated cardiac hypertrophy

221 overload LVH (VOH) is less profibrotic than pressure overload LVH (POH).

222 mice (Pak2-CKO) under tunicamycin stress or pressure overload manifested a defective ER response, ca

223 Pressure overload-mediated changes in overall cardiac RN

224 we show that HKL blocks agonist-induced and pressure overload-mediated, cardiac hypertrophic respons

225 ogical hearts from Galphaq-overexpressing or pressure-overloaded mice after ovary removal; however, e

226 n in calcified valves and in an experimental pressure overload model was assessed.

227 omoting endothelial dysfunction in a chronic pressure overload model.

228 nhibitor, gallein, in a clinically relevant, pressure-overload model of HF.

229 nalysis of chromatin organization with mouse pressure-overload model of myocardial stress (transverse

230 d contractile performance in postinfarct and pressure overload models of HF by in vivo echocardiograp

231 ly, induction of RBFox1 expression in murine pressure overload models substantially attenuated cardia

232 ted in whole heart tissue in multiple murine pressure overload models.

233 ated at the RNA and protein levels in murine pressure overload models.

234 of miR-1 as treatment with beta-blockers in pressure-overloaded mouse hearts prevented its down-regu

235 ance to Rho-mediated maladaptive fibrosis in pressure-overloaded mouse hearts.

236 elopment and exercise) and pathologic (i.e., pressure overload) myocardial hypertrophy.

237 d that galectin-3 may be up-regulated in the pressure-overloaded myocardium and regulate hypertrophy

238 s of activated cardiac myofibroblasts in the pressure-overloaded myocardium are, at least in part, be

239 In the pressure-overloaded myocardium, TGF-beta/Smad3-activated

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 In mice subjected to pressure overload, nicotinamide riboside reduced cardiom

244 se and have higher mortality after sustained pressure overload of the heart, owing to mTORC1 hyperact

245 tive beta1 integrin in adult CM; (5) in vivo pressure overload of the wild-type heart results in incr

246 excellent models for studying the impact of pressure overload on RV structure.

247 gitation (AR) imposes significant volume and pressure overload on the left ventricle (LV), but such p

248 In addition, pressure overload or CTCF depletion remodeled long-range

249 Pressure overload or CTCF depletion selectively altered

250 adverse heart remodeling following sustained pressure overload or Gq agonist stimulation.

251 d reduced myocardial fibrosis in response to pressure overload or myocardial infarction.

252 ted well beyond that observed in response to pressure overload or Sirt3 deficiency alone.

253 posed to aortic constriction-induced cardiac pressure-overload or in response to systemic tunicamycin

254 The imposition of cardiac stress by pressure overload, or muscle stress by myotonia, did not

255 During chronic pressure overload, overactivation of the sympathetic ner

256 knockout mice (n=31) died in the 16 weeks of pressure overload (P=0.02).

257 modeling response to a left ventricular (LV) pressure overload (PO) stimulus.

258 e the importance of YAP in response to acute pressure overload (PO).

259 Cardiac pressure overload produced a consistent downregulation o

260 hanisms by which the heart adapts to chronic pressure overload, producing compensated hypertrophy and

261 Instead, pressure overload promoted comparable proliferation and

262 ngenital alteration of SR Ca(2+) release and pressure overload promoted eccentric remodeling and HF d

263 s have found that an increase in Nox4 during pressure overload protects the heart against failure.

264 ctivation of AMPK preceding left ventricular pressure overload reduces adverse remodeling and preserv

265 Cardiac pressure overload resulted in a modest increase in c-kit

266 Cardiac pressure overload resulting from trans-aortic constricti

267 gulatory events occurring exclusively during pressure overload revealed signaling networks that may b

268 y help prevent ventricular dilatation in the pressure-overloaded RV.

269 in murine models of primary and secondary RV pressure overload (RVPO) and further explore biventricul

270 RV fibrosis has a dual role in patients with pressure-overloaded RVs of idiopathic pulmonary arterial

271 e VCP in the heart was able to normalize the pressure overload-stimulated hypertrophic signals by act

272 he overall cardiac response to TGF-beta when pressure overload stimulation was applied.

273 enuated the cardiac hypertrophic response to pressure overload stimulation.

274 llot, the right ventricle (RV) is subject to pressure overload stress, leading to RV hypertrophy and

275 hypertrophy and heart failure in response to pressure overload stress.

276 ks related to homeostasis are disturbed upon pressure overload stress.

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 ilure (HF) are apparent using a trans-aortic pressure overload (TAC) model.

281 l molecular regulation mediated by VCP under pressure overload that may bring new insight into the me

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 intaining cardiac oxidative metabolism under pressure overload to ensure survival.

287 ncRNA expression in murine CFs after chronic pressure overload to identify CF-enriched lncRNAs and in

288 Ras gene knockout mice and subjected them to pressure overload to induce cardiac hypertrophy and dysf

289 performed between 2 murine models of cardiac pressure overload, transverse aortic constriction bandin

290 Pressure overload triggers early activation of a matrix-

291 3, and ZO-1 was significantly perturbed upon pressure overload, underscored by disorganization of the

292 fibrosis, and dysfunction induced by chronic pressure overload via transverse aorta constriction or c

293 These 3 processes (pressure overload, volume overload, and RV cardiomyopath

294 Pressure overload was induced in TNC knockout and wild-t

295 Pressure overload was induced in wild-type (WT) and IL10

296 After pressure overload, we monitored the cardiac myocyte tran

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 nts concentric cardiac remodeling induced by pressure overload, while inhibition of PP2A signaling pr