ライフサイエンスコーパス: endothelial dysfunction

1 ERK5 signalling may be useful to counteract endothelial dysfunction.

2 ized (i.e., microvascular and macrovascular) endothelial dysfunction.

3 emic inflammation and coronary microvascular endothelial dysfunction.

4 ing fibrosis, immunologic abnormalities, and endothelial dysfunction.

5 nhealing wounds, and diabetes often involves endothelial dysfunction.

6 antigen levels as a marker for intrahepatic endothelial dysfunction.

7 ction of impaired renal microcirculation and endothelial dysfunction.

8 red to be a hallmark feature of pathological endothelial dysfunction.

9 ric oxide and prostanoid signalling underlie endothelial dysfunction.

10 rs to be particularly effective in reversing endothelial dysfunction.

11 scular microRNA-Sirtuin1 nexus that leads to endothelial dysfunction.

12 iovascular diseases that are associated with endothelial dysfunction.

13 ted with beta-cell strain, dyslipidemia, and endothelial dysfunction.

14 k between impaired potentiation and vascular endothelial dysfunction.

15 nuated the hypertensive response to systemic endothelial dysfunction.

16 significantly increased vasoconstriction and endothelial dysfunction.

17 ractive candidates for modulation in corneal endothelial dysfunction.

18 receptor CX3CR1 that has been implicated in endothelial dysfunction.

19 ostasis and prevent oxidative stress-induced endothelial dysfunction.

20 y be modified by genetic variants related to endothelial dysfunction.

21 ed to treat vision loss secondary to corneal endothelial dysfunction.

22 d antiproliferative effects that might limit endothelial dysfunction.

23 abolism, oxidative stress, inflammation, and endothelial dysfunction.

24 dicating that other critical factors trigger endothelial dysfunction.

25 SAM develop endothelial dysfunction.

26 Short-term exposure to CAP induced vascular endothelial dysfunction.

27 ic inhibition of iNOS prevented ATII-induced endothelial dysfunction.

28 ts without any pre-existing risk factors for endothelial dysfunction.

29 limits VEGFA-driven tumor growth and causes endothelial dysfunction.

30 phosphate oxidase-2 (NOX2) activation causes endothelial dysfunction.

31 ce, and steatosis that may also be linked to endothelial dysfunction.

32 nsplantation in patients with blindness from endothelial dysfunction.

33 leading to intracellular Ca(2+) overload and endothelial dysfunction.

34 flammation caused by TTP deficiency leads to endothelial dysfunction.

35 tive stress, endothelial cell apoptosis, and endothelial dysfunction.

36 protein glutathione peroxidase 1 (GPx-1) and endothelial dysfunction.

37 ting in accelerated apoptosis and consequent endothelial dysfunction.

38 phenomenon is directly linked with pulmonary endothelial dysfunction.

39 HS) in preventing insulin resistance-induced endothelial dysfunction.

40 ast, JunD overexpression blunted age-induced endothelial dysfunction.

41 o reflect the common underlying pathology of endothelial dysfunction.

42 ve protein (CRP), and circulating markers of endothelial dysfunction.

43 e maternal circulation that cause a systemic endothelial dysfunction.

44 angiotensin-converting enzyme expression and endothelial dysfunction.

45 or individuals with blindness due to corneal endothelial dysfunction.

46 he vasculature, p66Shc-induced ROS engenders endothelial dysfunction.

47 effect of GATA2 and NF-kappaB and consequent endothelial dysfunction.

48 on Willebrand factor (vWF) is a biomarker of endothelial dysfunction.

49 improved NO bioavailability, and ameliorated endothelial dysfunction.

50 ay a facilitating role, probably mediated by endothelial dysfunction.

51 from diabetic oxidative stress and vascular endothelial dysfunction.

52 filtration rate and showed evidence of renal endothelial dysfunction.

53 d to cell-based therapy for treating corneal endothelial dysfunction.

54 otects against systemic inflammation-induced endothelial dysfunction.

55 One of the first events in MVD is endothelial dysfunction.

56 tic milieu characterized by blood stasis and endothelial dysfunction.

57 F3 as an important protective factor against endothelial dysfunction.

58 (DMEK) for the surgical treatment of corneal endothelial dysfunction.

59 inducing oxidative stress, inflammation, and endothelial dysfunction.

60 of pro-atherogenic genes and the subsequent endothelial dysfunction.

61 ythematosus (SLE) is a known risk factor for endothelial dysfunction.

62 ammation and thrombogenicity associated with endothelial dysfunction.

63 ture cell therapy products destined to treat endothelial dysfunctions.

64 rative medicine for the treatment of corneal endothelial dysfunctions.

65 in the fetal heart, and promoted peripheral endothelial dysfunction (70.9 +/- 5.6% AUC of normoxic c

66 ged exposure to phosphate is associated with endothelial dysfunction, a direct effect of phosphate, w

67 Age-related arterial endothelial dysfunction, a key antecedent of the develop

68 RATIONALE: Endothelial dysfunction, a major predictor of late cardi

69 toid arthritis (RA) has been associated with endothelial dysfunction, a pathophysiological feature of

70 e to ambient particulate matter (PM) induces endothelial dysfunction, a risk factor for cardiovascula

71 Endothelial dysfunction accompanies cardiac hypertrophy

72 ma) and its co-regulators in cerebrovascular endothelial dysfunction after stroke is unclear.

73 xidative stress, sympathetic activation, and endothelial dysfunction, all of which are critical media

74 injury, inflammation, oxidative stress, and endothelial dysfunction, all of which may perpetuate a n

75 (.)) production, but the direct link between endothelial dysfunction and aggravation of CHF is not di

76 , antecedent hypoglycemia results in greater endothelial dysfunction and an increased proatherothromb

77 almitoyltransferase with myriocin reinstates endothelial dysfunction and angiotensin II-induced hyper

78 ers of the arteries, predominantly caused by endothelial dysfunction and arterial stiffening.

79 This could promote the development of endothelial dysfunction and cardiovascular disease in SL

80 hough lipid signaling has been implicated in endothelial dysfunction and cardiovascular disease, spec

81 (MPs) have emerged as a surrogate marker of endothelial dysfunction and cardiovascular risk.

82 provide direct evidence of the link between endothelial dysfunction and CHF.

83 Because microvesicles (MV) are biomarkers of endothelial dysfunction and coagulation but are also inv

84 evident after the occurrence of age-related endothelial dysfunction and diminished distensibility.

85 otential efficacy of OO and FO in mitigating endothelial dysfunction and disruption of hemostasis cau

86 capacity in SCCOR participants, and between endothelial dysfunction and FEV1 or FEV1/FVC in HeartSCO

87 However, there was no association between endothelial dysfunction and FEV1, FEV1/FVC, low-attenuat

88 Albuminuria is a marker of endothelial dysfunction and has been associated with adv

89 tance (IHVR) and intrahepatic vascular tone (endothelial dysfunction and hyperresponsiveness to metho

90 of endothelial PGC-1alpha sensitized mice to endothelial dysfunction and hypertension in response to

91 ension, and activation of TLR4 and -9 causes endothelial dysfunction and hypertension.

92 ation in mice (Gata5-null) leads to vascular endothelial dysfunction and hypertension.

93 ecause of SOD2 hyperacetylation and promotes endothelial dysfunction and hypertension.

94 e increased vascular permeability and edema, endothelial dysfunction and impaired vasomotion, microem

95 The longitudinal effects of dialysis on endothelial dysfunction and in particular the effects of

96 Vascular endothelial dysfunction and increased arterial stiffness

97 administering PTX3 to wild-type mice induced endothelial dysfunction and increased blood pressure, an

98 Selective brain endothelial dysfunction and increased permeability of th

99 with systemic lupus erythematosus (SLE) have endothelial dysfunction and increased risk of cardiovasc

100 oid receptor blockade blunted leptin-induced endothelial dysfunction and increases in cardiac fibroti

101 lin-induced Akt and eNOS activation, causing endothelial dysfunction and inflammation.

102 Endothelial dysfunction and injury are thought to play a

103 oadiponectinaemia is closely associated with endothelial dysfunction and insulin resistance in obesit

104 oadiponectinaemia is closely associated with endothelial dysfunction and insulin resistance, and micr

105 be attributable to the relationship between endothelial dysfunction and intrinsic myocardial dysfunc

106 mechanisms will expand our understanding of endothelial dysfunction and its dynamic interaction with

107 s revealed that glucose flux via AR mediates endothelial dysfunction and leads to lesional hemorrhage

108 esis that the vascular amylin deposits cause endothelial dysfunction and microvascular injury and are

109 on of a blood pressure cuff protects against endothelial dysfunction and myocardial injury in percuta

110 etion in vascular endothelial cells mediates endothelial dysfunction and premature senescence in dive

111 vation is an important cause of postischemic endothelial dysfunction and presents a novel therapeutic

112 High-fat diet (HFD) promotes endothelial dysfunction and proinflammatory monocyte act

113 represent a novel therapeutic tool to fight endothelial dysfunction and promote vascular reparative

114 lar quercetin, have been shown to ameliorate endothelial dysfunction and reduce blood pressure (BP),

115 fetoplacental resistance and in FGR exhibit endothelial dysfunction and reduced flow-mediated vasodi

116 Endothelial dysfunction and reduced nitric oxide (NO) bi

117 RYGB rapidly reverses obesity-induced endothelial dysfunction and restores the endothelium-pro

118 low and is triggered by an interplay between endothelial dysfunction and subendothelial lipoprotein r

119 PM2.5-induced endothelial dysfunction and systemic inflammation have b

120 butes to cardiovascular disease by promoting endothelial dysfunction and the expression of profibroti

121 tho deficiency lead to chronic inflammation, endothelial dysfunction and vascular calcifications.

122 ndings, we observed elevations in markers of endothelial dysfunction and vascular damage in the serum

123 ted with maternal ancestry may contribute to endothelial dysfunction and vascular disease.

124 T1DM mice or ATP7A mutant T1DM mice augment endothelial dysfunction and vascular O2(*-) production v

125 ertension is a progressive disorder in which endothelial dysfunction and vascular remodeling obstruct

126 thout SDB, which seems to be associated with endothelial dysfunction and, in part, increased MSNA res

127 m that describes overlapping "hyperhemolytic-endothelial dysfunction" and "high hemoglobin-hypervisco

128 apy can also cause myocardial damage, induce endothelial dysfunction, and alter cardiac conduction.

129 nase activation, endothelial NOS uncoupling, endothelial dysfunction, and atherogenesis.

130 metabolism, homocysteine, oxidative stress, endothelial dysfunction, and cardiovascular and potentia

131 investigated blood markers of inflammation, endothelial dysfunction, and damage to both the native a

132 derpinned by impaired basal NO contribution, endothelial dysfunction, and enhanced vascular responsiv

133 endothelial nitric oxide synthase activity, endothelial dysfunction, and impairment of tissue repair

134 on in renal vascular resistance, reversal of endothelial dysfunction, and increased activation of the

135 lic dysfunction, pulmonary vascular disease, endothelial dysfunction, and peripheral abnormalities.

136 ial nitric oxide synthase signaling, rescues endothelial dysfunction, and reduces blood pressure leve

137 lar ER stress and ER stress-induced vascular endothelial dysfunction, and that miR-204 promotes vascu

138 mic and nongenomic effects that by promoting endothelial dysfunction, and vascular and cardiorenal ad

139 have been associated with disease severity, endothelial dysfunction, and vasodilation.

140 inary results suggest that microvascular and endothelial dysfunction are associated with severity of

141 Inflammation and endothelial dysfunction are considered two primary insti

142 Oxidative/nitrosative stress and endothelial dysfunction are hypothesized to be central t

143 n, high VWF:Ag levels, probably representing endothelial dysfunction, are associated with prognosis i

144 WD feeding resulted in aortic stiffness and endothelial dysfunction as determined in vivo by pulse w

145 n patients with HFpEF, which is in line with endothelial dysfunction as potential mediator in the pat

146 D (SAM-WD) and SAM on regular diet displayed endothelial dysfunction, as evidenced by impaired acetyl

147 n grass antioxidant properties might prevent endothelial dysfunction associated to an oxidative imbal

148 Conversely, laminar flow protects against endothelial dysfunction, at least in the initial phases

149 that global deletion of collectrin leads to endothelial dysfunction, augmented salt sensitivity, and

150 Endothelial dysfunction begins in early CKD and contribu

151 Shear stress antagonises endothelial dysfunction by increasing nitric oxide forma

152 e artery stiffness can cause cerebral artery endothelial dysfunction by reducing NO bioavailability a

153 In conclusion, shear stress counteracts endothelial dysfunction by suppressing the pro-inflammat

154 04 (miR-204) promotes vascular ER stress and endothelial dysfunction by targeting the Sirtuin1 (Sirt1

155 Prevention of endothelial dysfunction, by endothelial PTP1B deficiency

156 Oxidative stress and endothelial dysfunction can prevail during advanced age

157 Endothelial dysfunction caused by the combined action of

158 We hypothesized that pulmonary endothelial dysfunction, characterized by abnormal fibro

159 Endothelial dysfunction, characterized by the lowered bi

160 KEY POINTS: Ageing-induced endothelial dysfunction contributes to organ dysfunction

161 Endothelial dysfunction contributes to the pathology of

162 We hypothesized that endothelial dysfunction could be associated with high RP

163 Endothelial dysfunction does not mediate the association

164 of adult age, the R6/2 mouse developed overt endothelial dysfunction due to an inability to increase

165 ve populations may have in common underlying endothelial dysfunction due to genetic or environmental

166 These data support the concept that endothelial dysfunction due to high circulating sFLT1 ma

167 From 66 patients with irreversible corneal endothelial dysfunction dues to Fuchs' dystrophy who enr

168 cysteinemia (HHcy) and hyperglycemia (HG) on endothelial dysfunction (ED) and the underlying mechanis

169 ns are associated with an increased risk for endothelial dysfunction (ED) in children, an early risk

170 Endothelial dysfunction (ED) is a parameter of early ACD

171 Endothelial dysfunction (ED) is involved in the developm

172 IR is responsible for Endothelial Dysfunction (ED) through the impairment of e

173 -standing anterior uveitis increases risk of endothelial dysfunction, especially in the setting of in

174 inally, chronic high-salt ingestion produces endothelial dysfunction, even in salt-resistant subjects

175 ciation between FEV1 and atherosclerosis for endothelial dysfunction had no impact.

176 ndothelial keratoplasty (DSAEK) for isolated endothelial dysfunction has become the preferred surgica

177 Endothelial dysfunction has been considered an important

178 Endothelial dysfunction has been recently shown to play

179 Age-induced endothelial dysfunction has been reported in most skelet

180 However, the role of CIRP in causing endothelial dysfunction has not been investigated.

181 Specifically, disruption of CNP leads to endothelial dysfunction, hypertension, atherogenesis, an

182 pulmonary artery pressure in volunteers with endothelial dysfunction (impaired endothelial production

183 ry arterial hypertension is characterized by endothelial dysfunction, impaired bone morphogenetic pro

184 retains eNOS substrate activity and reverses endothelial dysfunction: implications for the COX-2/ADMA

185 m uric acid levels with allopurinol improves endothelial dysfunction in 80 participants >/=18 years o

186 shear adaptation is an essential part of the endothelial dysfunction in all forms of PAH and tested w

187 on and reduced high-glucose or lipid-induced endothelial dysfunction in arterioles ex vivo.

188 elial cells and its causal relationship with endothelial dysfunction in atherosclerosis are less unde

189 es CHF and further suggest a causal role for endothelial dysfunction in CHF development.

190 Hyperuricemia may contribute to endothelial dysfunction in CKD.

191 and systemic inflammation may contribute to endothelial dysfunction in COPD.

192 ns, has been described to be associated with endothelial dysfunction in different cardiovascular diso

193 ents and lipid oxidation products may induce endothelial dysfunction in HIV infection that could be p

194 and prevented high-glucose and lipid-induced endothelial dysfunction in human arterioles.

195 ma hemoglobin (Hb) in pulmonary and systemic endothelial dysfunction in humans.

196 esponse leading to arterial inflammation and endothelial dysfunction in mice during early stage obesi

197 antioxidant, MitoQ, in ameliorating vascular endothelial dysfunction in old mice.

198 Chronic heart failure (CHF) induces endothelial dysfunction in part because of decreased nit

199 oscillatory shear stress further exacerbates endothelial dysfunction in patients with moderate-severe

200 ive against oscillatory shear stress-induced endothelial dysfunction in patients with moderate-severe

201 -media thickness, and circulating markers of endothelial dysfunction in patients.

202 tant mechanism underlying the development of endothelial dysfunction in primary ageing.

203 on is an early manifestation and mediator of endothelial dysfunction in pulmonary hypertension.

204 udy were to determine how IFN-alpha promotes endothelial dysfunction in SLE, focusing on its regulati

205 ghting DECT-PBV as a biomarker of reversible endothelial dysfunction in smokers with CAE.

206 PC4 provides a Ca(2+) source associated with endothelial dysfunction in the pathophysiology of PAH.

207 rize the unidentified factor(s) that trigger endothelial dysfunction in the postischemic heart.

208 asty has been validated in the management of endothelial dysfunction in the setting of a number of co

209 The endothelial dysfunction in TTP(-/-) mice was associated

210 esults illustrate the importance of studying endothelial dysfunction in vitro over prolonged periods.

211 Endothelial dysfunction, including endothelial hyporespo

212 The loss of NOSTRIN in mice leads to endothelial dysfunction, increased blood pressure, and d

213 xcretion, and vascular inflammation leads to endothelial dysfunction, increased vascular resistance,

214 elet activation, oxidation and inflammation, endothelial dysfunction, increased vascular stiffness, c

215 ), which was associated with protection from endothelial dysfunction induced by Ang II.

216 A defining feature of endothelial dysfunction induced by cardiovascular risk f

217 In CKD, uremic solutes may induce endothelial dysfunction, inflammation, and oxidative str

218 e most apparent for biomarkers of adiposity, endothelial dysfunction, inflammatory cell recruitment,

219 on, attenuated oxidative stress, ameliorated endothelial dysfunction, inhibited inflammation, and sup

220 Endothelial dysfunction is a central pathomechanism in d

221 Endothelial dysfunction is a characteristic of many vasc

222 Vision loss secondary to corneal endothelial dysfunction is a common indication for trans

223 Endothelial dysfunction is a critical factor in many car

224 Endothelial dysfunction is a hallmark of systemic inflam

225 es underlying PRES are not fully understood, endothelial dysfunction is a key factor.

226 Endothelial dysfunction is an early event in cardiovascu

227 Endothelial dysfunction is characterised by aberrant red

228 itric oxide (NO) dilator system to cutaneous endothelial dysfunction is currently unknown in PCOS.

229 It is also known that pulmonary endothelial dysfunction is intertwined with the initiati

230 direct evidence of vascular inflammation and endothelial dysfunction is lacking.

231 Endothelial dysfunction is of interest in relation to sm

232 e remained unaffected, thus the mechanism of endothelial dysfunction is poorly defined.

233 Endothelial dysfunction is seen as an early indicator of

234 primary ageing, but its role in age-related endothelial dysfunction is unknown.

235 Endothelial dysfunction is widely implicated in cardiova

236 Endothelin-1, a marker of endothelial dysfunction, is a potent vasoconstrictor rel

237 d sublingual glycerol trinitrate, markers of endothelial dysfunction), kidney function by Chronic Kid

238 thelial cells (ECs), one of the hallmarks of endothelial dysfunction leading to cardiovascular disord

239 Endothelial dysfunction links thrombotic microangiopathy

240 xic pregnancy in young offspring accelerated endothelial dysfunction (maximal arterial relaxation to

241 Vascular endothelial dysfunction may play an important role in th

242 Endothelial dysfunction may pose a particularly signific

243 Improvement of endothelial dysfunction may reduce colorectal cancer ris

244 Endothelial dysfunction may underlie this; however, the

245 hIRECO demonstrated significant endothelial dysfunction measured by blunted endothelium-

246 METHODS AND hIRECO demonstrated significant endothelial dysfunction measured by blunted endothelium-

247 Portal venous pressure and intrahepatic endothelial dysfunction might account for the selective

248 Microvascular and endothelial dysfunction might underlie hypovolaemic shoc

249 l for targeting novel pathways implicated in endothelial dysfunction, mitochondrial oxidative stress,

250 adipokines, and biomarkers of inflammation, endothelial dysfunction, myocyte injury and stress, and

251 ul effects, ranging from oxidative stress to endothelial dysfunction, nitric oxide disarrays, renal i

252 Endothelial dysfunction/NO bioavailability is associated

253 RBC dysfunction, analogous to endothelial dysfunction, occurs early during diet-induce

254 (ER) stress has been implicated in vascular endothelial dysfunction of obesity, diabetes, and hypert

255 According to this concept, endothelial dysfunction of the renal microcirculation ca

256 is study sought to investigate the effect of endothelial dysfunction on the development of cardiac hy

257 rther research into possible causes, such as endothelial dysfunction or concurrent psychological como

258 conditions, i.e. vascular remodelling after endothelial dysfunction or damage, contractile SMCs foun

259 reperfusion at rest that are associated with endothelial dysfunction, oxidant stress, inflammation, a

260 epletion blunted Ang II-induced SBP rise and endothelial dysfunction (P<0.05), compared with isotype

261 Peripheral endothelial dysfunction (PED) has been described in HF a

262 Endothelial dysfunction plays a pivotal role in the path

263 utic strategy to limit the development of an endothelial dysfunction post-ACS.

264 vessel wall stiffening, and microcirculatory endothelial dysfunction, precedes hypertension and thus

265 Endothelial dysfunction present in patients with periphe

266 Endothelial dysfunction promoted podocyte apoptosis, and

267 option for the management of PAH, improving endothelial dysfunction, pulmonary vascular remodeling,

268 ved circulating PAR2 agonist and mediator of endothelial dysfunction-related microvascular diabetes c

269 Instead, airflow limitation and endothelial dysfunction seem to be unrelated and mutuall

270 biota promotes atherosclerosis, and vascular endothelial dysfunction, signalled by impaired endotheli

271 We demonstrate that IFN-alpha promotes an endothelial dysfunction signature in HUVECs that is char

272 in angiotensin-converting enzyme expression, endothelial dysfunction, smooth muscle contractility, an

273 isoprostane and total carbonyl content), and endothelial dysfunction (soluble vascular cell adhesion

274 hk1(-/-) mice were characterized by enhanced endothelial dysfunction, suggesting a local protective r

275 re both associated with oxidative stress and endothelial dysfunction, suggesting common mechanistic o

276 Taking into account the potential role of endothelial dysfunction, systemic inflammation, arterios

277 c microangiopathy (TMA) leads to generalized endothelial dysfunction that can progress to multiorgan

278 ent of treatments for vision loss because of endothelial dysfunction that do not rely on donor cornea

279 netically predisposed and is associated with endothelial dysfunction that is induced by oxidative str

280 ular amylin deposition as a trigger of brain endothelial dysfunction that is modulated by plasma apol

281 Oxidative stress and inflammation promote endothelial dysfunction thereby hampering cerebral perfu

282 Given statins' ability to repair endothelial dysfunction, this economical approach may al

283 BT) protects against hypertension-associated endothelial dysfunction through alleviation of ER stress

284 rkers of inflammation, oxidative stress, and endothelial dysfunction to the 20-year cumulative incide

285 nt of patients with concomitant cataract and endothelial dysfunction, triple DMEK is an effective str

286 use endothelial damage and contribute to the endothelial dysfunction typical for PE.

287 Accordingly, endothelial dysfunction underpins many cardiovascular di

288 It has been shown to protect against endothelial dysfunction, vascular smooth muscle cell pro

289 CHF-induced endothelial dysfunction was less marked in endoPTP1B(-/-

290 Endothelial dysfunction was manifested by decreased leve

291 e marker whose expression is associated with endothelial dysfunction, was only expressed on CD4+CD28-

292 Fourteen obese adults with endothelial dysfunction were enrolled in a randomized cr

293 xide signalling contributes significantly to endothelial dysfunction, whereas in resistance arteriole

294 iodontal disease is associated with systemic endothelial dysfunction, which has been implicated in pr

295 t EC Kir channels could be targeted to treat endothelial dysfunction, which is a hallmark of vascular

296 apnea syndrome (OSAS) and provokes systemic endothelial dysfunction, which is associated with oxidat

297 Endothelial dysfunction, which is caused by endothelial

298 te to arteriosclerosis, atherosclerosis, and endothelial dysfunction, which seem to be major risk fac

299 IFN-gamma ex vivo caused significant endothelial dysfunction, which was reduced by superoxide

300 sights into the molecular mechanisms linking endothelial dysfunction with the pathogenesis of Alzheim