ライフサイエンスコーパス: endothelial injury

1 ial regeneration in the endotoxemia model of endothelial injury.

2 tory T-cell (Treg) activity fails to control endothelial injury.

3 mpaired reannealing of endothelial AJs after endothelial injury.

4 elopment of neointimal hyperplasia following endothelial injury.

5 or simply reveals the presence of underlying endothelial injury.

6 C reparative function after diabetes-related endothelial injury.

7 ession in vivo and noninvasive assessment of endothelial injury.

8 ame concentrated in the adventitia following endothelial injury.

9 in part, by less severe lung epithelial and endothelial injury.

10 respectively, aHUS is characterized by renal endothelial injury.

11 is a complex disease characterized by severe endothelial injury.

12 in the pathogenesis of diseases that involve endothelial injury.

13 osure to hand-held vibrating tools may cause endothelial injury.

14 tributes to the cellular injury in shock and endothelial injury.

15 ting arterial lesion growth in conditions of endothelial injury.

16 geting as a drug delivery strategy to reduce endothelial injury.

17 ythrocyte, provokes inflammation, and causes endothelial injury.

18 otid artery following experimentally induced endothelial injury.

19 predispose to atherosclerosis by inflicting endothelial injury.

20 ts with active SLE may represent a marker of endothelial injury.

21 r CAD, may cause atherosderosis by oxidative endothelial injury.

22 ic systems, neutrophil release products, and endothelial injury.

23 ant role in platelet adhesion to the site of endothelial injury.

24 ese findings likely represent sepsis-induced endothelial injury.

25 n cytolytic activity may contribute to graft endothelial injury.

26 tory response that in turn causes functional endothelial injury.

27 ischemia-reperfusion (I-R) occurs because of endothelial injury.

28 lial barrier and in preventing lung vascular endothelial injury.

29 s in the promoters of other genes induced by endothelial injury.

30 icating NK cell and macrophage activation in endothelial injury.

31 ocking this pathway abolished FBN1-triggered endothelial injury.

32 n vascular remodeling following wire-induced endothelial injury.

33 severe manifestation of kidney microvascular endothelial injury.

34 entified potential mediators of the observed endothelial injury.

35 roparticle formation, a functional marker of endothelial injury.

36 e complement activation, likely triggered by endothelial injury.

37 lity, multiple markers of ICU morbidity, and endothelial injury.

38 dothelial cell regeneration in rabbits after endothelial injury.

39 , ICU morbidity, and biochemical evidence of endothelial injury.

40 improves renal and lung function by reducing endothelial injury.

41 A pathogenic consequence of hyperoxia is endothelial injury.

42 t blocking APC-mediated pathways or inducing endothelial injury.

43 hanges were accompanied by evidence of acute endothelial injury.

44 e the restoration of vascular function after endothelial injury.

45 tly in response to systemic inflammation and endothelial injury.

46 renchyma, and decreased hepatic ischemia and endothelial injury.

47 as well as pulmonary epithelial and systemic endothelial injury.

48 MN activation and recruitment at the site of endothelial injury.

49 t, but had little effect on antibody-induced endothelial injury.

50 ics of inflammation, hypercoagulability, and endothelial injury.

51 athway dysregulation and is characterized by endothelial injury.

52 the protective effects of olive oil against endothelial injuries.

53 ur groups of C57BL/6 mice underwent denuding endothelial injury 1 day after systemic injection of rec

54 e venous and arterial thrombi in response to endothelial injury, a defect that was phenocopied using

55 their adhesion at the site of laser-induced endothelial injury, a necessary step leading to the gene

56 in a mouse model of type 1 diabetes promotes endothelial injury accelerating the progression of glome

57 terleukin-8 (anti-IL-8) therapy reduces lung endothelial injury after acid instillation, there is no

58 ng the postoperative days, presumably due to endothelial injuries and the infusion of vWF concentrate

59 Epithelial and endothelial injury and a cascade of immune and interstit

60 adhesion molecule-1 (sVCAM-1) is a marker of endothelial injury and a potent predictor of cardiovascu

61 mportant role in the mechanism of glomerular endothelial injury and activation and the formation of m

62 uremic syndrome (D+HUS) is characterized by endothelial injury and activation of inflammatory cytoki

63 ory cytokines, alveolar fluid clearance, and endothelial injury and activation.

64 s, blunts leukocyte homing, protects against endothelial injury and atherosclerosis in a manner invol

65 esponses and leukocyte homing and alleviated endothelial injury and atherosclerosis in vivo.

66 (iv) MYDGF alleviated endothelial injury and atherosclerosis through mitogen-a

67 We hypothesized that microvascular endothelial injury and attendant interstitial edema woul

68 hat because AMR is associated with allograft endothelial injury and C4d deposition, plasma microvesic

69 eases and renal fibrosis are associated with endothelial injury and capillary rarefaction.

70 th factor 23 (FGF23) axis is associated with endothelial injury and cardiovascular risk.

71 important missing piece is the link between endothelial injury and complement activation.

72 NETs may serve as a mechanistic link between endothelial injury and complement activation.

73 activator inhibitor-1 (PAI-1) is a marker of endothelial injury and could be a prognostic marker for

74 onocytes, contributing to lung microvascular endothelial injury and DAH susceptibility.

75 Endothelin-1 (ET-1) is an indicator of endothelial injury and dysfunction and is elevated in wo

76 sociation with this condition, the extent of endothelial injury and dysfunction has been difficult to

77 Endothelial injury and dysfunction precede accelerated a

78 inflammation, mitochondrial dysfunction, and endothelial injury and dysfunction, and can lead to chro

79 y investigated whether biomarkers related to endothelial injury and endothelial repair discriminate b

80 These MPs induce endothelial injury and facilitate acute vaso-occlusive e

81 thin 5 d; the histology was characterized by endothelial injury and fibrin thrombi.

82 have shown that smoke inhalation causes lung endothelial injury and formation of pulmonary edema, the

83 marker of classic complement activation and endothelial injury and has been described in preliminary

84 or EndMT in the response to kidney capillary endothelial injury and highlight the contribution of end

85 Aggravated endothelial injury and impaired endothelial repair capac

86 of these studies suggest new mechanisms for endothelial injury and impaired vascular function associ

87 lveolar fluid clearance could be due to lung endothelial injury and increased fluid flux from the blo

88 nt in the pathogenesis of diseases linked to endothelial injury and inflammation in smokers.

89 ients with SP2, characterized by more severe endothelial injury and inflammation, had higher 28-day m

90 e complement alternative pathway exacerbates endothelial injury and inflammation.

91 sition was accompanied by extensive vascular endothelial injury and intravascular release of von Will

92 diabetic D2 mice demonstrated early signs of endothelial injury and loss of fenestrae.

93 , increases the susceptibility to glomerular endothelial injury and microangiopathy in two genetic mu

94 e a critical role in kidney injury, as might endothelial injury and microvascular thrombi.

95 Endothelial injury and microvascular/macrovascular throm

96 d suggest that cross talk between glomerular endothelial injury and podocytes leads to defects and de

97 e of this study was to assess how indices of endothelial injury and repair change during different st

98 in patients an unfavorable imbalance between endothelial injury and repair, as indicated by increased

99 ause the mechanisms by which FeCl(3) induces endothelial injury and subsequent thrombus formation are

100 unknown role for ADAM10 in sepsis-associated endothelial injury and suggest that understanding pathog

101 ides mechanistic insight into toxin-mediated endothelial injury and suggests new therapeutic approach

102 se data suggest that NETs contribute to lung endothelial injury and that targeting NET formation may

103 their use is limited by the resulting acute endothelial injury and the long-term development of inti

104 Systemic organ endothelial injury and V(O2)-D(O2) relationship alterati

105 relationship, if any, between systemic organ endothelial injury and V(O2)-D(O2) relationship alterati

106 This was due to hepatic ischemia, endothelial injury, and activation of neutrophils, Kupff

107 d vascular inflammation, adhesion responses, endothelial injury, and atherosclerosis in vivo.

108 hondrial reactive oxygen species generation, endothelial injury, and ICAM-1 expression after LPS admi

109 iated with multiple markers of inflammation, endothelial injury, and impaired oxygenation on Day 1 of

110 flammation, alveolar epithelial and systemic endothelial injury, and the development of acute lung in

111 embolic but rather result from inflammation, endothelial injury, and the hypercoagulable state caused

112 g coronary artery by creation of a stenosis, endothelial injury, and thrombus formation followed by t

113 a clinical risk score (LqSOFA) to markers of endothelial injury (Ang-1, Ang-2, sFlt-1), immune activa

114 n end products and surfactant protein D) and endothelial injury (angiopoietin-2) and inflammation (in

115 1beta; tumor necrosis factor-alpha and -R2), endothelial injury (angiopoietin-2, von Willebrand facto

116 due to features of PAH: in situ thrombi and endothelial injury, angioproliferative remodeling, and r

117 rs reduced extravascular lung water and lung endothelial injury as measured by protein permeability (

118 tive vascular features, consisting of severe endothelial injury associated with the presence of intra

119 To detect endothelial injury at the early and reversible stage of

120 It was shown that ELIPs specifically enhance endothelial injury/atheroma components.

121 ium of the diabetic retina, which results in endothelial injury, blood-retina barrier breakdown, and

122 has been widely associated with tubular and endothelial injury but rarely has been shown to induce p

123 le in the process of platelet adhesion after endothelial injury by serving as a bridge between consti

124 advanced glycation end products and systemic endothelial injury by the urine albumin-creatinine ratio

125 Endothelial injury (caused by infection or intravenous d

126 To determine endothelial injury component enhancement, anti-fibrinoge

127 he vascular system and its inhibition due to endothelial injury contributes to cardiovascular disease

128 ition of nitric oxide-mediated vasodilation, endothelial injury due to increased release of free fatt

129 than reactive oxygen species as mediators of endothelial injury during ANCA-associated systemic vascu

130 Objectives: To describe alveolar and endothelial injury dynamics and associations with COVID-

131 accompanied by increased pulmonary vascular endothelial injury, enhanced pulmonary accumulation of n

132 bles and plasma biomarkers representative of endothelial injury, epithelial injury, or inflammation w

133 Ventilation with either 6 or 3 ml/kg reduced endothelial injury equally as measured by plasma vWf:Ag

134 fts in C6+ recipients demonstrated extensive endothelial injury evidenced by release of von Willebran

135 lement plays a significant role in mediating endothelial injury following oxidative stress.

136 development depends on Virchow's triad (ie, endothelial injury from myocardial infarction, blood sta

137 matory condition precipitated in response to endothelial injury from various environmental challenges

138 ific integrin Mac-1, neutrophil recruitment, endothelial injury, glomerular thrombosis, and acute ren

139 in initial platelet accumulation at sites of endothelial injury, however, is the subject of debate.

140 timulated leukocyte shape change at sites of endothelial injury; however, only thrombi were capable o

141 usoidal platelet microthrombi and sinusoidal endothelial injury identified via immunohistology and si

142 on and fibrin generation after laser-induced endothelial injury in a single developing thrombus.

143 neutrophil-derived histones responsible for endothelial injury in acute inflammatory conditions such

144 sue of the JCI, Hippensteel et al. show that endothelial injury in animal models of sepsis or endotox

145 iopoietin-2 is a proinflammatory mediator of endothelial injury in animal models, and increased plasm

146 detrimental inflammatory response seen post-endothelial injury in arteries undergoing revascularizat

147 ir, representing a novel mechanism promoting endothelial injury in CAD patients.

148 d inflation--on alveolar epithelial and lung endothelial injury in experimental acute lung injury.

149 whereas both CPAP-30 and STEP-30/30 yielded endothelial injury in extrapulmonary acute lung injury.

150 This mechanism may well be relevant to acute endothelial injury in inflammation and other pathologica

151 of LOX-1 in monocyte adhesion to HCAECs and endothelial injury in response to ox-LDL.

152 yte-dependent and -independent mechanisms of endothelial injury in sepsis.

153 Here, we examined retinal microvascular endothelial injury in streptozotocin (STZ)-diabetic rats

154 , low-sugar diet does not exacerbate retinal endothelial injury in streptozotocin-induced diabetes.

155 These findings suggest that endothelial injury in the absence of sufficient circulat

156 cular imaging and quantitative evaluation of endothelial injury in the choriocapillaris of live anima

157 ffects of WEB and GB in reducing LPS-induced endothelial injury in the choroid indicate an important

158 f hepatocytes in viral hepatitis and also in endothelial injury in the cold perfusion-warm reperfusio

159 y rise of Ang-2 emphasizes the importance of endothelial injury in the early pathogenesis of ALI.

160 roduces noninvasive subclinical detection of endothelial injury in the iris vasculature, providing a

161 tory cytokines and chemokines, microvascular endothelial injury in the liver, lungs, heart, and kidne

162 idence for the role of potential triggers of endothelial injury in the pathophysiology of CAV and dis

163 se, suggesting that in vivo diabetes-related endothelial injury in the retina may be due to glucose-i

164 in WD exacerbated leukocyte accumulation and endothelial injury in the retinas of STZ-diabetic rats.

165 iciency of eNOS-derived NO causes glomerular endothelial injury in the setting of diabetes and result

166 increased retinal leukocyte accumulation and endothelial injury in the STZ-diabetic rat model but tha

167 increased retinal leukocyte accumulation and endothelial injury in the STZ-diabetic rats.

168 itically discuss the potential mechanisms of endothelial injury in this disease.

169 th, replicating the characteristics of acute endothelial injury in transfused lungs in vivo.

170 findings shed light on a novel mechanism of endothelial injury in transplant-TMA and may therefore g

171 study was to investigate the role of PAF in endothelial injury in uveitis.

172 imaging agents for noninvasive detection of endothelial injury in vivo.

173 ly, reendothelialization after focal carotid endothelial injury in WT mice was significantly increase

174 c Organ Dysfunction score, and biomarkers of endothelial injury, including angiopoietin-2, von Willeb

175 irculatory events included hepatic ischemia, endothelial injury, including with gene expression array

176 fies non-HLA Abs and strongly predicts graft endothelial injury independent of HLA-DSAs.

177 First, widespread endothelial injury indicates antibody-mediated rejection

178 expression may be an important mechanism of endothelial injury induced by TNF-alpha.

179 er, these data provide in vivo evidence that endothelial injury is a key feature of COVID-19.

180 Endothelial injury is a major manifestation of septic sh

181 Endothelial injury is central to the development of pulm

182 Endothelial injury is central to the pathogenesis of vas

183 As endothelial injury is central to the pathogenesis of vas

184 Endothelial injury is considered critical for progressio

185 Vascular endothelial injury is responsible for many of the clinic

186 The mechanism of endothelial injury is still elusive, yet endothelial apo

187 Endothelial injury is the first step in atherosclerosis,

188 ear adaptation, which promotes shear-induced endothelial injury, is a newly identified dysfunction sp

189 ies suggest that albuminuria, a biomarker of endothelial injury, is increased in patients with COPD.

190 exposure can result in hemolysis and direct endothelial injury leading to HUS phenotype.

191 Alveolar and endothelial injury likely contribute at different times

192 -mediated dilatation (R = -0.3, P < 0.01) or endothelial injury marker von Willebrand factor (R = +0.

193 Endothelial injury markers increase later and are associ

194 Our data indicate that the degree of endothelial injury may also be an important component of

195 Rationale: Alveolar and endothelial injury may be differentially associated with

196 Rationale: Endothelial injury may provoke emphysema, but molecular

197 Vessel instability, an early response to endothelial injury, may reflect a shared mechanism and e

198 c properties, favor an indirect mechanism of endothelial injury mediated locally by an augmented infl

199 This review focuses on epithelial and endothelial injury mediators, interactions, and targets

200 Utilizing a mouse endothelial injury model we show that thrombin cleavage

201 Using a laser-induced endothelial injury model, we examined thrombus formation

202 Glomerular inflammation correlates with endothelial injury, monocyte influx, and IL-6 and IL-bet

203 a MMP profiles associated with inflammation, endothelial injury, morbidity, and mortality.

204 mice were studied in a model of transluminal endothelial injury of the femoral artery.

205 Concomitant endothelial injury of the microvasculature was also note

206 Stimuli that can cause endothelial injury or death include environmental stress

207 e in vascular disease states associated with endothelial injury or dysfunction.

208 vention and search for additional targetable endothelial injury pathways.

209 have multiple beneficial effects of reducing endothelial injury, platelet retention, and NET release

210 Endothelial injury plays a central role in the pathophys

211 elial cells and ameliorated diabetes-induced endothelial injury, podocyte loss, albuminuria, and glom

212 which are biomarkers of lung epithelial and endothelial injury previously found to be prognostic in

213 Diabetic NGRs showed substantial retinal endothelial injury, primarily in the microvessels, inclu

214 ed rat lungs upon I/R in order to assess the endothelial injury produced.

215 posure accelerated lethal pulmonary vascular endothelial injury, reduced the inspired oxygen threshol

216 injury, but the signaling pathways mediating endothelial injury remain incompletely understood.

217 he precise molecular mechanisms that lead to endothelial injury remain poorly understood.

218 Although endothelial injury represents the final common pathway o

219 upregulation (P<0.05) of markers related to endothelial injury response and cellular activation of E

220 COVID-19 has been associated with endothelial injury, resultant microvascular inflammation

221 monstrated both alveolar epithelial and lung endothelial injury, resulting in accumulation of protein

222 O by HIV-1 Tat plays a pivotal role in brain endothelial injury, resulting in the irreversible loss o

223 rved with kidneys obtained from NHBDs is the endothelial injury seen on protocol core biopsies after

224 ted ECs may promote adhesion of platelets to endothelial injury sites to assure wound healing, simult

225 ctivation (elastase/alpha 1 antitrypsin) and endothelial injury (soluble thrombomodulin).

226 ficantly higher sensitivity for detection of endothelial injury than singly conjugated MSs (rPSGL-1-

227 In a rabbit model of arterial endothelial injury, the infusion of 51Cr-labeled micropa

228 oncerning its pathogenesis focus on vascular endothelial injury, the oxidation of low-density lipopro

229 chanisms and signaling pathways that mediate endothelial injury, the regulatory mechanisms responsibl

230 ion represents a logical strategy to prevent endothelial injury, thereby preserving humoral immunity

231 (polymorphonuclear leukocytes, PMNs) mediate endothelial injury, thrombosis, and vascular remodeling.

232 In an in vivo model of light/dye-induced endothelial injury/thrombosis in the cremasteric venules

233 nterior descending coronary artery stenosis, endothelial injury, thrombus formation and thrombolysis.

234 a regulator of arterial thrombosis following endothelial injury through effects on vascular wall IGF-

235 eleased by intravascular hemolysis initiates endothelial injury through nitric oxide (NO) scavenging

236 mote platelet activation, leukocyte-mediated endothelial injury, tissue damage, and death.

237 Studies using a model of endothelial injury to the carotid artery reveal that the

238 d-/-) mice underwent photochemically induced endothelial injury to trigger arterial thrombosis.

239 derived toxins (or possibly other sources of endothelial injury), together with additional genetic su

240 Using mouse models of endothelial injury (traumatic or ischemia reperfusion),

241 injury using X203 significantly reduced post-endothelial injury vessel wall thickness, and injury-rel

242 Although initial reports suggested that endothelial injury was caused directly by the virus, rec

243 unts than non-ICU patients and the extent of endothelial injury was correlated with putative markers

244 Brain endothelial injury was measured with cytotoxicity and di

245 ets; however, time to vessel occlusion after endothelial injury was significantly shorter in Pf4-Lox(

246 trial of gene therapy to reduce CTL-mediated endothelial injury, we stably transduced early passage H

247 The cellular markers of endothelial injury were associated with disease severity

248 n Willebrand factor (a traditional marker of endothelial injury) were measured in 931 subjects with a

249 lesions characterized by atherosclerosis and endothelial injury, whereas anticoagulant agents are fav

250 challenge resulted in more severe glomerular endothelial injury, whereas the glomerular injury after

251 This suggests that the virus may initiate endothelial injury, which is believed to be an early eve

252 These factors cause maternal vascular endothelial injury, which leads to hypertension and mult

253 ne cell infiltration but suggested capillary endothelial injury with interstitial edema and early fib

254 e used for 1% of births yet may also lead to endothelial injury with long-term adverse consequences f

255 l phenotype conferring enhanced capacity for endothelial injury, with a corresponding signature of ne

256 Electron microscopy showed endothelial injury within 6 hours following CP, and, aft

257 We observed extensive endothelial injury without Kupffer cell or hepatocyte da

258 Following vascular endothelial injury, Wnt activation in MVPC was sufficien

259 Endothelial injury worsens over time on dialysis but imp