ライフサイエンスコーパス: neointimal hyperplasia

1 ed Akt activity in a stretch injury model of neointimal hyperplasia.

2 ures at six months, possibly attributable to neointimal hyperplasia.

3 n of p27(kip1) in the VSMC and inhibition of neointimal hyperplasia.

4 cell loss, heterophils/eosinophils, and late neointimal hyperplasia.

5 ituted endothelium, leading to inhibition of neointimal hyperplasia.

6 all at the time of angioplasty might prevent neointimal hyperplasia.

7 1) in EPCs enhances their ability to inhibit neointimal hyperplasia.

8 ffect of flow disturbances on the pattern of neointimal hyperplasia.

9 grity in injured vessels, thereby inhibiting neointimal hyperplasia.

10 smooth muscle cell apoptosis and subsequent neointimal hyperplasia.

11 tatus and suggest a novel target to minimize neointimal hyperplasia.

12 nificantly to late vein graft failure due to neointimal hyperplasia.

13 with dexamethasone (DEX) to reduce in-stent neointimal hyperplasia.

14 in foreign body contamination and increased neointimal hyperplasia.

15 migration and proliferation contributing to neointimal hyperplasia.

16 hanced vascular NO production, and decreased neointimal hyperplasia.

17 ulnerable to restenosis, caused primarily by neointimal hyperplasia.

18 sma cholesterol levels and drug treatment on neointimal hyperplasia.

19 may therefore be therapeutically useful for neointimal hyperplasia.

20 apeutic agents targeted to inhibit localized neointimal hyperplasia.

21 y agonists implicated in the pathogenesis of neointimal hyperplasia.

22 an arrest cell cycle progression and inhibit neointimal hyperplasia.

23 xtracellular matrix deposition, and vascular neointimal hyperplasia.

24 ed differences existed in the development of neointimal hyperplasia.

25 d vice versa, that were also associated with neointimal hyperplasia.

26 tic obstruction occurring on a foundation of neointimal hyperplasia.

27 However, dexamethasone did not decrease neointimal hyperplasia.

28 In-stent restenosis results primarily from neointimal hyperplasia.

29 ly reduces in-stent restenosis by inhibiting neointimal hyperplasia.

30 nd late arterial remodeling while triggering neointimal hyperplasia.

31 al contributor to experimental stent-induced neointimal hyperplasia.

32 uld contribute to AVF failure as a result of neointimal hyperplasia.

33 ls and vascular smooth muscle cells and thus neointimal hyperplasia.

34 d both BRSs to be patent with nonobstructive neointimal hyperplasia.

35 s NFkappaB activation, SMC inflammation, and neointimal hyperplasia.

36 s, perivascular inflammation, and asymmetric neointimal hyperplasia.

37 utics; NP delivering rapamycin inhibit patch neointimal hyperplasia.

38 dings reveal a pathological role for CD47 in neointimal hyperplasia.

39 e studied the role of CD47 in injury-induced neointimal hyperplasia.

40 0 activity increased NFkappaB activation and neointimal hyperplasia.

41 promotes inflammation in atherosclerosis and neointimal hyperplasia.

42 ing atherogenesis, plaque stabilization, and neointimal hyperplasia.

43 ession, accompanied by a reduction in venous neointimal hyperplasia.

44 e involved in the preventive action of E2 on neointimal hyperplasia.

45 case 2 (70.9%) without evidence of excessive neointimal hyperplasia.

46 contribution of late scaffold recoil versus neointimal hyperplasia.

47 t Orai3 knockdown inhibited LRC currents and neointimal hyperplasia.

48 e injured using balloon angioplasty to cause neointimal hyperplasia.

49 hus contributing to vascular remodelling and neointimal hyperplasia.

50 xide production in medial VSMCs and enhanced neointimal hyperplasia.

51 s a potential therapeutic strategy to reduce neointimal hyperplasia.

52 be centrally involved in the development of neointimal hyperplasia.

53 ormal vascular homeostasis and regulation of neointimal hyperplasia.

54 novel regulators for VSMC proliferation and neointimal hyperplasia.

55 or anacetrapib, prevents vein bypass-induced neointimal hyperplasia.

56 rolimus effectively inhibits leptin-enhanced neointimal hyperplasia.

57 heparin (90 mg/kg BID) effectively inhibited neointimal hyperplasia (0.11+/-0.02 and 0.09+/-0.07 mm(2

58 The LFA-1 blockade profoundly attenuated neointimal hyperplasia (61.6 vs 23.8%; P < 0.05), CAV-af

59 lockade of the IIb/IIIa receptor, may reduce neointimal hyperplasia after arterial balloon injury.

60 A central role for leukocytes in neointimal hyperplasia after arterial injury is suspecte

61 vascular inflammation, atherosclerosis, and neointimal hyperplasia after arterial injury.

62 rapy with mTOR and PI3K inhibitors, inhibits neointimal hyperplasia after arterial injury.

63 ble ceramide as a novel therapy for reducing neointimal hyperplasia after balloon angioplasty.

64 We studied the effects of calcification on neointimal hyperplasia after balloon injury in the rat c

65 frequent (BID) subcutaneous dosing inhibits neointimal hyperplasia after balloon injury or stent imp

66 rin beta-subunit CD18 was required to reduce neointimal hyperplasia after balloon injury.

67 t studies have demonstrated reduction in the neointimal hyperplasia after intracoronary radiation (IR

68 Neointimal hyperplasia after percutaneous coronary inter

69 de that nonablative infrared laser inhibited neointimal hyperplasia after PTCA in cholesterol-fed rab

70 Neointimal hyperplasia after PTCA is an important compon

71 ed antisense oligonucleotides (Resten-NG) on neointimal hyperplasia after stenting in a pig model.

72 P-1 receptor CCR2, was effective at reducing neointimal hyperplasia after stenting.

73 n tip of an embolectomy catheter would limit neointimal hyperplasia after stretch injury.

74 e the effects of orally delivered heparin on neointimal hyperplasia after varying forms of arterial i

75 ever, the role of RAGE/ligand interaction in neointimal hyperplasia after vascular injury remains unc

76 l tetrahydrobiopterin availability modulates neointimal hyperplasia after vascular injury via acceler

77 Deletion of mPGES-1 in mice attenuates neointimal hyperplasia after vascular injury, in part by

78 the genes that influence the development of neointimal hyperplasia after vascular injury.

79 nt of arterial thrombosis, inflammation, and neointimal hyperplasia after vascular injury.

80 ys) of nitro-oleic acid (OA-NO(2)) inhibited neointimal hyperplasia after wire injury of the femoral

81 Colchicine is associated with less neointimal hyperplasia and a decreased ISR rate when adm

82 s, in fact, been developed that inhibits the neointimal hyperplasia and accelerated atherosclerosis t

83 he response to vascular injury that leads to neointimal hyperplasia and accelerated atherosclerosis.

84 central to the initiation and progression of neointimal hyperplasia and arterial stenosis.

85 e intima during vascular remodelling such as neointimal hyperplasia and arteriosclerosis.

86 Increased endothelial BH4 reduces vein graft neointimal hyperplasia and atherosclerosis through a red

87 s the potential to advance the fight against neointimal hyperplasia and atherosclerosis.

88 otes vascular inflammatory disorders such as neointimal hyperplasia and atherosclerosis.

89 ion of CaMKII delta prevented injury-induced neointimal hyperplasia and cell proliferation in the int

90 ion is a major contributor to injury-induced neointimal hyperplasia and depends on alteration of the

91 tency, the cell-seeded TEV demonstrated less neointimal hyperplasia and fewer proliferating cells tha

92 ESS with the localization and progression of neointimal hyperplasia and in-stent clotting.

93 Neointimal hyperplasia and inflammation around stent str

94 ery, NAD(P)H oxidase activity contributes to neointimal hyperplasia and is involved in vascular cell

95 affords mice with a protected status against neointimal hyperplasia and lumen narrowing in vivo.

96 d a significant dose-dependent inhibition of neointimal hyperplasia and luminal encroachment in the p

97 he time of angioplasty significantly reduced neointimal hyperplasia and prevented restenosis.

98 inhibitor of NOS activity, increased venous neointimal hyperplasia and pro-inflammatory gene express

99 tent-based therapies that can both attenuate neointimal hyperplasia and promote re-endothelialization

100 ent with that of a bare metal stent (BMS) on neointimal hyperplasia and re-endothelialization in a ra

101 s relevant to vascular remodeling along with neointimal hyperplasia and relevant histological changes

102 n and devising strategies that may interrupt neointimal hyperplasia and relevant pathogenetic pathway

103 or later obstruction by vein graft disease (neointimal hyperplasia and remodelling).

104 C) migration and proliferation contribute to neointimal hyperplasia and restenosis after vascular inj

105 ial cell layer lining the lumen and prevents neointimal hyperplasia and restenosis.

106 vascular injury may reduce the incidence of neointimal hyperplasia and restenosis.

107 ion of drugs to a vascular segment to reduce neointimal hyperplasia and restenosis.

108 from diabetic mice developed more extensive neointimal hyperplasia and showed greater proliferation

109 Systemic treatment produced the least neointimal hyperplasia and significantly reduced in-sten

110 apy of experimental vein grafts inhibits the neointimal hyperplasia and subsequent accelerated athero

111 dependent risk factor for the development of neointimal hyperplasia and subsequent vein graft failure

112 Both neointimal hyperplasia and the intima/media ratio of the

113 ction of these anastomoses, primarily due to neointimal hyperplasia and the resulting narrowing of th

114 ll migration and proliferation contribute to neointimal hyperplasia and vascular stenosis after endot

115 Acute thrombosis, neointimal hyperplasia, and accelerated atherosclerosis

116 11 reduced vessel wall thickness, attenuated neointimal hyperplasia, and has favorable effects on vas

117 constitutes a key event in atherosclerosis, neointimal hyperplasia, and the response to vascular inj

118 ivation of membrane ERalpha does not prevent neointimal hyperplasia; and (3) ERalphaAF1 is necessary

119 Furthermore, SMC migration and neointimal hyperplasia are promoted by degradation of th

120 hile there was no difference with regards to neointimal hyperplasia area (P=0.132).

121 oints were late absolute scaffold recoil and neointimal hyperplasia area as assessed by optical coher

122 Neointimal hyperplasia area was smaller among patients w

123 Histologic assessment demonstrated neointimal hyperplasia around the IVC filter within 2 we

124 nti-CD4 mAb-treated mice exhibited prominent neointimal hyperplasia associated with endothelial morph

125 The neointimal hyperplasia associated with this injury was l

126 causes an inflammatory cascade that leads to neointimal hyperplasia at the anastomosis site.

127 l roles in vascular restenosis by preventing neointimal hyperplasia at the early stage via suppressio

128 Neointimal hyperplasia at the site of surgical intervent

129 Neointimal hyperplasia (at 14 d) was notably attenuated

130 regulatory gene expression inhibits not only neointimal hyperplasia, but also diet-induced, accelerat

131 Intracoronary ultrasound showed severe neointimal hyperplasia, but only at the proximal interfa

132 elium-dependent vasoconstriction and promote neointimal hyperplasia, but the intracellular signaling

133 In vivo, siHIF1/2a, Eve and TOPO decreased neointimal hyperplasia by 32%-50%, 7 days after treatmen

134 d thrombocytopenia and suppressed postinjury neointimal hyperplasia by 88%.

135 rtery SMC after balloon angioplasty prevents neointimal hyperplasia by blocking SMC proliferation and

136 Although inhibition of neointimal hyperplasia by cell cycle gene blockade thera

137 is feasible and effectively reduces in-stent neointimal hyperplasia by inhibiting cellular proliferat

138 esulting in decreased O2*-, would lessen the neointimal hyperplasia caused by balloon injury to the c

139 tenosis, although early stent thrombosis and neointimal hyperplasia causing vessel renarrowing were k

140 Neointimal hyperplasia characterized by abnormal accumul

141 Stenotic lesions caused by neointimal hyperplasia commonly occur resulting in patie

142 ed femoral arteries showed a 20% increase in neointimal hyperplasia compared with similarly injured w

143 l activation, less inflammation, and reduced neointimal hyperplasia compared with the E1-AV vector-tr

144 2, p = 0.044) owing to significantly reduced neointimal hyperplasia (cross-sectional area, 0.46 +/- 0

145 Neointimal hyperplasia, defined by post-procedure prolif

146 lack of endothelium and compliance mismatch, neointimal hyperplasia develops aggressively, resulting

147 otection against aneurysm and injury-induced neointimal hyperplasia, diseases linked to loss of vascu

148 sion revascularization (consistent with less neointimal hyperplasia), especially after PES implantati

149 selectin antagonism using rPSGL-Ig decreases neointimal hyperplasia following balloon injury, by inhi

150 nd both agents attenuated the development of neointimal hyperplasia following endothelial injury.

151 s of OA-NO(2) in vivo, because inhibition of neointimal hyperplasia following femoral artery injury w

152 dels of angioplasty have suggested a role in neointimal hyperplasia for endothelins (ETs), potent vas

153 elivery in a manner that virtually abolishes neointimal hyperplasia for months after stent implantati

154 lymer could produce a sustained reduction in neointimal hyperplasia for up to six months after stenti

155 r, and antibody-deficient mice had decreased neointimal hyperplasia formation in vivo.

156 A) receptor antagonism significantly reduced neointimal hyperplasia forming over porcine coronary ste

157 Three weeks after injury, neointimal hyperplasia (from alpha-smooth muscle actin-p

158 helialization, but also effectively improved neointimal hyperplasia, hypercoagulability, and vasoreac

159 ar ultrasound (IVUS) measurement of in-stent neointimal hyperplasia (IH) volumes.

160 ery of drugs targeting HIF-1/2 could inhibit neointimal hyperplasia in a mouse model of AVF.

161 ent and selective ET(A) antagonist to reduce neointimal hyperplasia in a porcine coronary artery sten

162 al nonablative infrared laser irradiation on neointimal hyperplasia in a rabbit balloon injury model.

163 fibrin turnover/deposition, (3) exacerbates neointimal hyperplasia in an experimental model of stasi

164 erial injury correlates with the severity of neointimal hyperplasia in animal models and postangiopla

165 , and persistently suppress inflammation and neointimal hyperplasia in both leporine and swine models

166 pterin, in an EC-specific manner and reduced neointimal hyperplasia in experimental vein grafts in GC

167 The examination of neointimal hyperplasia in injured animal artery models h

168 gamma-irradiation reduces recurrent in-stent neointimal hyperplasia in long, diffuse ISR lesions; how

169 overexpression of the apoE gene also reduces neointimal hyperplasia in mice after endothelial denudat

170 PES compared with BMS significantly reduce neointimal hyperplasia in patients with ST-segment eleva

171 , named W9, inhibited balloon injury-induced neointimal hyperplasia in rabbit carotid arteries.

172 sutures provided a significant reduction in neointimal hyperplasia in rats over a period of 14 days

173 angiogenesis in tumor implants and sustained neointimal hyperplasia in response to arterial injury, i

174 direct effect of apoE in protection against neointimal hyperplasia in response to mechanically induc

175 in (apo) E in vivo was explored by measuring neointimal hyperplasia in response to vascular injury in

176 ion and degradation of p27(Kip1) accentuates neointimal hyperplasia in response to wire injury.

177 , the rat subtotal nephrectomy model, venous neointimal hyperplasia in the arteriovenous fistula was

178 s been shown to attenuate the development of neointimal hyperplasia in the balloon injury model, this

179 Ad2/betaARKct significantly reduced neointimal hyperplasia in the graft/vein anastomosis.

180 switching in human and mouse aortic SMCs and neointimal hyperplasia in the mouse.

181 AV-W9 treatment significantly inhibited neointimal hyperplasia in this porcine arterial balloon

182 enhance endothelial regeneration and reduce neointimal hyperplasia in vascular injury states.

183 injury and were able to show a reduction in neointimal hyperplasia in wild-type mice.

184 defects, improve EPC survival, and decrease neointimal hyperplasia in Zucker fatty rats postangiopla

185 gulator of SMC proliferation, migration, and neointimal hyperplasia, in part through modulating endos

186 linically significant outcome, inhibition of neointimal hyperplasia induced by arterial injury.

187 ated balloon catheters significantly reduced neointimal hyperplasia induced by balloon angioplasty in

188 n into Kit(W-sh/W-sh) mice, not only was the neointimal hyperplasia induced, but the neutrophil, macr

189 Atherosclerosis and arterial injury-induced neointimal hyperplasia involve medial smooth muscle cell

190 Neointimal hyperplasia involves activation of smooth mus

191 Neointimal hyperplasia is a critical component of resten

192 These data suggest that neointimal hyperplasia is accelerated in calcified arter

193 Exaggerated neointimal hyperplasia is considered as the primary mech

194 ysis arteriovenous fistulas, and that venous neointimal hyperplasia is exacerbated when this model is

195 ggest that apoE inhibition of injury-induced neointimal hyperplasia is not due to the inhibition of i

196 Recalcitrant neointimal hyperplasia is postulated to be involved in t

197 ver, and if the media is not made quiescent, neointimal hyperplasia is simply delayed rather than pre

198 In addition to neointimal hyperplasia, late scaffold recoil contributed

199 Patches delivering rapamycin developed less neointimal hyperplasia, less smooth muscle cell prolifer

200 articles, causing a significant reduction in neointimal hyperplasia, lipid burden, cholesterol clefts

201 t the process of smooth muscle cell-mediated neointimal hyperplasia may occur separately from a macro

202 1 to negatively regulate cell proliferation (neointimal hyperplasia) may have an antiatherogenic effe

203 is characterized by increased vascular tone, neointimal hyperplasia, medial hypertrophy, and adventit

204 , a retinal ischemia/reperfusion model and a neointimal hyperplasia model of the femoral artery.

205 remodeling, morphometry, graft patency, and neointimal hyperplasia (NH) development.

206 In view of the inflammatory nature of neointimal hyperplasia (NIH), we tested the hypothesis t

207 ss was 0.04, 0.05, and 0.06 mm, whereas mean neointimal hyperplasia obstruction was 4.5+/-2.4%, 5.2+/

208 Neointimal hyperplasia occurred in variable degrees by 5

209 Neointimal hyperplasia of restenosis after coronary arte

210 vulnerability in atherosclerosis and in the neointimal hyperplasia of restenosis.

211 To trigger neointimal hyperplasia of VSMC, we used a mouse model of

212 asty model, control patches developed robust neointimal hyperplasia on the patch luminal surface char

213 sis within Palmaz-Schatz stents results from neointimal hyperplasia or chronic stent recoil and occur

214 fer from in-stent restenosis associated with neointimal hyperplasia or stent thrombosis.

215 ese EPCs given to Zucker fatty rats decrease neointimal hyperplasia post-carotid angioplasty.

216 nactivation of ERalpha in VSMC abrogates the neointimal hyperplasia protection induced by E2, whereas

217 implantation may lower the intensity of late neointimal hyperplasia, reducing the incidence of in-ste

218 only used in cardiovascular surgery, however neointimal hyperplasia remains a significant concern, es

219 C phenotypic switching or its implication in neointimal hyperplasia remains unclear.

220 Because ISR is due to neointimal hyperplasia, rotational ablation may be a mor

221 Moreover, the reduction in neointimal hyperplasia seen in beta-arrestin2(-/-) mice

222 and at 4 weeks, the venous segment displayed neointimal hyperplasia, smooth muscle proliferation, and

223 , especially negative remodeling, influences neointimal hyperplasia suppression after implantation of

224 USP20-S334A mice developed ~50% less neointimal hyperplasia than congenic WT mice after carot

225 e sirolimus drug-eluting stent in inhibiting neointimal hyperplasia, the process underlying restenosi

226 Although much attention has focused on neointimal hyperplasia, the repetitive trauma to vessel

227 ents (42 lesions) with no difference in mean neointimal hyperplasia thickness between groups at 13 mo

228 The median neointimal hyperplasia thickness was 0.04, 0.05, and 0.0

229 oherence tomography substudy (endpoint: mean neointimal hyperplasia thickness) and an angiography sub

230 A20 prevents neointimal hyperplasia through combined anti-inflammator

231 Also, CCN5rp promoted EC repair to suppress neointimal hyperplasia via interaction with Cd9 extracel

232 Few therapies prevent venous neointimal hyperplasia (VNH) and venous stenosis (VS) fo

233 e-year patency rate is 60% because of venous neointimal hyperplasia (VNH) and venous stenosis (VS) fo

234 Venous neointimal hyperplasia (VNH) at the outflow vein of hemo

235 AVFs fail because of venous neointimal hyperplasia (VNH) resulting in venous stenosi

236 nfiltration and accumulation, causing venous neointimal hyperplasia (VNH)/venous stenosis (VS) in art

237 tively, and intravascular ultrasound percent neointimal hyperplasia was 8.10+/-5.81 and 8.85+/-7.77,

238 Neointimal hyperplasia was assayed 8 weeks after the vas

239 Neointimal hyperplasia was assessed after carotid balloo

240 e recruitment (41%) were reduced at 3 d, and neointimal hyperplasia was attenuated (29%) at 28 d by R

241 Neointimal hyperplasia was enhanced in beta-arrestin1(-/

242 of EPCs was done at various time points, and neointimal hyperplasia was measured 3 weeks later.

243 ablishing the fistula, and by 16 weeks, such neointimal hyperplasia was progressive and pronounced; a

244 After balloon catheter injury, neointimal hyperplasia was significantly increased in ra

245 Accordingly, the origin of neointimal hyperplasia-was examined in porcine arteriali

246 smooth muscle cell (VSMC) proliferation and neointimal hyperplasia were evaluated in cultured VSMCs

247 d of intima (percentage intima) secondary to neointimal hyperplasia were noted among the different ra

248 ected from the development of injury-induced neointimal hyperplasia, whereas LPA1(-/-) mice developed

249 es including atherosclerosis but its role in neointimal hyperplasia which contributes to restenosis h

250 odeling, including interstitial fibrosis and neointimal hyperplasia, which are characteristic of chro

251 Control allografts showed severe neointimal hyperplasia, which consists mainly of alpha-a

252 s in venous endothelial cells (ECs) to cause neointimal hyperplasia, which correlated with the high e

253 d activation and degranulation, resulting in neointimal hyperplasia, which was not observed in MC-def

254 ice exhibited exacerbation of injury-induced neointimal hyperplasia, while CCN5 gain-of-function alle

255 Cav-1 in mice stimulates SMC proliferation (neointimal hyperplasia), with concomitant activation of

256 The frequency of neointimal hyperplasia within the stent was also decreas