ライフサイエンスコーパス: neointimal

1 as hemocompatibility, thereby improving anti-neointimal activity of synthetic vascular grafts.

2 ignificantly reduced neointima formation and neointimal alphaSMA cells.

3 association plays a protective role against neointimal and atherosclerotic plaque formations.

4 pulmonary arteriopathy, including concentric neointimal and complex plexiform-like lesions.

5 y chain (CD98hc) is markedly up-regulated in neointimal and cultured VSMCs, and that activated but no

6 Akt activity was suppressed in neointimal and medial VSMCs from injured vessels at 2 we

7 characterized by the formation of occlusive neointimal angioproliferative lesions that worsened with

8 21 mm(2) [1.22] at 6 months) with a low mean neointimal area (0.08 mm(2) [0.09]), and optical coheren

9 Furthermore, the mean neointimal area (1.55+/-0.51 versus 1.58+/-0.34 mm(2); P

10 In vivo, PVDF-HFP revealed more neointimal area (P<0.01) and residual parastrut fibrin (

11 Both neointimal area and vascular stenosis were significantly

12 months indicating a potential difference in neointimal area at follow-up (O-SES, 0.16+/-0.33 mm(2) v

13 Mean neointimal area by intravascular ultrasound was higher i

14 phy results demonstrated significantly lower neointimal area in FP-PES (8.01 mm(2) [7.65-9.21]) compa

15 Neointimal area was reduced after treatment with an aden

16 Neointimal area, uncovered struts, and fibrin deposition

17 oth muscle resulted in a 20-fold increase in neointimal area, with a 3-fold increase in the cell prol

18 ction and maximum cross-sectional narrowing (neointimal area/stent area) were not significantly diffe

19 Neointimal atherosclerotic change (neoatherosclerosis) a

20 n >30 days were examined for the presence of neointimal atherosclerotic disease.

21 -marked minority subset of SMCs as the major neointimal cell of origin.

22 Neointimal cell proliferation in calcified arteries as a

23 uman coronary endothelium and in a subset of neointimal cells and medial smooth muscle cells.

24 Neointimal cells expressed SMC markers and did not deriv

25 ury and shared a similar phenotype with many neointimal cells.

26 rating) alpha smooth muscle actin (alphaSMA) neointimal cells.

27 esign, examining thromboresistance, speed of neointimal coverage and completeness of healing, includi

28 Lack of re-endothelialization and neointimal coverage on stent struts has been put forward

29 oherence tomography at 2 years showed 99% of neointimal coverage with optical and ultrasonic signs of

30 ce tomography at 6 and 12 months showed full neointimal coverage, with stabilization of the mean scaf

31 y, the role of vascular SMC p38alpha MAPK in neointimal development was examined.

32 e defined by interstitial fibrosis, vascular neointimal development, and graft dysfunction.

33 lization strategy of heparin and potent anti-neointimal drug (Mitogen Activated Protein Kinase II inh

34 Neointimal endothelium and smooth muscle cells in the in

35 xpression significantly reduces pathological neointimal expansion consequent to injury.

36 cts ligands, thereby regulating pathological neointimal expansion.

37 l integrity was confirmed as a key factor of neointimal foam cell formation following stent implantat

38 Neointimal foam cell formation was induced in rabbits (n

39 /- and smN1+/- mice showed a 70% decrease in neointimal formation after carotid artery ligation.

40 Adamts7 knockout mice also showed reduced neointimal formation after femoral wire injury.

41 Immune modulation of neointimal formation after vascular injury has been inve

42 than Notch3, mediates SMC proliferation and neointimal formation after vascular injury through CHF1/

43 This may contribute to neointimal formation after vascular injury.

44 smooth muscle cells (SMCs) may contribute to neointimal formation after vascular injury.

45 eceptor antagonism prevented the exacerbated neointimal formation and ECM synthesis conferred by loss

46 d on the other hand, PDGF signaling mediates neointimal formation and exacerbates chronic rejection i

47 Using this model, we found that increased neointimal formation and macrophage recruitment occurs i

48 Sunitinib decreased neointimal formation and smooth muscle cell proliferatio

49 SMCs following vascular insult is central to neointimal formation and the development of vascular pat

50 eatment rescued Ang II-mediated increases in neointimal formation and vascular remodeling in a vein g

51 Neointimal formation at IEL disruptions in the ascending

52 eletion of the Klf4 gene in mice accelerated neointimal formation but delayed down-regulation of smoo

53 te accumulation, cellular proliferation, and neointimal formation compared with wild-type mice.

54 C/R247C) mice showed significantly increased neointimal formation due to increased SMC proliferation

55 Acta2(-/-) mice showed increased neointimal formation following vascular injury in vivo,

56 veral diverse approaches aimed at preventing neointimal formation have been devised which have yielde

57 High rates of restenosis and neointimal formation have driven increasing interest in

58 h an inhibitory action of cortistatin on the neointimal formation in 2 models of carotid arterial lig

59 itutively active I-1 gene transfer decreased neointimal formation in an angioplasty rat model by prev

60 sfer significantly reduced proliferation and neointimal formation in balloon angioplasty-injured rat

61 ese phenotypic changes culminated in reduced neointimal formation in cultured human saphenous vein.

62 ablation of the miR-21 stem loop attenuated neointimal formation in mice post-stenting.

63 Klf4 mutant mice exhibited enhanced neointimal formation in response to vascular injury caus

64 increased re-endothelialization and reduced neointimal formation in samples at 4 weeks after implant

65 Interruptions in the IEL resulted in neointimal formation in the ascending aorta but not in m

66 Erlotinib ameliorated neointimal formation in the dose response study.

67 naling lipid phosphatidic acid (PA), reduced neointimal formation in the mouse carotid artery ligatio

68 helial cell function, resulting in decreased neointimal formation in the porcine coronary injury mode

69 age accumulation in a model of lipid-induced neointimal formation in vivo.

70 Neointimal formation induced by carotid artery ligation

71 tion for preventing thrombotic occlusion and neointimal formation of synthetic vascular grafts.

72 arterial injury, with VSMC proliferation and neointimal formation serving as the final outcomes of th

73 More importantly, injury-induced neointimal formation was significantly attenuated by PDE

74 Neointimal formation was significantly less at the flow

75 However, neointimal formation was similar between wild-type and N

76 nd Acta2(-/-) SMC proliferation in vitro and neointimal formation with vascular injury in vivo.

77 es that regulates vascular calcification and neointimal formation, and inhibits inflammation in diffe

78 wire injury, PRCP(gt/gt) mice had increased neointimal formation, CD45 staining, and Ki-67 expressio

79 Further, visfatin-induced neointimal formation, endothelial inflammasome formation

80 lobal or SMC-specific LMO7 deletion enhanced neointimal formation, TGF-beta signaling, ECM deposition

81 VSMC synthetic phenotype in vivo and reduce neointimal formation, thereby implicating miRNAs as exci

82 y were found to have significantly increased neointimal formation, which was correlated with increase

83 attenuates VSM proliferation and consequent neointimal formation.

84 down FSP-1 expression in BM cells prevented neointimal formation.

85 cell migration, resulting in lower levels of neointimal formation.

86 ell-induced but not interferon-gamma-induced neointimal formation.

87 le cell (VSMC) migration, a key component of neointimal formation.

88 that is required for effective inhibition of neointimal formation.

89 essed re-endothelialization and HHcy-induced neointimal formation.

90 These neointimal founder cells subsequently undergoing massive

91 s specifically required for the selection of neointimal founder cells, and Notch inhibition significa

92 ormation in native coronary bifurcations and neointimal growth after DES implantation was significant

93 present in such patients, the comparison of neointimal growth after percutaneous coronary interventi

94 Despite greater suppression of global neointimal growth in DES, both DES and BMS+DEB effective

95 ow-up, a modest but significant reduction of neointimal growth was demonstrated in a dose range from

96 th markedly increased medial hyperplasia and neointimal growth, and evidence of higher SMC mitochondr

97 oliferative VSMCs and in vascular walls with neointimal growth.

98 oon-injured arteries via Ad-miR-145 inhibits neointimal growth.

99 Neointimal healing tends to reduce ISA, with the malappo

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

101 Neointimal hyperplasia (at 14 d) was notably attenuated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 Neointimal hyperplasia area was smaller among patients w

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

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

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

132 Neointimal hyperplasia characterized by abnormal accumul

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

149 Exaggerated neointimal hyperplasia is considered as the primary mech

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

168 Acute thrombosis, neointimal hyperplasia, and accelerated atherosclerosis

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

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

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

172 In addition to neointimal hyperplasia, late scaffold recoil contributed

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

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

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

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

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

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

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

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

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

182 t Orai3 knockdown inhibited LRC currents and neointimal hyperplasia.

183 e injured using balloon angioplasty to cause neointimal hyperplasia.

184 contribution of late scaffold recoil versus neointimal hyperplasia.

185 hus contributing to vascular remodelling and neointimal hyperplasia.

186 s a potential therapeutic strategy to reduce neointimal hyperplasia.

187 xide production in medial VSMCs and enhanced neointimal hyperplasia.

188 be centrally involved in the development of neointimal hyperplasia.

189 ormal vascular homeostasis and regulation of neointimal hyperplasia.

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

191 novel regulators for VSMC proliferation and neointimal hyperplasia.

192 rolimus effectively inhibits leptin-enhanced neointimal hyperplasia.

193 apeutic agents targeted to inhibit localized neointimal hyperplasia.

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

195 utics; NP delivering rapamycin inhibit patch neointimal hyperplasia.

196 0 activity increased NFkappaB activation and neointimal hyperplasia.

197 promotes inflammation in atherosclerosis and neointimal hyperplasia.

198 ing atherogenesis, plaque stabilization, and neointimal hyperplasia.

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

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

201 cortistatin-deficient mice developed higher neointimal hyperplasic lesions than wild-type mice.

202 icient mice exhibited a markedly exaggerated neointimal hyperplastic response to wire injury of the f

203 odules, diffuse adventitial infiltrates, and neointimal infiltrates.

204 Neointimal inhibition by limus-coated balloons has been

205 es suppressed VSMC proliferation in vivo and neointimal lesion formation after angioplasty.

206 tly downregulated in the vascular walls with neointimal lesion formation and in cultured dedifferenti

207 temic depletion of miR-126 in mice inhibited neointimal lesion formation of carotid arteries induced

208 ht ventricular pressures, medial thickening, neointimal lesion formation, elastin breakdown, increase

209 gement of vascular diseases that course with neointimal lesion formation.

210 dulator that is able of controlling vascular neointimal lesion formation.

211 vascular disease but often cause deleterious neointimal lesion formation.

212 that generates robust and diffuse occlusive neointimal lesions across the pulmonary vascular bed and

213 Typically, the graft developed neointimal lesions after 2 weeks, resulting in lumen clo

214 sia, whereas LPA1(-/-) mice developed larger neointimal lesions after injury.

215 on exists between the percentage of PAs with neointimal lesions and elastin fragmentation in S100A4 m

216 we demonstrate that VSMCs in injury-induced neointimal lesions and in atherosclerotic plaques are ol

217 the treatment of occluded blood vessels, but neointimal lesions commonly occur.

218 etic agent resulted in marked attenuation of neointimal lesions in a murine arterial injury model.

219 y arterial smooth muscle cells and decreased neointimal lesions in lung organ culture.

220 68 (M1-MHV-68) induces pulmonary artery (PA) neointimal lesions in S100A4-overexpressing, but not in

221 r murine erythrocyte membrane injection into neointimal lesions of hypercholesterolemic apolipoprotei

222 erentiate into smooth muscle cells that form neointimal lesions of the vessel wall.

223 ts from vehicle-treated recipients developed neointimal lesions predominantly consisting of alphaSMA-

224 ecause of medial thickening and occlusion by neointimal lesions, resulting in elevated pulmonary vasc

225 direct relationship between elastase and PA neointimal lesions, the nature and source of the enzyme,

226 thrombin prior to injection promoted florid neointimal lesions, whereas those incubated with PAR ant

227 the intima and proliferate to contribute to neointimal lesions.

228 elastase and attenuates later development of neointimal lesions.

229 ted to inflammation or viral load and before neointimal lesions.

230 ersus that in control lungs and localizes to neointimal lesions.

231 Arterial injury results in the formation of neointimal lesions.

232 g massive clonal expansion to form occlusive neointimal lesions.

233 However, RR6 significantly reduced neointimal macrophage influx that was accompanied by inc

234 At follow-up, neointimal obstruction and maximum cross-sectional narro

235 of necrotic core facing border of FC and the neointimal presence of macrophages and calcification con

236 ted the hypothesis that CaMKIIdelta mediates neointimal proliferation after carotid artery ligation b

237 arrest in the synthetic state with excessive neointimal proliferation after carotid injury, as well a

238 (fluoropolymer-based versus polymer-free) on neointimal proliferation and healing response in the fam

239 uting stents (DES) are effective in reducing neointimal proliferation and in-stent restenosis.

240 ude local inflammation leading to aggressive neointimal proliferation and late neoatherosclerosis.

241 PB-PES, PF-PES was associated with increased neointimal proliferation and subsequent clinical resteno

242 ion of an FP-PES resulted in lower levels of neointimal proliferation and sustained biological effect

243 but have retained the capability to inhibit neointimal proliferation by eluting immunosuppressive dr

244 Drug elution by BVS prevents neointimal proliferation in a similar fashion to drug-el

245 hy analysis showed significantly more global neointimal proliferation in the BMS+DEB group (15.7+/-7.

246 sirolimus-coated balloons effectively reduce neointimal proliferation in the porcine coronary model b

247 Neointimal proliferation in vivo and platelet-derived gr

248 In this randomized trial, strut coverage and neointimal proliferation of a therapy of bare metal sten

249 Two patients developed significant neointimal proliferation requiring valve-in-valve treatm

250 ilator actions, inhibition of thrombosis and neointimal proliferation, and both pro- and antiinflamma

251 ISR mainly results from aggressive neointimal proliferation, but recent data also suggest t

252 vasculopathy is characterized by progressive neointimal proliferation, leading to ischemic failure of

253 consistent with chronic rejection, including neointimal proliferation, transplant vasculopathy, vesse

254 processes initiating excessive and prolonged neointimal proliferation.

255 g enough to explain persistent inhibition of neointimal proliferation.

256 Activation of the PDGF pathway leads to neointimal proliferative responses to artery injury; it

257 i3 is upregulated in an animal model of VSMC neointimal remodeling, and in vivo Orai3 knockdown inhib

258 Neointimal SMC proliferation and medial SMC matrix metal

259 raft inflammation and increased apoptosis of neointimal SMC.

260 In addition, PDE1C was highly induced in neointimal SMCs of human coronary arteries.

261 utations show increased numbers of medial or neointimal SMCs.

262 M and dynein coordinate division fidelity in neointimal SMCs.

263 HAMM) regulate division fidelity in cultured neointimal SMCs.

264 y, matrix metalloproteinase 9 expression and neointimal smooth muscle cell (SMC) proliferation were a

265 Because many neointimal smooth muscle cells (VSMCs) derive from circu

266 carotid arteries to determine the effects on neointimal structure.

267 iferation and migration in vitro and reduces neointimal thickening and macrophage and lipid accumulat

268 utes to atherosclerotic plaque formation and neointimal thickening in other occlusive vascular diseas

269 These fibroproliferative lesions lead to neointimal thickening of arteries in all transplanted al

270 ce were protected from wire injury with less neointimal thickening, leukocyte infiltration, and cellu

271 Neointimal thickness >=40 mum by OCT yielded the most ac

272 Neointimal thickness (0.17+/-0.07 mm vs. 0.28+/-0.11 mm)

273 aphy at 9 months, which demonstrated similar neointimal thickness among lesions allocated to O-SES an

274 Neointimal thickness and inflammatory scores were compar

275 1% at 6 months (P<0.01), with 0.19+/-0.09-mm neointimal thickness at follow-up.

276 gation resulted in a significant increase of neointimal thickness compared with ApoE-KO mice.

277 At 28 days, GS exhibited lower neointimal thickness compared with either NGS (21.1%, P=

278 n the neointima strongly correlated with the neointimal thickness following injury.

279 CrP decreased lipid burden and neointimal thickness in aortic root lesions of hyperglyc

280 Although neointimal thickness in the AMI culprit site was signifi

281 mm(2) to 2x7 mug/mm(2), for example, maximum neointimal thickness of 0.38+/-0.13 versus 0.65+/-0.21 m

282 as to assess the appropriate cutoff value of neointimal thickness of stent strut coverage by OCT with

283 Both platforms demonstrated increased neointimal thickness over time where values were greater

284 179 stents in 151 patients in which the mean neointimal thickness was >100 microm.

285 Strut-level neointimal thickness was 0.19+/-0.09 mm and 0.20+/-0.11

286 Neointimal thickness was comparable among the groups, wh

287 The OCT assessment without consideration of neointimal thickness yielded a poor specificity of 37.5%

288 ed with the culprit site in stable patients (neointimal thickness: 0.11 mm [IQR, 0.07 to 0.21 mm], P=

289 By identifying the presence or absence of neointimal tissue at the site of LRP detected by NIRS, i

290 te of LRP, intravascular ultrasound found no neointimal tissue in 35% of cases.

291 Computed tomography scans identified neointimal tissue ingrowth within the stent frame in bot

292 asound was used to determine the presence of neointimal tissue.

293 Explanted cultures of neointimal tissues displayed heterogeneous outgrowth in

294 CaMKIIdelta-dependent VSM cell function and neointimal VSM hyperplasia induced by vascular injury.

295 ble to those found in obese humans, promotes neointimal VSMC hyperplasia in a murine femoral artery w

296 pression of myosin heavy chain in medial and neointimal VSMC.

297 samples after occlusion by dedifferentiated neointimal VSMC.

298 LRC currents were up-regulated in medial and neointimal VSMCs after vascular injury and that Orai3 kn

299 otron-based x-ray fluorescence microscopy at neointimal VSMCs in wire injury model.

300 e identified that QKI is highly expressed by neointimal VSMCs of human coronary restenotic lesions, b