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

22 Neointimal cells expressed SMC markers and did not deriv

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

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

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

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

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

28 Levels of serum complement (C3), neointimal deposition of complement (C3d), and cellular

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

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

31 h in arteries and that S1P is a regulator of neointimal development.

32 promise for the prevention and treatment of neointimal disease.

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

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

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

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

41 This may contribute to neointimal formation after vascular injury.

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

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

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

45 ties of SMCs to migrate in vitro and inhibit neointimal formation and MMP9 expression in vivo.

46 deling in response to injury with pronounced neointimal formation and reduced vascular compliance.

47 Sunitinib decreased neointimal formation and smooth muscle cell proliferatio

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

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

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

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

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

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

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

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

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

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

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

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

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

61 o profound changes in their phenotype during neointimal formation in response to vessel injury or wit

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

63 Erlotinib ameliorated neointimal formation in the dose response study.

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

65 cellular and molecular pathways of increased neointimal formation in the setting of diabetes.

66 in grafting to investigate the mechanisms of neointimal formation in the setting of type 2 diabetes.

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

68 Neointimal formation induced by carotid artery ligation

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

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

71 A significant increase in neointimal formation was noted in lepr(db/db) mice (139+

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

73 Neointimal formation was significantly less at the flow

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

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

76 impacts collagen type I and III deposition, neointimal formation, and dedifferentiation of smooth mu

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

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

82 attenuates VSM proliferation and consequent neointimal formation.

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

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

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

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

87 that is required for effective inhibition of neointimal formation.

88 llular matrix proteins, thus contributing to neointimal formation.

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

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

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

92 Neointimal growth and negative remodelling were the main

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

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

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

96 oliferative VSMCs and in vascular walls with neointimal growth.

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

98 Neointimal healing tends to reduce ISA, with the malappo

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

100 Neointimal hyperplasia (at 14 d) was notably attenuated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

130 Neointimal hyperplasia characterized by abnormal accumul

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

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

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

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

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

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

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

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

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

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

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

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

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

144 Exaggerated neointimal hyperplasia is considered as the primary mech

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

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

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

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

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

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

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

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

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

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

155 A20 prevents neointimal hyperplasia through combined anti-inflammator

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

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

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

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

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

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

162 Acute thrombosis, neointimal hyperplasia, and accelerated atherosclerosis

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

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

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

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

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

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

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

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

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

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

173 hus contributing to vascular remodelling and neointimal hyperplasia.

174 xide production in medial VSMCs and enhanced neointimal hyperplasia.

175 be centrally involved in the development of neointimal hyperplasia.

176 ormal vascular homeostasis and regulation of neointimal hyperplasia.

177 novel regulators for VSMC proliferation and neointimal hyperplasia.

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

179 utics; NP delivering rapamycin inhibit patch neointimal hyperplasia.

180 rolimus effectively inhibits leptin-enhanced neointimal hyperplasia.

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

182 0 activity increased NFkappaB activation and neointimal hyperplasia.

183 promotes inflammation in atherosclerosis and neointimal hyperplasia.

184 ing atherogenesis, plaque stabilization, and neointimal hyperplasia.

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

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

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

188 apeutic agents targeted to inhibit localized neointimal hyperplasia.

189 t Orai3 knockdown inhibited LRC currents and neointimal hyperplasia.

190 e injured using balloon angioplasty to cause neointimal hyperplasia.

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

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

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

194 odules, diffuse adventitial infiltrates, and neointimal infiltrates.

195 Neointimal inhibition by limus-coated balloons has been

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

197 thrc1 transgenic mice developed normally but neointimal lesion formation and adventitial collagen dep

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

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

200 Neointimal lesion formation was induced in sphingosine 1

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

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

203 vascular disease but often cause deleterious neointimal lesion formation.

204 k-down) had a significant negative effect on neointimal lesion formation.

205 st that miRNAs are novel regulatory RNAs for neointimal lesion formation.

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

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

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

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

210 Atherosclerotic plaques and neointimal lesions at the aortic root and descending aor

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

212 After 28 days, large neointimal lesions developed in S1P2-null but not in wil

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

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

215 theroma and occlusive, inflammatory arterial neointimal lesions in response to injury was suppressed

216 68 (M1-MHV-68) induces pulmonary artery (PA) neointimal lesions in S100A4-overexpressing, but not in

217 However, expression of A20 in established neointimal lesions leads to their regression through inc

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

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

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

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

222 elastase and attenuates later development of neointimal lesions.

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

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

225 Arterial injury results in the formation of neointimal lesions.

226 onically hypoxic rats that have no occlusive neointimal lesions.

227 the intima and proliferate to contribute to neointimal lesions.

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

229 or this hypothesis (such as the finding that neointimal microvessels may increase delivery of cellula

230 ollagen type 8 (an isoform that promotes the neointimal migration of vascular smooth muscle cells).

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

232 However, by immunofluorescence a neointimal population of F4/80+CRP+ cells was revealed o

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

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

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

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

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

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

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

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

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

242 ted vascular disease and in the treatment of neointimal proliferation in other settings.

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

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

245 Neointimal proliferation in vivo and platelet-derived gr

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

247 Neointimal proliferation was similar between PP and non-

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

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

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

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

252 processes initiating excessive and prolonged neointimal proliferation.

253 g enough to explain persistent inhibition of neointimal proliferation.

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

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

256 Neointimal SMC proliferation and medial SMC matrix metal

257 herapeutic potential by uniquely sensitizing neointimal SMC to apoptosis.

258 raft inflammation and increased apoptosis of neointimal SMC.

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

260 utations show increased numbers of medial or neointimal SMCs.

261 M and dynein coordinate division fidelity in neointimal SMCs.

262 HAMM) regulate division fidelity in cultured neointimal SMCs.

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

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

265 ative and sometimes proapoptotic function in neointimal smooth muscle cells, we hypothesize that thei

266 carotid arteries to determine the effects on neointimal structure.

267 medial "contractile" VSMCs but is nuclear in neointimal "synthetic" VSMCs.

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

269 Twenty-eight days later neointimal thickening in CRPtg/Fc gamma RI(-/-) and CRPt

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

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

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

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

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

275 Neointimal thickness and inflammatory scores were compar

276 1% at 6 months (P<0.01), with 0.19+/-0.09-mm neointimal thickness at follow-up.

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

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

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

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

281 Although neointimal thickness in the AMI culprit site was signifi

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

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 gamma RIIb(-/-) and CRPtg/Fc gamma RIII(-/-) neointimal thickness was equal to or greater than in CRP

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 asound was used to determine the presence of neointimal tissue.

292 Explanted cultures of neointimal tissues displayed heterogeneous outgrowth in

293 age results from the development of immature neointimal vasa vasorum.

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 samples after occlusion by dedifferentiated neointimal VSMC.

297 pression of myosin heavy chain in medial and 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