ライフサイエンスコーパス: atherosclerotic plaque

1 , lymph nodes, and inflammatory lesions (eg, atherosclerotic plaques).

2 n that calcification serves to stabilize the atherosclerotic plaque.

3 u and disseminates to distant sites, such as atherosclerotic plaque.

4 number of typical hallmarks of ageing in the atherosclerotic plaque.

5 ia other mechanisms than inflammation in the atherosclerotic plaque.

6 on macrophages, an abundant cell type in the atherosclerotic plaque.

7 exclusively linked to destabilization of the atherosclerotic plaque.

8 isease, promoting atherogenesis and unstable atherosclerotic plaque.

9 bustly increased collagen fibrillogenesis in atherosclerotic plaque.

10 ctor-alpha, a macrophage M1 marker, in human atherosclerotic plaque.

11 e has long been a hallmark of the vulnerable atherosclerotic plaque.

12 in removing lipids and debris present in the atherosclerotic plaque.

13 L3 deficiency showed no evidence of coronary atherosclerotic plaque.

14 (inflammatory) from stable (noninflammatory) atherosclerotic plaque.

15 number of apoptotic macrophages in advanced atherosclerotic plaques.

16 in murine infarcts and both mouse and rabbit atherosclerotic plaques.

17 the progression and promote the stability of atherosclerotic plaques.

18 served VSMC accumulation after injury and in atherosclerotic plaques.

19 ifically needed for CD4 T-cell homing to the atherosclerotic plaques.

20 ) play an essential role in the formation of atherosclerotic plaques.

21 mmation and are involved in the formation of atherosclerotic plaques.

22 utor to atherogenesis and the progression of atherosclerotic plaques.

23 able and vulnerable regions of human carotid atherosclerotic plaques.

24 osis, or inflammatory parameters in advanced atherosclerotic plaques.

25 f calcification in diseased heart valves and atherosclerotic plaques.

26 or the evaluation of metabolic activities in atherosclerotic plaques.

27 ells that amplify immune cell recruitment in atherosclerotic plaques.

28 hways they can contribute to inflammation in atherosclerotic plaques.

29 c heart, and reduced myeloid cell numbers in atherosclerotic plaques.

30 is, a common feature of high-risk/vulnerable atherosclerotic plaques.

31 s that control growth and destabilization of atherosclerotic plaques.

32 erosis but becomes dysfunctional in advanced atherosclerotic plaques.

33 t1(fl/fl)SM-MHC-CreER(T2E)) the formation of atherosclerotic plaques.

34 high levels of oxidized lipid-free apoA-I in atherosclerotic plaques.

35 scular cell adhesion molecule 1 (VCAM-1), in atherosclerotic plaques.

36 as surrounding the calcium deposits in human atherosclerotic plaques.

37 tive detection of (18)F-FDG uptake by murine atherosclerotic plaques.

38 tress in the initiation of advanced coronary atherosclerotic plaques.

39 ges to the lipid-laden foam cells present in atherosclerotic plaques.

40 fications play a major role in destabilizing atherosclerotic plaques.

41 and neutrophils in the perivascular area of atherosclerotic plaques.

42 markedly decreases inflammation in advanced atherosclerotic plaques.

43 y held notions that calcifications stabilize atherosclerotic plaques.

44 /wk group had a higher prevalence of CAC and atherosclerotic plaques.

45 cle carrier vehicle that delivers statins to atherosclerotic plaques.

46 cy in reducing macrophage burden in advanced atherosclerotic plaques.

47 er and hence should lead to the reduction of atherosclerotic plaques.

48 smooth muscle cells in coronary and carotid atherosclerotic plaques.

49 ng with CXCR4 transcript expression in human atherosclerotic plaques.

50 both the development and the progression of atherosclerotic plaques.

51 heir efficacy to reduce macrophage burden in atherosclerotic plaques.

52 ivation of platelets at the site of ruptured atherosclerotic plaques.

53 ey autophagy markers in both mouse and human atherosclerotic plaques.

54 o identify a protein signature for high-risk atherosclerotic plaques.

55 se uptake in cultured macrophages and murine atherosclerotic plaques.

56 se-7 (Mmp-7) reduced VSMC apoptosis in mouse atherosclerotic plaques.

57 esterol fecal excretion and reduces inflamed atherosclerotic plaques.

58 a key factor in the development of necrotic atherosclerotic plaques.

59 e platforms accumulated to similar levels in atherosclerotic plaques.

60 vents, such as thrombosis, is the rupture of atherosclerotic plaques.

61 on of calcium phosphate minerals in advanced atherosclerotic plaques.

62 ound on the surface of inflamed and ruptured atherosclerotic plaques.

63 the assessment of macrophage infiltration in atherosclerotic plaques.

64 oteolytic inactivation by other proteases in atherosclerotic plaques.

65 In the atherosclerotic plaques, amyloid deposition increases wi

66 iseases; although their contributory role to atherosclerotic plaque and abdominal aortic aneurysm sta

67 ction, both important factors in maintaining atherosclerotic plaque and aneurysm stability.

68 Here we show that Rgs1 is upregulated in atherosclerotic plaque and aortic aneurysms.

69 ascular photoacoustic imaging of lipid-laden atherosclerotic plaque and perivascular fat was demonstr

70 irst, a strong association was noted between atherosclerotic plaque and plasma TMAO levels in a mouse

71 Monocyte recruitment to atherosclerotic plaque and the ischemic heart depends on

72 ne, could attenuate progression of preformed atherosclerotic plaque and to identify molecular mechani

73 rvous system, bone marrow, and spleen to the atherosclerotic plaque and to the infarcting myocardium.

74 -181b was overexpressed in symptomatic human atherosclerotic plaques and abdominal aortic aneurysms a

75 -181b was overexpressed in symptomatic human atherosclerotic plaques and abdominal aortic aneurysms a

76 we revealed that CPB isolated from calcified atherosclerotic plaques and artificially synthesised CPB

77 el mechanistic link between NE expression in atherosclerotic plaques and concomitant pro-inflammatory

78 es was located in macrophage-rich regions of atherosclerotic plaques and correlated with the intensit

79 ed increased expression of SMILR in unstable atherosclerotic plaques and detected increased levels in

80 modalities combined could help characterize atherosclerotic plaques and differentiate plaques with a

81 and extracellular matrix deposition both in atherosclerotic plaques and in vascular smooth muscle ce

82 KB1 expression was examined in human carotid atherosclerotic plaques and in western diet-fed atherosc

83 Monochromatic regions in atherosclerotic plaques and injury-induced neointima did

84 und that LINC00305 expression is enriched in atherosclerotic plaques and monocytes.

85 inflammatory state and macrophage burden of atherosclerotic plaques and potentially identify vulnera

86 Cholesterol crystals (CC) are abundant in atherosclerotic plaques and promote inflammatory respons

87 SIRT1 expression was reduced in human atherosclerotic plaques and VSMCs both derived from plaq

88 des insights into the biological activity of atherosclerotic plaques and, in particular, plaque infla

89 CRP in inflamed human striated muscle, human atherosclerotic plaque, and infarcted myocardium (rat an

90 ivity promotes the development of vulnerable atherosclerotic plaques, and elevated plasma levels of t

91 se-2 (15-LOX-2) is highly expressed in large atherosclerotic plaques, and its activity has been linke

92 ly, miR-146a expression is elevated in human atherosclerotic plaques, and polymorphisms in the miR-14

93 ing disease, but the origins of cells within atherosclerotic plaques are not well defined.

94 in injury-induced neointimal lesions and in atherosclerotic plaques are oligoclonal, derived from fe

95 Atherosclerotic plaques are one of the primary complicat

96 phages surrounding calcium deposits in human atherosclerotic plaques are phenotypically defective bei

97 Atherosclerotic plaques are populated with smooth muscle

98 erm-line Akt2-deficient mice develop similar atherosclerotic plaques as wild-type mice despite higher

99 d physiology, and determine the formation of atherosclerotic plaques at regions of disturbed flow.

100 l to catalyze further progress in imaging of atherosclerotic plaque biology.

101 Atherosclerotic plaques build up in arteries in a slow p

102 trated choline diet-dependent enhancement in atherosclerotic plaque burden as compared with recipient

103 ced endothelial cell activation and elevated atherosclerotic plaque burden compared with Ldlr(-/-) mi

104 The distribution of atherosclerotic plaque burden in the human coronary arte

105 n Myocardial Infarction patients with severe atherosclerotic plaque burden were statistically signifi

106 f syndecan 4 (S4(-/-)) drastically increased atherosclerotic plaque burden with the appearance of pla

107 dosis occurs as a nonhereditary condition in atherosclerotic plaques, but it can also manifest as a h

108 optotic markers have been observed in Hp 2-2 atherosclerotic plaques, but the mechanism responsible f

109 ticipated in the STABILITY (Stabilization of Atherosclerotic Plaque by Initiation of Darapladib Thera

110 (The Stabilization of Atherosclerotic Plaque by Initiation of Darapladib Thera

111 rosclerosis, allowing noninvasive imaging of atherosclerotic plaque by MRI.

112 e presence of activated macrophages in human atherosclerotic plaques by (99m)Tc-folate imaging and to

113 nhibitor reduced (125)I-pentixafor uptake in atherosclerotic plaques by approximately 40%.

114 fold induction of (18)F-FDG uptake in murine atherosclerotic plaques by both M-CSF and GM-CSF.

115 that IL-19 can halt progression of preformed atherosclerotic plaques by regulating both macrophage in

116 Coronary artery calcified atherosclerotic plaque (CAC) predicts cardiovascular dis

117 Inflamed atherosclerotic plaques can be visualized by noninvasive

118 Thrombus formation over a ruptured atherosclerotic plaque cap can occlude an artery with fa

119 that LOY is associated with the severity of atherosclerotic plaque characteristics and outcome in me

120 ression of atherosclerosis results in larger atherosclerotic plaques characterized by bigger necrotic

121 ce in haematopoietic cells results in larger atherosclerotic plaques, characterized by bigger necroti

122 cally active Ly-6C(high) monocytes, enhanced atherosclerotic plaque chemokine expression, and monocyt

123 Ruptured coronary atherosclerotic plaques commonly cause acute myocardial

124 3a/b was markedly increased in human carotid atherosclerotic plaques compared with normal arteries, a

125 e-contrast CT can help identify and quantify atherosclerotic plaque components, with excellent correl

126 n of Cdnk2b promoted advanced development of atherosclerotic plaques composed of large necrotic cores

127 Increased atherosclerotic plaque correlated with reduced serum nit

128 In vivo uptake of (18)F-FCH in human carotid atherosclerotic plaques correlated strongly with degree

129 Histologic assessment in atherosclerotic plaque demonstrated that RO5444101 reduc

130 oprotected areas of mouse arteries and human atherosclerotic plaques demonstrated the preferential ex

131 Atherosclerotic plaque destabilization is the major dete

132 methods to interrogate the biology of MPs in atherosclerotic plaques developed in the past few years

133 by plasma cells and determine the impact on atherosclerotic plaque development in mice with and with

134 t-endothelial interactions may contribute to atherosclerotic plaque development, although in vivo stu

135 t-induced aortic macrophage accumulation and atherosclerotic plaque development.

136 g lymphatic function to lipid metabolism and atherosclerotic plaque development.

137 ontrast, VSMC Akt1 inhibition in established atherosclerotic plaques does not influence lesion size b

138 Human atherosclerotic plaques express increased mtDNA damage.

139 ccurately identified high-risk locations for atherosclerotic plaque formation along the entire aorta,

140 they may play a causative role in triggering atherosclerotic plaque formation and arterial thrombosis

141 inflammation thought to precede and underlie atherosclerotic plaque formation and instability.

142 Interleukin 18 (IL-18) promotes atherosclerotic plaque formation and is increased in pat

143 ntify microRNAs that exert a broad effect on atherosclerotic plaque formation and stability in the ca

144 ntation does not significantly contribute to atherosclerotic plaque formation and stability.

145 inical goal, and treatments that can reverse atherosclerotic plaque formation are actively being soug

146 eatment similarly reduced early diet-induced atherosclerotic plaque formation associated with both di

147 deficiency of Hck and Fgr led to attenuated atherosclerotic plaque formation by abrogating endotheli

148 thelial autophagic flux under high SS limits atherosclerotic plaque formation by preventing endotheli

149 We induced atherosclerotic plaque formation in hypercholesterolemic

150 mation from ox-LDL associated with decreased atherosclerotic plaque formation in hyperlipidemia.

151 NAC also significantly reduced atherosclerotic plaque formation in hyperlipidemic LDLR(

152 Atherosclerotic plaque formation results from chronic in

153 In addition, atherosclerotic plaque formation was significantly reduc

154 ophages and Th1 cells (both of which mediate atherosclerotic plaque formation) lacking sortilin had r

155 n high-fat diet-fed Ldlr(-/-) mice decreased atherosclerotic plaque formation, associated with decrea

156 (-/-)Apoe(-/-) knockout mice show diminished atherosclerotic plaque formation, characterized by reduc

157 olesterol diet, Tcad/ApoE-DKO mice increased atherosclerotic plaque formation, despite a 5-fold incre

158 ndothelial cell (EC) dysfunction, leading to atherosclerotic plaque formation.

159 nd ERK5 by disturbed flow contributes to the atherosclerotic plaque formation.

160 olipids (OxPL) by oxidative stress promoting atherosclerotic plaque formation.

161 to ER stress, is a hallmark of all stages of atherosclerotic plaque formation.

162 ays a protective role against neointimal and atherosclerotic plaque formations.

163 ation, is abundantly expressed in ECs and in atherosclerotic plaques from mice and humans.

164 Here Htun et al. demonstrate that vulnerable atherosclerotic plaques generate near-infrared autofluor

165 In conclusion, over the past decade, atherosclerotic plaques harvested during carotid endarte

166 asible assessment of inflammation within the atherosclerotic plaques has been demonstrated to enhance

167 gs indicate that the contribution of SMCs to atherosclerotic plaques has been greatly underestimated,

168 Noninvasive imaging of atherosclerotic plaques has substantially advanced over

169 modelling of the stress distribution within atherosclerotic plaques has suggested that subcellular m

170 and FBS showed lower adjusted odds of having atherosclerotic plaques (ICHS odds ratio [OR]: 0.41; 95%

171 In human atherosclerotic plaques, IL-1beta localizes predominantl

172 sues for the distinct imaging modalities for atherosclerotic plaque imaging.

173 eset, is a surrogate marker of rupture-prone atherosclerotic plaque in a rabbit model.

174 ke have increased risk of developing carotid atherosclerotic plaque in adulthood.

175 ibutes to the formation of necrotic cores in atherosclerotic plaque in animal models.

176 ection of hypoxic and potentially vulnerable atherosclerotic plaque in human subjects.

177 has pursued the quest to identify vulnerable atherosclerotic plaque in patients for decades, hoping t

178 coupled eNOS and reduced the size of carotid atherosclerotic plaque in rats feeding with high fat die

179 cannot distinguish between intima, media, or atherosclerotic plaque in the carotid artery.

180 hletes despite the presence of more coronary atherosclerotic plaque in the most active participants.

181 passive smoking was associated with carotid atherosclerotic plaque in young adults.

182 nvasive in vivo detection of inflammation in atherosclerotic plaques in a mouse model of atherosclero

183 lating CCR2(+) monocytes and the size of the atherosclerotic plaques in both the carotid artery and t

184 h cortistatin reduced the number and size of atherosclerotic plaques in carotid artery, heart, aortic

185 Snail was also expressed in EC overlying atherosclerotic plaques in coronary arteries from patien

186 B gene has been linked to the development of atherosclerotic plaques in humans and in a mouse model o

187 Macrophages in necrotic and symptomatic atherosclerotic plaques in humans as well as advanced at

188 morphometry of the aorta demonstrated larger atherosclerotic plaques in Itgbeta6(-/-) mice than in wi

189 ty lipoprotein (LDL) levels and formation of atherosclerotic plaques in Ldlr(-/-) mice.

190 otes macrophage emigration and regression of atherosclerotic plaques in part by liver X receptor (LXR

191 /kidney transplantation, arterial stiffness, atherosclerotic plaques in the aorta or lower limbs, and

192 via paradoxical embolism, and non-occlusive atherosclerotic plaques in the aortic arch, cervical, or

193 NP-HDL accumulation within atherosclerotic plaques in vivo and ex vivo was estimate

194 n across endothelial monolayers in vitro and atherosclerotic plaques in vivo, as assessed by intravit

195 F-FDG uptake within inflamed tissues such as atherosclerotic plaques in vivo.

196 nism that leads to amyloid deposition in the atherosclerotic plaques in vivo.

197 NP-HDL(59Fe-SPIOs) uptake into atherosclerotic plaques increased significantly after in

198 Anti-GPVI antibodies inhibit atherosclerotic plaque-induced platelet aggregation unde

199 Human atherosclerotic plaque-induced platelet aggregation was

200 of fluoro-deoxyglucose-PET/CT for imaging of atherosclerotic plaque inflammation.

201 )F-FDG PET/CT can be used to detect arterial atherosclerotic plaque inflammation.

202 (ESTA-MSV) to inflamed endothelium covering atherosclerotic plaques inhibits atherosclerosis.

203 helial interactions also contribute to early atherosclerotic plaque initiation and growth.

204 In this review, we discuss mechanisms of atherosclerotic plaque initiation and progression; how p

205 are compounds interfering with platelet GPVI-atherosclerotic plaque interaction to improve current an

206 Collagen content in atherosclerotic plaque is a hallmark of plaque stability

207 Contrast enhancement of intracranial atherosclerotic plaque is associated with its likelihood

208 Progressive inflammation in atherosclerotic plaques is associated with increasing ri

209 The formation of cholesterol crystals in atherosclerotic plaques is associated with the onset of

210 on imaging and early detection of high-risk atherosclerotic plaques is important for risk stratifica

211 LOY was also present in atherosclerotic plaque lesions (n=8/242, 3%).

212 mulation of adiponectin in the neointima and atherosclerotic plaque lesions, and the adiponectin-T-ca

213 Atherosclerotic plaque localization correlates with regi

214 cruitment into plaques, leading to increased atherosclerotic plaque macrophage content and inflammati

215 : cardiac mast cells are key constituents of atherosclerotic plaques; mast cell mediators play an imp

216 regimen reducing FABP4 expression within the atherosclerotic plaque may promote lesion stability thro

217 y GM-CSF and M-CSF in either cell culture or atherosclerotic plaques may not be distinguishable by th

218 te hypoxia, a condition that prevails in the atherosclerotic plaque, may conspire with inflammation a

219 role in the development of advanced coronary atherosclerotic plaques, no causal relationship has been

220 Human atherosclerotic plaques obtained by endarterectomy were

221 expression on inflammatory cells present in atherosclerotic plaques of an experimental rabbit model.

222 Male athletes had a higher prevalence of atherosclerotic plaques of any luminal irregularity (44.

223 evation in smooth muscle accumulation within atherosclerotic plaques of ApoE KO mice, suggesting plaq

224 ctor-1 (IGF-1) increases collagen content in atherosclerotic plaques of Apoe(-/-) mice.

225 lung, as they were also highly expressed in atherosclerotic plaques of human aorta, supporting a rol

226 ture microdissected CD68(+) macrophages from atherosclerotic plaques of Ldlr(-/-) mice devoid of Ager

227 iobank study that includes the collection of atherosclerotic plaques of patients undergoing primary c

228 were detected in vivo with PET/MR imaging in atherosclerotic plaques of the abdominal aorta and right

229 were detected in vivo with PET/MR imaging in atherosclerotic plaques of the abdominal aorta and right

230 occlusion localized at the site of high-risk atherosclerotic plaques, of which early detection and th

231 f USF1 gene had decreased USF1 expression in atherosclerotic plaques (P = 0.028 and 0.08, respectivel

232 ighly expressed in human and murine diabetic atherosclerotic plaques, particularly in macrophages.

233 a peptide, LyP-1, which specifically targets atherosclerotic plaques, penetrates into plaque interior

234 sted LOY for association with (inflammatory) atherosclerotic plaque phenotypes and cytokines and asse

235 essel formation inside the arterial wall and atherosclerotic plaques plays a critical role in pathoge

236 l atherosclerosis, NE was detected in mature atherosclerotic plaques, predominantly in the endotheliu

237 therogenic effects of systemic risk factors, atherosclerotic plaques preferentially develop at sites

238 he identification of patients with high-risk atherosclerotic plaques prior to the manifestation of cl

239 meostasis pathways that alter the balance of atherosclerotic plaque progression and regression.

240 own an association of ADAM10 expression with atherosclerotic plaque progression, a causal role of ADA

241 However, the role of GM-CSF in advanced atherosclerotic plaque progression, the process that giv

242 ion, demonstrating an enhanced potential for atherosclerotic plaque progression.

243 imaging techniques employed to visualize the atherosclerotic plaque provide information of diagnostic

244 d to proximal RCA thickening, independent of atherosclerotic plaque quantified by CT.

245 Although the directed treatment of atherosclerotic plaques remains elusive, macrophages are

246 gated temporal changes in the composition of atherosclerotic plaques removed from patients undergoing

247 Microscopic examination of atherosclerotic plaques revealed essential colocalizatio

248 Characterization of human and mouse atherosclerotic plaques revealed that MC1-R expression l

249 Atherosclerotic plaque rupture and subsequent acute even

250 onnection between myocardial infarctions and atherosclerotic plaque rupture events in the coronary ar

251 Atherosclerotic plaque rupture is accompanied by an acut

252 Coronary artery thrombosis is dominated by atherosclerotic plaque rupture, complex pulsatile flows

253 Inflammation drives atherosclerotic plaque rupture.

254 faceted hypothesis of the natural history of atherosclerotic plaque rupture.

255 ancer cell proliferation and metastasis, and atherosclerotic plaque rupture.

256 f microcalcifications that are implicated in atherosclerotic plaque rupture; however, the mechanisms

257 ously demonstrated that both human and mouse atherosclerotic plaques show elevated expression of EphA

258 tilized the apoE(-/-) mouse model to compare atherosclerotic plaque size and composition after inorga

259 ice exhibited a significant reduction of the atherosclerotic plaque size at the aortic root and the a

260 e (WT) mice but no significant difference in atherosclerotic plaque size between mice with polybacter

261 1 (Trem-1(-/-)) showed a strong reduction of atherosclerotic plaque size in both the aortic sinus and

262 -helper type-1 immune responses, and reduced atherosclerotic plaque size without altering the plasma

263 kaged in ESTA-MSV but not in PEG/PEI reduced atherosclerotic plaque size.

264 al expansion and led to a marked increase in atherosclerotic plaque size.

265 GAPDH levels were reduced in atherosclerotic plaque SMCs, and this effect correlated

266 duced thrombin generation, may also increase atherosclerotic plaque stability, as has been shown in m

267 laque's collagen content-two determinants of atherosclerotic plaque stability-are interlinked.

268 ADAM10 may play a causal role in modulating atherosclerotic plaque stability.

269 hich may play an important role in promoting atherosclerotic plaque stability.

270 eractions may be a novel therapy to increase atherosclerotic plaque stability.

271 peptide expressed in the vascular system and atherosclerotic plaques that regulates vascular calcific

272 lial nitric oxide synthase, the stability of atherosclerotic plaques, the production of proinflammato

273 In atherosclerotic plaques, the risk of rupture is increase

274 ivo histopathologic quantitative measures of atherosclerotic plaque tissue characteristics, as well a

275 component determining the susceptibility of atherosclerotic plaque to rupture.

276 Atherosclerotic plaques transplanted into WT or Ccr5-/-

277 ammatory M2 state is a key characteristic of atherosclerotic plaques undergoing regression.

278 Atherosclerotic plaques underlying most myocardial infar

279 n vivo MRI and ex vivo multimodal imaging of atherosclerotic plaque using NP-HDL is feasible, and int

280 ET and CT to identify ruptured and high-risk atherosclerotic plaques using the radioactive tracers (1

281 ed lipids in endarterectomized human carotid atherosclerotic plaques using three-dimensional (3D) ele

282 Human atherosclerotic plaque VSMCs show increased DNA damage,

283 Human atherosclerotic plaque VSMCs showed increased expression

284 but also HAMP and PLAUR, which contribute to atherosclerotic plaque vulnerability.

285 attenuated, and local antibody deposition in atherosclerotic plaque was absent.

286 tion on apoA-I that is abundant within human atherosclerotic plaque, was further investigated by usin

287 Because HILPDA is highly expressed in atherosclerotic plaques, we examined its regulation and

288 Methods: Atherosclerotic plaques were induced by endothelial abra

289 Atherosclerotic plaques were induced by endothelial abra

290 Mice with carotid atherosclerotic plaques were injected with the optical o

291 ol size of iodinated LDL particles of aortic atherosclerotic plaques were not reduced until after 4 w

292 MIs result spontaneously from instability of atherosclerotic plaque, whereas type 2 MIs occur in the

293 dothelium predisposes it toward formation of atherosclerotic plaque, which may be a subsequent risk f

294 k allele had reduced expression of CDKN2B in atherosclerotic plaques, which was associated with impai

295 he underlying media) and a diseased portion (atherosclerotic plaque with the underlying media).

296 -) mice show reduced progression to advanced atherosclerotic plaques with diminished smooth muscle an

297 vel technology that allows identification of atherosclerotic plaques with intraplaque hemorrhage and

298 Although the atherosclerotic plaques with large necrotic cores (indep

299 Here, I review the evolution of atherosclerotic plaques with respect to changes in the M

300 g to identify ruptured or high-risk coronary atherosclerotic plaques would represent a major clinical