ライフサイエンスコーパス: atherosclerotic lesion

1 rrowing of coronary lumen space caused by an atherosclerotic lesion.

2 , progression, and subsequent rupture of the atherosclerotic lesion.

3 lls (SMCs), and endothelial cells from mouse atherosclerotic lesions.

4 IRF5 affects the formation and phenotype of atherosclerotic lesions.

5 plasma cholesterol and TG levels and reduced atherosclerotic lesions.

6 ay allow for molecular imaging of vulnerable atherosclerotic lesions.

7 ulation is a key characteristic of advancing atherosclerotic lesions.

8 que inflammation and progression to advanced atherosclerotic lesions.

9 and macrophage-derived foam cells and cause atherosclerotic lesions.

10 f bifurcated vessels that are susceptible to atherosclerotic lesions.

11 ) mice have a significant increase of aortic atherosclerotic lesions.

12 etion in myeloid cells increased the size of atherosclerotic lesions.

13 lipid-laden macrophages that infiltrate the atherosclerotic lesions.

14 -specific ABCG1 deficiency protected against atherosclerotic lesions.

15 ced endothelial inflammation and the size of atherosclerotic lesions.

16 e circulation and alter cellular behavior in atherosclerotic lesions.

17 notypes and the consequential development of atherosclerotic lesions.

18 via reduction of macrophage recruitment into atherosclerotic lesions.

19 es of stability, and monocyte recruitment to atherosclerotic lesions.

20 rosclerosis, to resolution and regression of atherosclerotic lesions.

21 kine production, and increased cell death in atherosclerotic lesions.

22 ce inhibited monocyte recruitment to nascent atherosclerotic lesions.

23 ct >80% of SMC-derived cells within advanced atherosclerotic lesions.

24 ion of vascular cell migration and matrix in atherosclerotic lesions.

25 studies of HDL-like particles recovered from atherosclerotic lesions.

26 duced the development of both early and late atherosclerotic lesions.

27 g VSMC-specific Aadac showed amelioration of atherosclerotic lesions.

28 quantification of VCAM-1 expression in mouse atherosclerotic lesions.

29 ndothelial activation and the development of atherosclerotic lesions.

30 regulates the site-specific distribution of atherosclerotic lesions.

31 g emerges as a new tool for the detection of atherosclerotic lesions.

32 ) have long been recognized as a hallmark of atherosclerotic lesions.

33 percholesterolemia and a marked elevation in atherosclerotic lesions.

34 on and make up a major component of advanced atherosclerotic lesions.

35 imaging agent for the detection of inflamed atherosclerotic lesions.

36 the in vivo imaging of VCAM-1 expression in atherosclerotic lesions.

37 ue to inconsistent detection of the virus in atherosclerotic lesions.

38 n in the lymphoid system and the presence in atherosclerotic lesions.

39 ration of both effector T cells and Tregs in atherosclerotic lesions.

40 ls, necrotic cores, and interleukin 1beta in atherosclerotic lesions.

41 demia to cause topographical distribution of atherosclerotic lesions.

42 n apoptotic cells, inflammatory tissues, and atherosclerotic lesions.

43 m the arterial lumen and the adventitia into atherosclerotic lesions.

44 nd are at great risk to develop obstructive, atherosclerotic lesions.

45 is a major contributor to the instability of atherosclerotic lesions.

46 in SPC migration and their recruitment into atherosclerotic lesions.

47 ges, and intensified with the progression of atherosclerotic lesions.

48 4 prevents cell death of SMCs and stabilizes atherosclerotic lesions.

49 numbers of circulating monocytes and smaller atherosclerotic lesions.

50 atterns determine the uneven distribution of atherosclerotic lesions.

51 ice lacking myeloid GLUT1 developed unstable atherosclerotic lesions.

52 lerosis by enhancing monocyte recruitment to atherosclerotic lesions.

53 racy of measurements and characterization of atherosclerotic lesions.

54 ival, as well as differentiation in advanced atherosclerotic lesions.

55 hancing recruitment of Ly6c(hi) monocytes to atherosclerotic lesions.

56 educe macrophage cholesterol accumulation in atherosclerotic lesions.

57 uld be useful to improve characterization of atherosclerotic-lesions.

58 In Apoe(-/-) mice with mature atherosclerotic lesions (5 months of high fat diet), we

59 less hepatic lipid accumulation and smaller atherosclerotic lesions (60% smaller in Ldlr(-/-);Gsk3a(

60 Although not detected in atherosclerotic lesions, Abcg4 was highly expressed in b

61 e marrow cells exhibited significantly fewer atherosclerotic lesions after high-fat and high-choleste

62 RI showed an increased uptake of NP-HDL into atherosclerotic lesions after intraperitoneal injection,

63 Moreover, analysis of human unstable atherosclerotic lesions also revealed a significant inve

64 A, inflammasome activation, and apoptosis in atherosclerotic lesions and also higher serum IL-1beta a

65 t-like structures have also been detected in atherosclerotic lesions and arterial thrombi in humans a

66 ice, Nef significantly increased the size of atherosclerotic lesions and caused vessel remodeling.

67 Because eRNA is associated with atherosclerotic lesions and contributes to inflammation-

68 markedly enhanced in patients with advanced atherosclerotic lesions and correlates with disease seve

69 phospho-IRE1, and GRP78 in macrophage-dense atherosclerotic lesions and in peritoneal macrophages.

70 one marrow into Ldlr(-/-) mice led to larger atherosclerotic lesions and increased IL-1beta productio

71 Furthermore, DMAG significantly reduced atherosclerotic lesions and induced a more stable plaque

72 d to alteration of monocyte recruitment into atherosclerotic lesions and inhibited toll-like receptor

73 AMPKalpha1(-/-) mice showed reduced sizes of atherosclerotic lesions and lesser numbers of macrophage

74 significantly upregulated on macrophages in atherosclerotic lesions and M1 macrophages in vitro.

75 Sections of human atherosclerotic lesions and non-atherosclerotic arteries

76 imaging system to identify the locations of atherosclerotic lesions and occlusion due to myocardial-

77 oaded foam cell macrophages are prominent in atherosclerotic lesions and play complex roles in both i

78 Monocyte-derived macrophages, located in atherosclerotic lesions and presenting heterogeneous phe

79 e more Ly-6C(high) monocytes, develop larger atherosclerotic lesions and produce less hypocretin-a st

80 rystal deposition that are characteristic of atherosclerotic lesions and pulmonary alveolar proteinos

81 sis factor-alpha, and interleukin-12) within atherosclerotic lesions and spleens of high-fat diet-fed

82 RT6 in the inflammatory pathways of diabetic atherosclerotic lesions and suggest its possible positiv

83 we observed that PIAS3 levels are reduced in atherosclerotic lesions and that PIAS3 expression decrea

84 Both the chronic development of atherosclerotic lesions and the acute changes in lesion

85 sms of the formation of clinically dangerous atherosclerotic lesions and the potential of pro-resolvi

86 NZW rabbit aorta for detection of lipid-rich atherosclerotic lesions, and (2) on live animals for dem

87 s of inflammation including amyloid plaques, atherosclerotic lesions, and arthritic joints.

88 ion, the content of monocytes/macrophages of atherosclerotic lesions, and attenuated atheroprogressio

89 PK1 protein and mRNA in both human and mouse atherosclerotic lesions, and used loss-of-function appro

90 In atherosclerotic lesions, apoA-I exhibits marked oxidativ

91 Advanced atherosclerotic lesions are further weakened by the pron

92 Atherosclerotic lesions are known for their cellular het

93 ioplasty for the treatment of infrapopliteal atherosclerotic lesions are not well characterized.

94 Finally, aortic atherosclerotic lesions are reduced by 90% and 70%, resp

95 Surprisingly, however, mean atherosclerotic lesion area in Pggt1btriangle up/triangl

96 MAO levels in donors and recipients and with atherosclerotic lesion area in recipients.

97 Aortic atherosclerotic lesion area was significantly decreased

98 se inhibition blocked NET formation, reduced atherosclerotic lesion area, and delayed time to carotid

99 ion of hematopoietic Dectin-2 did not affect atherosclerotic lesion area, immune cell composition, ex

100 ecule MAP4K4 inhibitor also markedly reduces atherosclerotic lesion area.

101 unostaining was observed in the left carotid atherosclerotic lesions as a consequence of artery ligat

102 ine, a specific by-product of MPO, in aortic atherosclerotic lesions as determined by both immunohist

103 unity, which can be regulated locally within atherosclerotic lesions, as well as in secondary lymphoi

104 nction of many cells that make up late-stage atherosclerotic lesions, as well as the mechanisms by wh

105 part, from decreased emigration of DCs from atherosclerotic lesions because of the high-cholesterol

106 PfnHet) exhibited a significant reduction in atherosclerotic lesion burden and vascular inflammation.

107 lationship between vascular risk factors and atherosclerotic lesion burden of intracranial arteries a

108 g (QKI) are low in monocytes and early human atherosclerotic lesions, but are abundant in macrophages

109 esolution of inflammation and development of atherosclerotic lesions, but the effects of the P387 TSP

110 r pathway is active in modulated SMCs in the atherosclerotic lesion cap.

111 inical practice, in vivo characterization of atherosclerotic lesions causing myocardial infarction, i

112 ckout (DKO; apoE-CD16 DKO) mice have reduced atherosclerotic lesions compared with apoE knockout mice

113 lipidemic mice lacking ABCG1 develop smaller atherosclerotic lesions compared with controls.

114 ays an important role in the localization of atherosclerotic lesions concomitant with LOX-1 dependent

115 Advanced atherosclerotic lesions contain senescent cells, but the

116 osphorylated p53 compared with controls, and atherosclerotic lesions contained fewer proliferating ma

117 (99m)Tc-cAbVCAM1-5 uptake in atherosclerotic lesions correlated with the level of VCA

118 lEVs accumulated in plaque atherosclerotic lesions depending on the progression of

119 but not interferon gamma failed to increase atherosclerotic lesions despite partial reconstitution i

120 Myeloid cells are central to atherosclerotic lesion development and vulnerable plaque

121 Intimal macrophage infiltration promotes atherosclerotic lesion development by facilitating the a

122 MitoOS in lesional macrophages amplifies atherosclerotic lesion development by promoting NF-kappa

123 oe deficiency) demonstrated no difference in atherosclerotic lesion development compared with apoe(-/

124 ry choline or TMAO significantly accelerates atherosclerotic lesion development in ApoE-deficient mic

125 ndogenous macrophage foam cell formation and atherosclerotic lesion development in apolipoprotein e(-

126 Moreover, perhexiline administration reduced atherosclerotic lesion development in apolipoprotein E-d

127 First, atherosclerotic lesion development in hyperlipidemic apo

128 Atherosclerotic lesion development in response to high-c

129 these in vitro findings were of relevance to atherosclerotic lesion development in vivo.

130 on of various cell types that participate in atherosclerotic lesion development, including endothelia

131 flow in promoting atheroprone phenotypes and atherosclerotic lesion development.

132 ifferentiation of leukocytes is important in atherosclerotic lesion development.

133 Macrophages accumulate in atherosclerotic lesions during the inflammation that is

134 erived cells within advanced mouse and human atherosclerotic lesions exhibit far greater phenotypic p

135 Intimal lymphatics in the atherosclerotic lesions exhibited an atypical phenotype,

136 Lipid-rich atherosclerotic lesions exhibited distinct positive TS (

137 essed a cleavage-resistant variant of MerTK, atherosclerotic lesions exhibited higher macrophage MerT

138 Atherosclerotic lesions exhibited inflammatory cells.

139 f the crucial step in the mechanism by which atherosclerotic lesions form.

140 y, deletion of hematopoietic CARD9 increased atherosclerotic lesion formation and lesion severity.

141 MAARS knockdown reduces atherosclerotic lesion formation by 52% in LDLR(-/-) mic

142 tes and macrophages promotes and accelerates atherosclerotic lesion formation by hyper-sensitizing mo

143 nd that exacerbated dyslipidemia may mediate atherosclerotic lesion formation caused by constant ligh

144 versed vascular inflammation and accelerated atherosclerotic lesion formation in cholesterol-fed Ldlr

145 cruitment into the arterial wall and limited atherosclerotic lesion formation in hyperlipidemic mice.

146 =12-15) or SMCs (n=13-24) markedly increased atherosclerotic lesion formation in hyperlipidemic mice.

147 ompartment and was associated with increased atherosclerotic lesion formation in low-density lipoprot

148 Reduced levels of MALAT1 augment atherosclerotic lesion formation in mice and are associa

149 R2 and its proresolving ligand annexin A1 to atherosclerotic lesion formation is largely undefined.

150 The rate of atherosclerotic lesion formation is profoundly influence

151 se to biochemical and biomechanical stimuli, atherosclerotic lesion formation occurs from the partici

152 rmation of lipid-filled foam cells, initiate atherosclerotic lesion formation, and deficient efferocy

153 on of FPR2 or its ligand annexin A1 enhances atherosclerotic lesion formation, arterial myeloid cell

154 MPhi-IGF1R-KO significantly increased atherosclerotic lesion formation, as assessed by Oil Red

155 cy in atherosclerosis-prone mice accelerates atherosclerotic lesion formation, but the underlying mec

156 tial to provide a comprehensive insight into atherosclerotic lesion formation, diagnostics and respon

157 of Ldlr-/- Arhgef1-/- with WT BM exacerbated atherosclerotic lesion formation, supporting Arhgef1 act

158 cells in Apoe(-/-) Malat1(+/+) mice enhanced atherosclerotic lesion formation, which suggests that he

159 Csn5 in Apoe(-/-) mice markedly exacerbated atherosclerotic lesion formation.

160 mice accelerated high-fat diet (HFD)-induced atherosclerotic lesion formation.

161 responses are recognized as major drivers of atherosclerotic lesion formation.

162 nd then analyzed for plasma lipid levels and atherosclerotic lesion formation.

163 ncrease susceptibility to EC dysfunction and atherosclerotic lesion formation.

164 s and how these may mediate their effects in atherosclerotic lesion formation.

165 a-like 1 homolog (Dlk1) and thereby prevents atherosclerotic lesion formation.

166 nd fed an atherogenic diet showed aggravated atherosclerotic lesion formation.

167 ncy of inflammatory monocytes that initiates atherosclerotic lesion formation.

168 nd 46 quantification methods to characterize atherosclerotic lesions from (18)F-FDG PET images.

169 The presence of eRNA was revealed in atherosclerotic lesions from high-fat diet-fed low-densi

170 Peritoneal macrophages and atherosclerotic lesions from Zfp148(gt/+)Apoe(-/-) mice

171 Atherosclerotic lesions grow via the accumulation of leu

172 sible for the development and progression of atherosclerotic lesions have not been fully established.

173 bin on the NLRP3 inflammasome inhibition and atherosclerotic lesion in ApoE2Ki mice fed a high-fat We

174 of cathepsin S attenuates the progression of atherosclerotic lesions in 5/6 nephrectomized mice, serv

175 rable uptake of [(18)F]FDM and [(18)F]FDG in atherosclerotic lesions in a rabbit model; [(18)F]FDM up

176 ize, stage, and inflammatory cell content of atherosclerotic lesions in Apoe(-/-) mice on high-fat di

177 miR-155 are selectively upregulated in early atherosclerotic lesions in Apoe(-/-) mice.

178 nockout significantly reduced SPC numbers in atherosclerotic lesions in apolipoprotein E (ApoE)-defic

179 RIPK1 expression is abundant in early-stage atherosclerotic lesions in both humans and mice.

180 Unstable atherosclerotic lesions in carotid arteries require surg

181 fter dexamethasone treatment and in advanced atherosclerotic lesions in fat-fed Ldlr(-/-) mice.

182 , however, an integrated omics assessment of atherosclerotic lesions in individual Apoe(-/-) mice has

183 graphy imaging, identifies acidic regions in atherosclerotic lesions in live mice, ushering a non-inv

184 d radiation-free imaging approach to monitor atherosclerotic lesions in live subjects.

185 (SPIOs) and quantum dots was able to detect atherosclerotic lesions in mice after intravenous and in

186 erotic plaques in humans as well as advanced atherosclerotic lesions in mice demonstrated activation

187 2) but not SphK1 aggravates the formation of atherosclerotic lesions in mice with ApoE deficiency.

188 type, and decreased the progression of early atherosclerotic lesions in mice.

189 disturbed flow, and is expressed in advanced atherosclerotic lesions in patients and in the Apoe(-/-)

190 interrogate the pharmacological response of atherosclerotic lesions in situ and in vivo.

191 ibited vascular inflammation, and suppressed atherosclerotic lesions in streptozotocin (STZ)-induced

192 acilitate the in vivo noninvasive imaging of atherosclerotic lesions in terms of intimal macrophage a

193 okines, alveolar bone loss, cholesterol, and atherosclerotic lesions in the aorta and aortic sinus co

194 at high levels, and after 12 weeks, mice had atherosclerotic lesions in the aorta.

195 r heterozygous Tet2 knockout mice had larger atherosclerotic lesions in the aortic root and aorta tha

196 Genesis of atherosclerotic lesions in the human arterial system is

197 ncy intravascular ultrasound (IVUS) revealed atherosclerotic lesions in the regions with augmented IS

198 alloon vs. Standard PTA for the Treatment of Atherosclerotic Lesions in the Superficial Femoral Arter

199 PACT SFA Clinical Study for the Treatment of Atherosclerotic Lesions in the Superficial Femoral Arter

200 atheter vs Standard PTA for the Treatment of Atherosclerotic Lesions in the Superficial Femoral Arter

201 pendent reduction of LKB1 levels occurred in atherosclerotic lesions in western diet-fed Ldlr(-/-) an

202 rosclerosis and show that they accumulate in atherosclerotic lesions in which they directly affect pl

203 -/-)LKB1(fl/fl)LysM(cre) mice developed more atherosclerotic lesions in whole aorta and aortic root a

204 Intimal macrophages play a critical role in atherosclerotic lesion initiation and progression by tak

205 echanisms that underlie its pivotal roles in atherosclerotic lesion initiation and progression; explo

206 now widely accepted that the development of atherosclerotic lesions involves a chronic inflammatory

207 (s) that regulates T-cell trafficking to the atherosclerotic lesions is also unknown.

208 olipoprotein A1 (apoA1) recovered from human atherosclerotic lesions is highly oxidized.

209 The molecular basis for the focal nature of atherosclerotic lesions is poorly understood.

210 e (MPO) secreted by activated macrophages in atherosclerotic lesions is the promoter of such apoA-I o

211 the observed gain of DNA methylation in the atherosclerotic lesions justifies efforts to develop DNA

212 d that CaMKIIgamma-deficient macrophages and atherosclerotic lesions lacking myeloid CaMKIIgamma had

213 that Ogg1 expression decreases over time in atherosclerotic lesion macrophages of low-density lipopr

214 ages, and Nhe1-FcepsilonR1 colocalization in atherosclerotic lesion macrophages support a role of IgE

215 In the atherosclerotic lesion, macrophages ingest high levels o

216 TREM-1 was expressed in human atherosclerotic lesions, mainly in lipid-rich areas with

217 cid (LPA), a potent bioactive lipid found in atherosclerotic lesions, markedly induces smooth muscle

218 DOL-induced dyslipidemia caused formation of atherosclerotic lesions of an intermediate stage, which

219 primarily by monocytes/macrophages in aortic atherosclerotic lesions of ApoE(-/-) mice and is secrete

220 tomic phenotype of modulated SMCs in vivo in atherosclerotic lesions of both mouse and human arteries

221 lood mononuclear cell (PBMC) accumulation in atherosclerotic lesions of cardiovascular (CV) patients

222 concurred with an increased MGC presence in atherosclerotic lesions of Mcl-1(-/-) mice.

223 in activated T cells that infiltrate in vivo atherosclerotic lesions of primary APS patients with ath

224 d NKT cells were identified in the liver and atherosclerotic lesions of recipient mice.

225 nce of MPO expression in the bone marrow and atherosclerotic lesions of the aorta in the CKD-bMPOKO m

226 determine whether their key roles are within atherosclerotic lesions or secondary lymphoid organs.

227 to describe the presence of T cells in mouse atherosclerotic lesions; other articles demonstrated the

228 the high levels of RIPK1 expression in human atherosclerotic lesions, our study suggests RIPK1 as a f

229 P2X7 receptor was higher expressed in murine atherosclerotic lesions, particularly by lesional macrop

230 ed more trafficking of Ly6c(hi) monocytes to atherosclerotic lesions, preferential differentiation of

231 It has been known for some time that atherosclerotic lesions preferentially develop in areas

232 The earliest atherosclerotic lesions preferentially develop in arteri

233 Development of atherosclerotic lesions probably requires low-density li

234 a role in macrophage-driven inflammation in atherosclerotic lesions, probably by augmenting the Ccl5

235 Inhibition of IL-17A markedly prevented atherosclerotic lesion progression (p = 0.001) by reduci

236 that functional blockade of IL-17A prevents atherosclerotic lesion progression and induces plaque st

237 tibodies in autoimmune mice that targeted 25 atherosclerotic lesion proteins, including essential com

238 Identifying metabolically active atherosclerotic lesions remains an unmet clinical challe

239 cardiovascular disease have well-established atherosclerotic lesions, rendering lesion regression of

240 tween this optical index and the severity of atherosclerotic lesions, represented by the age of the r

241 In early atherosclerotic lesions, Rgs1 regulates macrophage accum

242 Analyses of atherosclerotic lesions showed that Acat1(-M/-M) reduced

243 sed glomerular filtration rate and increased atherosclerotic lesion size and aortic leukocyte numbers

244 The absence of CARD9 unexpectedly increased atherosclerotic lesion size and severity, suggesting tha

245 ipopolysaccharide treatment rapidly enhanced atherosclerotic lesion size by expansion of the lesional

246 prisingly, the net effect was an increase in atherosclerotic lesion size due to an increase in the co

247 it did lead to a significant 60% increase in atherosclerotic lesion size in Pon3KO mice on the C57BL/

248 Analysis of atherosclerotic lesion size in the aortic root demonstra

249 ne levels, blood pressure, oxidative stress, atherosclerotic lesion size in the aortic roots, cell pr

250 cholesterol was reduced with pNAPE-EcN, but atherosclerotic lesion size showed only a non-significan

251 METHODS AND No difference in atherosclerotic lesion size was found in Ldlr(-/-) (low-

252 umber of circulating blood monocytes impacts atherosclerotic lesion size, and in mouse models, elevat

253 Neither diabetes nor MI led to increased atherosclerotic lesion size, but diabetes accelerated le

254 er, exogenous TWEAK administration increased atherosclerotic lesion size, lipids, and macrophages con

255 e burden, indicating that antibodies promote atherosclerotic lesion size.

256 ally, repeated treatment with Ac2-26 reduces atherosclerotic lesion sizes and lesional macrophage acc

257 , increased (18)F-FLT signal was observed in atherosclerotic lesions, spleen, and bone marrow (standa

258 the CORAL (Cardiovascular Outcomes in Renal Atherosclerotic Lesions) study, we performed exploratory

259 ines and chemokines in endothelial cells and atherosclerotic lesions, suggesting that CARD8 plays a s

260 e observe increased P2X7 expression in human atherosclerotic lesions, suggesting that our findings in

261 The focal nature of atherosclerotic lesions suggests an important role of lo

262 Increased TLR7 expression in human atherosclerotic lesions suggests its involvement in athe

263 17a1 x Apoe double KO XY mice developed more atherosclerotic lesions than Apoe KO male controls, rega

264 rol diet, P2X7-deficient mice showed smaller atherosclerotic lesions than P2X7-competent mice (0.162

265 ormoglycemic ApoE(-/-) mice developed larger atherosclerotic lesions than sham-operated on controls.

266 ase is often triggered by a distinct type of atherosclerotic lesion that displays features of impaire

267 eristics of dysregulated immune cells within atherosclerotic lesions that lead to clinical events suc

268 ists even in phenotypically modulated SMC in atherosclerotic lesions that show no detectable expressi

269 In atherosclerotic lesions, the miR-342-5p antagomir upregu

270 In advanced atherosclerotic lesions, the ratio between specialized p

271 led to an approximately fourfold increase in atherosclerotic lesions throughout the aorta, which were

272 ile at rest and angiographically significant atherosclerotic lesions to angioplasty with a paclitaxel

273 pHrodo probe localizes the acidic regions in atherosclerotic lesions to macrophages, IgE, and cell ap

274 f PTEN was observed in intimal SMCs of human atherosclerotic lesions underlying the potential clinica

275 th reduction in size and loss of lipids from atherosclerotic lesions upon plasma lipid lowering witho

276 s correlated to mediators of inflammation in atherosclerotic lesions using Biobank of Karolinska Enda

277 The pH in atherosclerotic lesions varies between individuals.

278 several independent human cohorts comparing atherosclerotic lesions versus healthy arteries, using t

279 ore, relative macrophage content in advanced atherosclerotic lesions was decreased.

280 frequent presence of T lymphocytes in human atherosclerotic lesions was first described in the 1980s

281 he endothelium, and accelerated formation of atherosclerotic lesions was observed in Senp2(+/-)/Ldlr(

282 Consequently, a marked reduction in atherosclerotic lesions was observed.

283 The influx of these cells into atherosclerotic lesions was significantly reduced, where

284 In murine atherosclerotic lesions, we found that macrophages turn

285 ly, structural and biochemical features from atherosclerotic lesions were acquired in ex vivo human c

286 Human atherosclerotic lesions were enriched in lEVs expressing

287 thirty-two patients with 158 infrapopliteal atherosclerotic lesions were enrolled.

288 Additionally, late atherosclerotic lesions were more common in patients wit

289 ecade ago, studies on macrophage behavior in atherosclerotic lesions were often limited to quantifica

290 as apoptosis and macrophage proliferation in atherosclerotic lesions were unaffected.

291 Moreover, L-sIDOL mice developed marked atherosclerotic lesions when fed a Western diet.

292 NCC is expressed in atherosclerotic lesions, where it colocalizes with IL18r

293 inantly expressed in foam cells found within atherosclerotic lesions, where MafB mediates the oxidize

294 Rupture and erosion of advanced atherosclerotic lesions with a resultant myocardial infa

295 Treatment with GSO-494 results in smaller atherosclerotic lesions with increased plaque stability.

296 and association between CVD risk factors and atherosclerotic lesions with LTL.

297 quencing from murine microdissected advanced atherosclerotic lesions with smooth muscle cell (SMC) an

298 -derived fibroblast-like cells are common in atherosclerotic lesions, with EndMT-derived cells expres

299 ificantly reduced between early and advanced atherosclerotic lesions, with no loss in ABCA1 expressio

300 ion of macrophages and their accumulation in atherosclerotic lesions without changing the size of les