ライフサイエンスコーパス: atherosclerosis

1 tic basis of this endogenous defense against atherosclerosis.

2 otic lesions depending on the progression of atherosclerosis.

3 participants from the Multi-Ethnic Study of Atherosclerosis.

4 active T(regs) as a novel cellular target in atherosclerosis.

5 ckpoints are critical negative regulators of atherosclerosis.

6 ogy in addition to their established role in atherosclerosis.

7 herapeutic target against the development of atherosclerosis.

8 epresent a translational target for treating atherosclerosis.

9 drivers and modifiers of the pathogenesis of atherosclerosis.

10 bone marrow MNCs was higher in patients with atherosclerosis.

11 1 as a potential target for the treatment of atherosclerosis.

12 tion plays a key role in the pathogenesis of atherosclerosis.

13 naling was dysregulated in symptomatic human atherosclerosis.

14 nt aspects of macrophage immunometabolism in atherosclerosis.

15 eat diseases of the vascular system, such as atherosclerosis.

16 kine that may be protective against coronary atherosclerosis.

17 s because of the detection of nonobstructive atherosclerosis.

18 al hypertension (SAH) and an early marker of atherosclerosis.

19 and as a risk factor in the pathogenesis of atherosclerosis.

20 ch groups to try to develop vaccines against atherosclerosis.

21 regulation of CARD8 in endothelial cells and atherosclerosis.

22 ially mediated by accelerated progression of atherosclerosis.

23 iet (WTD) to study the effects of CYP17A1 on atherosclerosis.

24 disease, especially intimal hyperplasia and atherosclerosis.

25 to a high fat diet, a known risk factor for atherosclerosis.

26 ys and chemokine-selectively interferes with atherosclerosis.

27 nrecognized inhibitor of VSMC senescence and atherosclerosis.

28 pment of several chronic diseases, including atherosclerosis.

29 aden macrophage foam cells are a hallmark of atherosclerosis.

30 lved in multifaceted disease responses, like atherosclerosis.

31 ding of the pathophysiology underlying human atherosclerosis.

32 nment that promotes vascular dysfunction and atherosclerosis.

33 ved in chronic inflammatory diseases such as atherosclerosis.

34 bined therapies in the treatment of advanced atherosclerosis.

35 d with receptors for other viruses linked to atherosclerosis.

36 ation and protect against the progression of atherosclerosis.

37 r disease such as vascular calcification and atherosclerosis.

38 studied commonly to elucidate mechanisms of atherosclerosis.

39 enes critical for inflammation, and prevents atherosclerosis.

40 (MMP) -2 and -9, which increase the risk of atherosclerosis.

41 or the prediction of generalized subclinical atherosclerosis.

42 s underlying sex as a biological variable in atherosclerosis.

43 ing is one of the strongest risk factors for atherosclerosis.

44 ms of how ageing influences the pathology of atherosclerosis.

45 ynergize, via IL-6 signalling, to accelerate atherosclerosis.

46 primary prevention and management of carotid atherosclerosis.

47 rting apoB(+) T(regs) failed to protect from atherosclerosis.

48 AC) is a highly specific marker for coronary atherosclerosis.

49 a novel circulating biomarker of subclinical atherosclerosis.

50 linical assessment and management of carotid atherosclerosis.

51 ade abolishes diabetes-driven aggravation of atherosclerosis.

52 apolipoprotein A-I (apoA-I) associated with atherosclerosis.

53 cacy in reducing disease in a mouse model of atherosclerosis.

54 h muscle cells (SMC) play a critical role in atherosclerosis.

55 bined therapies in the treatment of advanced atherosclerosis.

56 zed as a major player in the pathogenesis of atherosclerosis.

57 risk factors for cardiovascular diseases and atherosclerosis.

58 before hyperlipidemia may reduce age-related atherosclerosis.

59 trimethylamine oxide, a causative agent for atherosclerosis.

60 mmation, intimal hyperplasia and accelerated atherosclerosis.

61 ves inflammation and contributes directly to atherosclerosis.

62 or of 100 mg per deciliter or higher without atherosclerosis.

63 de insight into disease activity in coronary atherosclerosis.

64 rs of pathophysiological processes including atherosclerosis.

65 Why does poor-quality sleep lead to atherosclerosis?

66 opment and homeostasis but can also initiate atherosclerosis(1).

67 In MESA (Multi-Ethnic Study of Atherosclerosis), 1,992 participants free of CVD complet

68 o been implicated in Alzheimer's disease(4), atherosclerosis(5) and cancers(6).

69 analysis in the MESA (Multi-Ethnic Study of Atherosclerosis), a community-based cohort study that en

70 dary prevention in patients with established atherosclerosis: a systematic review and meta-analysis.

71 These results show that in patients with atherosclerosis, activation of innate immune cells occur

72 n tomography (PET) provides an assessment of atherosclerosis activity.

73 different time points following injection of atherosclerosis-affine Gadofluorine P as well as at diff

74 value of mass spectrometry imaging (MSI) of atherosclerosis-affine Gadofluorine P for molecular MRI

75 argets for the treatment of diseases such as atherosclerosis, Alzheimer's disease and cancer(2-7).

76 In patients with ischemic stroke and atherosclerosis, an LDL-C target of <70 mg/dL (1.8 mmol/

77 s with coronary artery disease due to severe atherosclerosis and 13 subjects without atherosclerosis

78 hether ICIs were associated with accelerated atherosclerosis and a higher risk of atherosclerosis-rel

79 poiesis under homeostatic conditions, during atherosclerosis and after myocardial infarction.

80 dings support an association between midlife atherosclerosis and development of vascular dementia and

81 imethylamine (TMA) in the gut can accelerate atherosclerosis and heart disease, and these TMA-produci

82 In mice, CHIP accelerates atherosclerosis and increases IL-6/IL-1beta expression,

83 uspid aortic valve, inflammatory vasculitis, atherosclerosis and infections).

84 ks arterial leukocyte adhesion, and inhibits atherosclerosis and inflammation in hyperlipidemic Apoe(

85 remodelling in macrophages in the context of atherosclerosis and inflammation, and provide a comprehe

86 nent role of HDAC (histone deacetylase)-9 in atherosclerosis and its clinical complications including

87 ytes are produced and how they contribute to atherosclerosis and its complications is, therefore, cri

88 ic inflammatory processes that are active in atherosclerosis and lead to myocardial infarction and st

89 a argue against a common primary trigger for atherosclerosis and multiple sclerosis but suggest that

90 ysfunction, but their role in early stage of atherosclerosis and on vascular smooth muscle cells (SMC

91 new therapeutic targets for the treatment of atherosclerosis and other diseases.

92 ge immunometabolism plays important roles in atherosclerosis and other inflammatory diseases.

93 Atherosclerosis and plaque disruption have a central pat

94 uals and found associations between cerebral atherosclerosis and reduced synaptic signaling and betwe

95 ost vascular pathological conditions such as atherosclerosis and restenosis.

96 living with HIV (PLWH) may have accelerated atherosclerosis and shorter TL than the general populati

97 erebral small vessel disease but not between atherosclerosis and subsequent AD dementia or AD patholo

98 otype of apoB-reactive autoimmune T cells in atherosclerosis and suggest an initially protective auto

99 ndex and, in men, associations with coronary atherosclerosis and systolic blood pressure.

100 ing array of impacts that exercise exerts on atherosclerosis and the cardiovascular system.

101 wledge on T cell subsets, their functions in atherosclerosis and the process of T cell homing to athe

102 l-, T(H)2 cell-, and T(H)17 cell-related and atherosclerosis and/or cardiovascular risk (CCL7, FGF21,

103 xcess of extracranial vascular disease (i.e. atherosclerosis) and/or of cerebral small vessel disease

104 d in the artery wall is a key autoantigen in atherosclerosis, and activation of antigen-specific T he

105 ich has been suggested as a novel marker for atherosclerosis, and coronary artery calcification (CAC)

106 lial Nck1 and IRAK-1 staining in early human atherosclerosis, and demonstrating that disturbed flow-i

107 els of NCDs, including diet-induced obesity, atherosclerosis, and inflammation-associated colorectal

108 kappaB-mediated inflammation, which promotes atherosclerosis, and provide Nck1 as a potential target

109 Composition Study, the Multi-Ethnic Study of Atherosclerosis, and the Framingham Offspring Study, kno

110 the cardiovascular setting, like decreasing atherosclerosis, angiogenesis, intimal hyperplasia, pulm

111 Moreover, plasma biomarkers of subclinical atherosclerosis are lacking.

112 ty epidemiological investigations on carotid atherosclerosis are needed to better address the global

113 d the effect of the knowledge of presence of atherosclerosis as assessed by bilateral carotid/femoral

114 , single-cell RNA sequencing showed cerebral atherosclerosis associated with higher oligodendrocyte a

115 better address the global burden of carotid atherosclerosis at finer levels.

116 s diseases, including inflammatory diseases, atherosclerosis, autoimmunity, and cancer.

117 t the inflammatory response that accompanies atherosclerosis, autoreactive CD4(+) T-helper cells accu

118 es regarding the role of T helper 2 cells in atherosclerosis based on studies that predated the disco

119 Thus, patients with a comparable calcified atherosclerosis burden generally carry a similar risk fo

120 Atherosclerosis burden was studied by histomorphometric

121 ophils are implicated in the pathogenesis of atherosclerosis but are seldom detected in atherosclerot

122 th inflammatory changes of myeloid cells and atherosclerosis, but the underlying mechanisms are only

123 are causally involved in the pathogenesis of atherosclerosis, but their role in cerebral small vessel

124 BA, a nonreactive analogue, 2-HOBA decreases atherosclerosis by 60% in en face aortas, without changi

125 that, during hypercholesterolemia, initiate atherosclerosis by being the first to accumulate cholest

126 Here, we report an in vitro model of early atherosclerosis by fabricating and perfusing multi-layer

127 RIPK1 as a central driver of inflammation in atherosclerosis by its ability to activate the NF-kappaB

128 Molecular imaging of atherosclerosis by Magnetic Resonance Imaging (MRI) has

129 R trial (Early Identification of Subclinical Atherosclerosis by Noninvasive Imaging Research) with lo

130 We hypothesized that AHR can affect atherosclerosis by regulating phenotypic modulation of S

131 n (AHA)/American College of Cardiology (ACC) atherosclerosis cardiovascular disease (ASCVD) risk scor

132 was reduced by 50% during the progression of atherosclerosis (chronic inflammation) and 70% during en

133 lumbia FH (n=262); Nutrition, Metabolism and Atherosclerosis Clinic (n=552); and UK Biobank cohorts (

134 heart disease, rhythm disorders, subclinical atherosclerosis, coronary heart disease, heart failure,

135 y targets in inflammatory diseases including atherosclerosis, cytokine storm, and chronic autoimmune

136 lations from MESA (The Multi-Ethnic Study of Atherosclerosis) data.

137 Early atherosclerosis depends upon responses by immune cells r

138 ing mechanisms for exercise-induced coronary atherosclerosis, determine the clinical relevance of cor

139 n but also prevents dedifferentiation during atherosclerosis development, resulting in reduced plaque

140 ion, aortic aneurysm, hypercholesterolaemia, atherosclerosis, diabetic vascular complications, cardia

141 nt monocyte adhesion to NETs and accelerates atherosclerosis during endotoxinemia.

142 The impact on carotid atherosclerosis evolution is not known.

143 A substantial global burden of carotid atherosclerosis exists.

144 levels were associated with higher coronary atherosclerosis extent and severity with a 2-fold increa

145 ents, in secondary prevention strategies for atherosclerosis following coronary revascularization for

146 fluorine P as well as at different stages of atherosclerosis formation (4, 8, 16 and 20 weeks of HFD)

147 ntribute to their functions in all stages of atherosclerosis, from lesion initiation to formation of

148 protein 43 pathology, hippocampal sclerosis, atherosclerosis, gross infarcts) were associated with gl

149 potential of CD31 as a therapeutic target in atherosclerosis has been considered ever since its cloni

150 s molecule in the biologic events underlying atherosclerosis has remained controversial, resulting in

151 68; 95% CI: 0.60, 0.77), a 26% lower risk of atherosclerosis (HR: 0.74; 95% CI: 0.62, 0.88), a 28% lo

152 poorly understood, but it is associated with atherosclerosis, hypercholesterolemia, and abnormal tran

153 lar disease (>=2 vascular beds affected with atherosclerosis), impaired renal function, heart failure

154 s) or incipient (0 to 2 plaques) subclinical atherosclerosis in 2 independent clinical cohorts (PESA

155 terns, and promote vascular inflammation and atherosclerosis in a murine model.

156 short-term progression of early subclinical atherosclerosis in a substantial proportion (41.5%) of a

157 vere atherosclerosis and 13 subjects without atherosclerosis in an exploratory study.

158 onse to HFD as an endogenous defense against atherosclerosis in ApoE(-/-) model.

159 l activity and exercise training on coronary atherosclerosis in athletes who are middle-aged and olde

160 ated with metabolic dysregulation leading to atherosclerosis in chickens.

161 Increased atherosclerosis in CYP17A1 XY KO mice lacking testostero

162 nding of their biology and role in promoting atherosclerosis in diabetes and other disorders.

163 e compared molecular and cellular aspects of atherosclerosis in high-fat diet (HFD)-fed L13a KO and i

164 roxybenzylamine (2-HOBA) on HDL function and atherosclerosis in Ldlr(-/-) mice, a model of FH.

165 estrate vascular development but also drives atherosclerosis in low shear stress regions of adult art

166 Constant light exposure exacerbated atherosclerosis in male, but not female, ApoE(-/-) mice.

167 i-inflammatory therapies and the accelerated atherosclerosis in many autoimmune diseases suggest that

168 NCE MDV disrupts lipid metabolism and causes atherosclerosis in MDV-infected chickens; however, the r

169 te the function of CYP17A1 and its impact on atherosclerosis in mice.

170 determine the clinical relevance of coronary atherosclerosis in middle-aged athletes and describe str

171 to carotid artery ligation and induction of atherosclerosis in mouse models.

172 s represents an accelerated manifestation of atherosclerosis in nascent neointima after stenting, ass

173 = 360] and NEFRONA [National Observatory of Atherosclerosis in Nephrology] [n = 394]).

174 erapeutic approaches to reduce the burden of atherosclerosis in old people.

175 n MPO and the development and progression of atherosclerosis in patients with CKD is unknown.

176 CSK9 and early as well as advanced stages of atherosclerosis in psoriasis.

177 fication of stenosis and characterization of atherosclerosis in relation to myocardial ischaemia.

178 umber of cases, and risk factors for carotid atherosclerosis in the general population globally and r

179 CD11b also protected against development of atherosclerosis in the setting of hyperlipidemia via red

180 the prospective MESA (Multi-Ethnic Study of Atherosclerosis) in relationship to incident ASCVD.

181 Yet whether aging increases the risk of atherosclerosis independently of chronic hyperlipidemia

182 icates that RSV prevents the exacerbation of atherosclerosis induced periodontitis by inhibiting loca

183 Atherosclerosis is a chronic inflammatory disease of the

184 Atherosclerosis is a chronic inflammatory vascular disea

185 Atherosclerosis is a fibroinflammatory disease, and FAP

186 Background Intracranial atherosclerosis is an important cause of ischemic stroke

187 Atherosclerosis is an inflammatory condition of the arte

188 Atherosclerosis is an inflammatory disease characterized

189 our understanding of the roles of T cells in atherosclerosis is based on findings from experimental m

190 ontrast, the influence of ART on subclinical atherosclerosis is not clear.

191 However, the role of epsins in atherosclerosis is poorly understood.

192 Arterial inflammation manifested as atherosclerosis is the leading cause of mortality worldw

193 Atherosclerosis is the major cause of cardiovascular dis

194 Atherosclerosis is the process that underlies heart atta

195 Atherosclerosis is the process underlying heart attack a

196 , its role in regulating VSMC senescence and atherosclerosis is unclear.

197 ribution of dyslipidemia and inflammation in atherosclerosis is well established.

198 The MESA (Multi-Ethnic Study of Atherosclerosis) is a prospective longitudinal study of

199 emic cardiovascular burden, and specifically atherosclerosis, is lower and cerebral small vessel dise

200 tic complications, sepsis, preeclampsia, and atherosclerosis, is summarized.

201 o the underlying mechanism into large-artery atherosclerosis (LAA), cardio-embolism (CE), small-vesse

202 of all impairments was high for large artery atherosclerosis (LAA), cardioembolism (CE), and stroke o

203 lesterol efflux capacity, favorably remodels atherosclerosis lesions, supporting the potential of the

204 specific lncRNA MAARS (Macrophage-Associated Atherosclerosis lncRNA Sequence).

205 In atherosclerosis, macrophages and monocytes are exposed t

206 SM22alpha-hSIRT6/ApoE(-/-) mice had reduced atherosclerosis, markers of senescence and inflammation

207 he association between exercise and coronary atherosclerosis measured using computed tomography, disc

208 ed relative to the vast literature exploring atherosclerosis mechanisms.

209 0 participating in the Multi-Ethnic Study of Atherosclerosis (MESA) from 1996 through December 31, 20

210 ity-based samples: the Multi-Ethnic Study of Atherosclerosis (MESA) Lung Study, which involved 2531 p

211 This atherosclerosis model can identify the role of drugs on

212 Most preclinical studies in animal atherosclerosis models do not examine both sexes, and ev

213 sterol homeostasis promotes the pathology of atherosclerosis, myocardial infarction and strokes.

214 nities; n=1595), MESA (Multi-Ethnic Study of Atherosclerosis; n=6632), and PREVEND (Prevention of Ren

215 orts (PESA [Progression of Early Subclinical Atherosclerosis] [n = 360] and NEFRONA [National Observa

216 the roles of macrophage immunometabolism in atherosclerosis, new exciting concepts and potential tar

217 vasospasm, acute thrombosis and accelerated atherosclerosis, of cancer therapies have gained greater

218 ed 90 patients with non-obstructive coronary atherosclerosis on baseline computed tomography coronary

219 esterol >40 and <=100 mg/dL and a history of atherosclerosis or diabetes mellitus to icosapent ethyl

220 level of 70 mg per deciliter or higher with atherosclerosis or of 100 mg per deciliter or higher wit

221 ohol maintained an association with coronary atherosclerosis (OR 1.02, 95% CI, 1.01-1.03, P value = 5

222 .95, P value = 1.9 x 10-6), and large artery atherosclerosis (OR = 2.4, 95% CI, 1.41-4.07, P value =

223 blished the role of treating inflammation in atherosclerosis, our understanding of endothelial activa

224 T and B lymphocytes, and lead to exacerbated atherosclerosis outcomes.

225 We studied 6507 Multi-Ethnic Study of Atherosclerosis participants aged 45 to 84 without basel

226 First, in 5481 MESA (Multi-Ethnic Study of Atherosclerosis) participants, the cross-sectional (exam

227 cient to rescue the hypercholesterolemia and atherosclerosis phenotypes seen in Apoe knockout mice.

228 ial contributory role of the presentation of atherosclerosis pictures, providing helpful information

229 ells likely to be detrimental for late-stage atherosclerosis plaque pathogenesis.

230 modalities (n = 432) also showed significant atherosclerosis progression (median: 1 plaque [interquar

231 Imaging detected short-term (3-year) atherosclerosis progression in 41.5% of participants (26

232 in an apolipoprotein E deficient (ApoE(-/-)) atherosclerosis progression murine model, T1317-sHDL sho

233 entation of effective therapies that prevent atherosclerosis progression, cardiac remodelling, and th

234 lation, resulting in foam cell formation and atherosclerosis progression.

235 ar mechanics, proliferation and migration in atherosclerosis progression.

236 cells, all of which play different roles in atherosclerosis progression.

237 r understanding of endothelial activation at atherosclerosis-prone sites remains limited.

238 ic efficacy of MNDEBs was evaluated using an atherosclerosis rabbit model.

239 of monocytes from patients with established atherosclerosis reduced the production of inflammatory c

240 progression, and whether they contribute to atherosclerosis regression is not known.

241 Using multiple independent mouse models of atherosclerosis regression, we demonstrate that an incre

242 lerated atherosclerosis and a higher risk of atherosclerosis-related cardiovascular events.

243 markers have been previously associated with atherosclerosis-related risk factors, but the nature of

244 We quantified 12 atherosclerosis-relevant phenotypes related to calcifica

245 geting a specific chemokine/receptor axis in atherosclerosis remains challenging.

246 ow SMCs contribute to the pathophysiology of atherosclerosis remains elusive.

247 s a major driver of various diseases such as atherosclerosis, rheumatoid arthritis and type 2 diabete

248 2013-2016) and longitudinal analyses of the Atherosclerosis Risk in Communities (ARIC) Study (baseli

249 ed 45 through 79 years, participating in the Atherosclerosis Risk in Communities (ARIC) study and 239

250 A previous Atherosclerosis Risk in Communities (ARIC) Study article

251 s (mean age, 62.5 years; 52.4% women) in the Atherosclerosis Risk in Communities (ARIC) study who com

252 y of Kidney Disease and Hypertension and the Atherosclerosis Risk in Communities (ARIC) Study.

253 c status (SES) with incident dementia in the Atherosclerosis Risk in Communities cohort.

254 We used the Atherosclerosis Risk in Communities study heart failure

255 Black and 8,707 White participants of the US Atherosclerosis Risk in Communities study using multivar

256 QT interval genes, SCN5A and NOS1AP, in the Atherosclerosis Risk in Communities Study, as a positive

257 cipants at the baseline (1996-1998) from the Atherosclerosis Risk in Communities study, we quantified

258 outcomes through 2017 were obtained from the Atherosclerosis Risk in Communities Study.

259 prospective epidemiologic cohort study, the Atherosclerosis Risk in Communities study.

260 sk of ESKD among individuals enrolled in the Atherosclerosis Risk in Communities study; the analysis

261 In the ARIC (Atherosclerosis Risk In Communities) cohort, VTE risk as

262 Among 12,149 ARIC (Atherosclerosis Risk In Communities) participants (54 ye

263 ase: DHS (Dallas Heart Study; n=2535), ARIC (Atherosclerosis Risk in Communities; n=1595), MESA (Mult

264 gy for lowering inflammatory status and thus atherosclerosis risk, reinforcing public health policies

265 edict the presence and extent of subclinical atherosclerosis (SA) in young, asymptomatic individuals.

266 utrophils and monocytes), thereby increasing atherosclerosis severity, even when other common risk fa

267 /RXR activation (- log[P-value] = 30-31) and atherosclerosis signaling (- log[P-value] = 10-11) were

268 wledge by the participant of the presence of atherosclerosis significantly boosted the intervention e

269 both sexes and to address age in mechanistic atherosclerosis studies are missed opportunities to unco

270 3,514 PESA (Progression of Early Subclinical Atherosclerosis) study participants (45.7 +/- 4.2 years

271 n the PESA (Progression of Early Subclinical Atherosclerosis) study.

272 he apolipoprotein E knock-out mouse model of atherosclerosis, suggest greater risk where there is an

273 AK-1) in NF-kappaB-mediated inflammation and atherosclerosis susceptibility.

274 significantly greater regression of carotid atherosclerosis than an LDL-C target of 90 to 110 mg/dL.

275 In stable atherosclerosis, the combination of aspirin plus rivarox

276 A central feature of atherosclerosis, the most prevalent chronic vascular dis

277 rphism in the incidence and complications of atherosclerosis, there are relatively limited data in th

278 (MIF) is an atypical chemokine that promotes atherosclerosis through CXC-motif chemokine receptor-4 (

279 linical management of athletes with coronary atherosclerosis to guide physicians in clinical decision

280 tients with established multivessel coronary atherosclerosis underwent (18)F-fluoride PET-computed to

281 Using data from the Multi-Ethnic Study of Atherosclerosis (United States, 2000-2015), 6,527 racial

282 dy sought to study short-term progression of atherosclerosis using different noninvasive imaging tech

283 ciated with developing an effective and safe atherosclerosis vaccine.

284 tribute to CVD in HIV/CMV coinfection and in atherosclerosis via CX3CR1-mediated trafficking and CD2/

285 anges in myeloid cell functions that promote atherosclerosis via inflammation, including a potential

286 gests that an experimental MI can accelerate atherosclerosis via monocytosis.

287 uscle cells (SMCs) play significant roles in atherosclerosis via phenotypic switching, a pathological

288 sis vintage are characterized by accelerated atherosclerosis, volume overload, and progressive left v

289 yme-linked immunosorbent assay, and coronary atherosclerosis was assessed using computed tomographic

290 Atherosclerosis was induced in miR-144 knockout mice by

291 Hardening of the arteries (atherosclerosis) was linked to dementia long ago, but su

292 In MESA (the Multi-Ethnic Study of Atherosclerosis), we evaluated the associations of basel

293 is review article, part of the Compendium on Atherosclerosis, we introduce the concepts of (1) intrac

294 e function of autoreactive CD4(+) T cells in atherosclerosis, we used a novel tetramer of major histo

295 unity and to inflammatory disease, including atherosclerosis, where monocyte egress into the intimal

296 c reduction of endothelial IP3R1 accelerates atherosclerosis, whereas deletion of endothelial epsins

297 s, disturbed flow- and high fat diet-induced atherosclerosis, whereas Nck2 deletion did not.

298 3 can drive inflammation in vivo, such as in atherosclerosis, while in other scenarios they can perfo

299 ed definition of cell communities at play in atherosclerosis will facilitate cell-based mapping of no

300 EN-PESA (Progression of Early Subclinical Atherosclerosis) yielded a c-statistic of 0.88 for the p