ライフサイエンスコーパス: atherogenesis

1 ar helper-germinal center B-cell axis during atherogenesis.

2 FPR2 and its resolving ligand annexin A1 in atherogenesis.

3 flammatory mechanism that may participate in atherogenesis.

4 migration, which is an important process in atherogenesis.

5 both had no detectable phenotypic impact on atherogenesis.

6 NOS uncoupling, endothelial dysfunction, and atherogenesis.

7 mechanisms may contribute to HIV-associated atherogenesis.

8 rbonyls also contributes to inflammation and atherogenesis.

9 events given its important etiologic role in atherogenesis.

10 endogenous danger signal that contributes to atherogenesis.

11 ports an important role of SMC plasticity in atherogenesis.

12 ophages and the arterial wall contributes to atherogenesis.

13 n factor participates in the acceleration of atherogenesis.

14 own expression and function of C5L2 in human atherogenesis.

15 ) macrophages to the aortic wall and trigger atherogenesis.

16 poprotein E(-/-) (ApoE(-/-)) mice attenuates atherogenesis.

17 odontal disease and to promote or exacerbate atherogenesis.

18 phagocytosis, thus possibly contributing to atherogenesis.

19 ols the expression of many genes involved in atherogenesis.

20 hat cytomegalovirus (CMV) may be involved in atherogenesis.

21 understanding how adaptive immunity affects atherogenesis.

22 iated with inflammation, hyperlipidemia, and atherogenesis.

23 ffects of n-3 fatty acids (FA) on inhibiting atherogenesis.

24 cells and other bone marrow-derived cells to atherogenesis.

25 arterial system protects arterial wall from atherogenesis.

26 ent, hematopoiesis, vascular remodeling, and atherogenesis.

27 lanine aminotransferase (ALT) and markers of atherogenesis.

28 n atherosclerotic lesions and is involved in atherogenesis.

29 r lipoprotein particles may actively enhance atherogenesis.

30 ulators that control foam cell formation and atherogenesis.

31 diverse roles of immune cells implicated in atherogenesis.

32 med vascular wall and absence of FKN reduces atherogenesis.

33 rns, thus affecting their susceptibility for atherogenesis.

34 ets, smooth muscle cells, and HDL to promote atherogenesis.

35 Oxidized LDL (ox-LDL) is a key factor in atherogenesis.

36 osclerotic plaques, are crucial promoters of atherogenesis.

37 pidemia and exacerbated Western diet-induced atherogenesis.

38 atherosclerotic lesions, the effects promote atherogenesis.

39 hages and bone marrow-derived cells mediates atherogenesis.

40 hages and may be important for regulation of atherogenesis.

41 smooth muscle cells (VSMCs) and superimposed atherogenesis.

42 ant enzyme, the deficiency of which promotes atherogenesis.

43 Wnt pathway proteins occurs in or regulates atherogenesis.

44 tes the importance of IL-1R/TLR signaling in atherogenesis.

45 and represents a therapeutic target in early atherogenesis.

46 upporting a link between innate immunity and atherogenesis.

47 t pathways in multiple processes involved in atherogenesis.

48 tion of multiple gene pathways implicated in atherogenesis.

49 ceptor-deficient mice (Ldlr(-/-)) from early atherogenesis.

50 sfunction, at least in the initial phases of atherogenesis.

51 as a valuable model to study early events of atherogenesis.

52 has been developed to study early events of atherogenesis.

53 of COX-2 in macrophages and T cells (TCs) to atherogenesis.

54 n macrophages, implicating monocytic Nox4 in atherogenesis.

55 n apolipoprotein E knockout mice accelerates atherogenesis.

56 reduced numbers of active T cells and resist atherogenesis.

57 and innate immunity play important roles in atherogenesis.

58 pathway is necessary for endotoxin-mediated atherogenesis.

59 l regulation of inflammation associated with atherogenesis.

60 nals within the vasculature, a key factor in atherogenesis.

61 he role of triglyceride-rich lipoproteins in atherogenesis.

62 subsets and commit to specific functions in atherogenesis.

63 nd inflammatory leukocyte recruitment during atherogenesis.

64 tes, contribute substantially to accelerated atherogenesis.

65 differentiation with possible relevance for atherogenesis.

66 -specific epitopes play an important role in atherogenesis.

67 resistance, proatherogenic dyslipidemia, and atherogenesis.

68 rophage phenotypic diversity is important in atherogenesis.

69 n the liver, which could then play a role in atherogenesis.

70 gioplasty, vein graft intimal thickening and atherogenesis.

71 efine the role of endogenous miR-146a during atherogenesis.

72 RNA miR-100 during vascular inflammation and atherogenesis.

73 phage retention at inflammatory sites during atherogenesis.

74 clerotic lesions suggests its involvement in atherogenesis.

75 l (EC) inflammation, one of the hallmarks of atherogenesis.

76 may permit further arterial inflammation and atherogenesis.

77 larly abdominal adiposity, dyslipidemia, and atherogenesis.

78 (rRNA) maturation and modulating pathways of atherogenesis.

79 el wall and in the circulation contribute to atherogenesis.

80 nfers hyperpinocytosis to macrophages during atherogenesis.

81 he causal role that VSMC senescence plays in atherogenesis.

82 ciency in monocytes and macrophages promotes atherogenesis.

83 nsities of CD11d to macrophage arrest during atherogenesis.

84 matory molecule expression, and experimental atherogenesis.

85 h dual (protective and detrimental) roles in atherogenesis.

86 nduced endothelial cell activation and early atherogenesis.

87 rotic arteries, suggesting its role in human atherogenesis.

88 tributes to the development of plaque during atherogenesis.

89 factor in the initiation and progression of atherogenesis.

90 of Akt1 during the initial and late steps of atherogenesis.

91 at hyperglycemic excursions are important in atherogenesis, 1,5-AG may provide independent informatio

92 of the innate and adaptive immune systems in atherogenesis; 2) the nature of many antigens that have

93 atherogenic factors, is a pivotal process in atherogenesis, a disorder in which monocytes adhere to e

94 sCD14 and sCD163 may play important roles in atherogenesis among HIV+ persons.

95 uld contribute to the pathogenic sequelae of atherogenesis and acute coronary events.

96 Indeed, deletion of mPGES-1 retards atherogenesis and angiotensin II-induced aortic aneurysm

97 factors impact processes highly relevant to atherogenesis and are involved in pathways common to sca

98 is an essential feedback loop that controls atherogenesis and athero-inflammation.

99 ploration of new avenues in the treatment of atherogenesis and atherothrombosis.

100 lvement of neutrophil extracellular traps in atherogenesis and atherothrombosis.

101 ch triggers of innate immunity appear during atherogenesis and by which pathways they can contribute

102 ct of oxidation products and inflammation on atherogenesis and carcinogenesis.

103 which suggests potential health benefits for atherogenesis and carcinogenesis.

104 To assess factors that promote atherogenesis and cardiovascular disease (CVD) in rheuma

105 s and are recognized as key risk factors for atherogenesis and cardiovascular disease, particularly i

106 ese cells participate in different stages of atherogenesis and comment on complexities, controversies

107 ne A(2) and prostaglandin (PG)E(2), promotes atherogenesis and exerts a restraint on enzyme expressio

108 Here, we investigated the role of Cdnk2b in atherogenesis and found that in a mouse model of atheros

109 des an update of the role of inflammation in atherogenesis and highlights how translation of these ad

110 le of alternatively activated macrophages in atherogenesis and highlights the impact of integrin alph

111 zed the cellular and molecular mechanisms of atherogenesis and identified specific aortic autoantigen

112 L5/LOX-1 complex may play a critical role in atherogenesis and illuminate important targets for disea

113 This ratio changed during atherogenesis and in different areas of the lesions, ref

114 e inflammatory state in subjects at risk for atherogenesis and in patients with myocardial infarction

115 LDL-C), which is associated with accelerated atherogenesis and increased cardiovascular risk.

116 intake of alpha-linolenic acid (ALA) reduces atherogenesis and inhibits arterial thrombosis.

117 Platelets have a key role in atherogenesis and its complications.

118 direct gateway to the processes involved in atherogenesis and its complications.

119 study examined the causative role of HHcy in atherogenesis and its effect on inflammatory MC differen

120 ing evidence supporting the role of LOX-1 in atherogenesis and its major complication, myocardial isc

121 Inflammatory pathways drive atherogenesis and link conventional risk factors to athe

122 innate and adaptive immunity operate during atherogenesis and link many traditional risk factors to

123 +)), and each may play distinct roles during atherogenesis and myocardial infarction.

124 hts possible mechanisms of neutrophil-driven atherogenesis and plaque destabilization.

125 vations provide new mechanistic insight into atherogenesis and provide a novel therapeutic opportunit

126 een IFN-gamma and TNF- alpha in inflammatory atherogenesis and provide rationale for dual cytokine an

127 for a causal role for col(V) autoimmunity in atherogenesis and providing insights into the potential

128 ins, such as fibronectin, occur early during atherogenesis and regulate shear stress-induced endothel

129 erpins vasculo-occlusive pathologies such as atherogenesis and restenosis after percutaneous coronary

130 o improved understanding of inflammation and atherogenesis and suggest new approaches to diagnosis an

131 elped to clarify the role of inflammation in atherogenesis and suggested new diagnostic modalities an

132 ions that macrophages proliferate throughout atherogenesis and that self-renewal is critical for main

133 s of certain inflammatory processes of early atherogenesis and the in vivo function of vascular cells

134 Understanding the pathophysiology of atherogenesis and the progression of atherosclerosis hav

135 tabolic stress may be a major contributor to atherogenesis and the progression of atherosclerotic pla

136 ertensive response to Ang II and accelerated atherogenesis and thrombogenesis.

137 oid receptor also predisposes to accelerated atherogenesis and thrombosis in mice.

138 ssociated cardiovascular risk, mechanisms of atherogenesis and thrombosis, clinical effects of smokin

139 Platelets play a critical role in atherogenesis and thrombosis-mediated myocardial ischemi

140 othelial KLF4 is an essential determinant of atherogenesis and thrombosis.

141 ssess the importance of macrophage mitoOS in atherogenesis and to explore the underlying molecular me

142 oxidized low-density lipoprotein (OxLDL) in atherogenesis and to test the efficacy of human antibody

143 diators of cardiovascular disease, promoting atherogenesis and unstable atherosclerotic plaque.

144 adib has been shown to be protective against atherogenesis and vascular leakage in diabetic and hyper

145 Macrophage inflammation marks all stages of atherogenesis, and AMPK is a regulator of macrophage inf

146 ds to endothelial dysfunction, hypertension, atherogenesis, and aneurysm.

147 ocal accumulation of ATP and ADP at sites of atherogenesis, and eventually, the exacerbation of ather

148 se 1 (mPGES-1) confers analgesia, attenuates atherogenesis, and fails to accelerate thrombogenesis, w

149 of a link between periodontal infections and atherogenesis, and have identified biological pathways b

150 C proliferation may be beneficial throughout atherogenesis, and not just in advanced lesions, whereas

151 he crucial role of leukocyte accumulation in atherogenesis, and the importance of Ccl5 chemokine rece

152 may play a role in the abnormal thrombosis, atherogenesis, and vasorelaxation that are characteristi

153 prandial excursions in serum lipoproteins to atherogenesis are less well-characterized.

154 the direct effects of DSBs in VSMCs seen in atherogenesis are unknown.

155 The cell selective roles of mPGES-1 in atherogenesis are unknown.

156 D11c in hypercholesterolemia and its role in atherogenesis are unknown.

157 cular smooth muscle cell (VSMC) function and atherogenesis are yet to be entirely elucidated.

158 iable risk factors appear to influence early atherogenesis as measured by coronary wall thickness and

159 cessive platelet production, thrombosis, and atherogenesis, as occurs in human myeloproliferative syn

160 ion into the arterial wall are key events in atherogenesis associated with hypercholesterolemia.

161 of RAGE was able to reduce inflammation and atherogenesis associated with MG exposure.

162 ing protein profilin-1 (pfn) plays a role in atherogenesis because pfn heterozygote mice (PfnHet) exh

163 ocyte-derived macrophages play a key role in atherogenesis because their transformation into foam cel

164 in models of disturbed flow and diet-induced atherogenesis but did not affect smooth muscle incorpora

165 s clearly influence vascular remodelling and atherogenesis but important, unrelated actions limit the

166 dem peptide Pro, effectively inhibited early atherogenesis but was ineffective against more mature le

167 VSMC DNA damage has minimal effects on atherogenesis, but alters plaque phenotype inhibiting fi

168 elial and smooth muscle cells participate in atherogenesis, but it is unclear whether other mesenchym

169 hese angiogenic cell populations may promote atherogenesis, but limited data are available on their r

170 and adaptive immune responses contribute to atherogenesis, but the identity of atherosclerosis-relev

171 receptor (IGF1R) and play a pivotal role in atherogenesis, but the potential effects of IGF-1 on the

172 vidence suggests that HDL might also inhibit atherogenesis by combating inflammation.

173 hear stress conditions and may promote early atherogenesis by enhancing vascular permeability.

174 receptor had no effect on the attenuation of atherogenesis by mPGES-1 deletion in the low-density lip

175 Promotion of atherogenesis by postnatal COX-2 deletion affords a mech

176 OGG1 plays a protective role in atherogenesis by preventing excessive inflammasome activ

177 ys a proatherogenic inflammatory role during atherogenesis by promoting monocyte/macrophage recruitme

178 ions and it protects against early stages of atherogenesis by removing toxic aldehydes generated in o

179 glucose uptake in cells that participate in atherogenesis by stimuli relevant to this process, to ga

180 CXCL4 may promote atherogenesis by suppressing CD163 in macrophages, which

181 Atherogenesis can be viewed as a chronic, maladaptive in

182 uggest that efferocytosis is impaired during atherogenesis caused by dysregulation of so-called eat m

183 Understanding how leukocytes impact atherogenesis contributes critically to our concept of a

184 In vivo, JNK activation at sites of early atherogenesis correlates with the deposition of fibronec

185 ammation and innate and adaptive immunity in atherogenesis, emerging clinical applications of oxidati

186 sis and inflammation are key determinants in atherogenesis, exemplified by the requirement of lipid-l

187 to mast cells, many cell types implicated in atherogenesis express FcepsilonR1, but whether IgE has a

188 necrotic core, but their appearance late in atherogenesis had been thought to disqualify them as pri

189 To date, the role of HCMV in atherogenesis has been explored only in static condition

190 To date, its role in atherogenesis has not been explored.

191 distribution of various lipid species during atherogenesis has remained unexplored.

192 and the direction of impact of this gene in atherogenesis have not been shown in relevant model syst

193 Experimental models of atherogenesis have provided a growing body of informatio

194 onic inflammation is a critical component of atherogenesis, however, reliable human translational mod

195 bed flow, whereas laminar flow protects from atherogenesis; however, the mechanisms involved are not

196 To mimic inflammation during atherogenesis, human myeloperoxidase was incubated with

197 e observed that myeloid CAPN6 contributed to atherogenesis in a murine model of bone marrow transplan

198 is a proinflammatory cytokine that promotes atherogenesis in animal models, but its role in plaque d

199 Therefore, TLR7 contributes to atherogenesis in Apoe (-/-) mice by regulating lesion an

200 of endothelial-specific Tie1 attenuation on atherogenesis in Apoe-/- mice and found a dose-dependent

201 n 2 (Plin2), and investigated its effects on atherogenesis in apolipoprotein E-deficient (ApoE(-/-))

202 erlipidemic mice, COX-2 deletion accelerated atherogenesis in both genders, with lesions exhibiting l

203 Inhibiting S100A8/A9 also decreased atherogenesis in diabetic mice.

204 le to increase vascular adhesion and augment atherogenesis in euglycemic apolipoprotein E knockout mi

205 selective cathepsin S inhibition attenuates atherogenesis in hypercholesterolemic mice with CRD.

206 stnatal global deletion of COX-2 accelerates atherogenesis in hyperlipidemic mice, a process delayed

207 In conclusion, myeloid cell mPGES-1 promotes atherogenesis in hyperlipidemic mice, coincident with iN

208 n resistance and hyperglycemia contribute to atherogenesis in key target tissues (liver, vessel wall,

209 y nitrate as a preventative strategy against atherogenesis in larger cohorts.

210 E2, elevated blood pressure, and accelerated atherogenesis in Ldlr knockout mice.

211 Heat shock protein-65 immunization enhanced atherogenesis in Ldlr(-/-) mice, but Ldlr(-/-) Cd74(-/-)

212 nce, proatherogenic dyslipidemia, and aortic atherogenesis in Ldlr(-/-) mice.

213 at macrophage alpha1AMPK deficiency promotes atherogenesis in LDLRKO mice and is associated with enha

214 PGs, TC composition in lymphatic organs, and atherogenesis in low-density lipoprotein receptor knocko

215 ic lesion analysis revealed markedly reduced atherogenesis in Mac-mPGES-1-KOs, which was concomitant

216 vascular cells does not detectably influence atherogenesis in mice.

217 ow plasma cholesterol levels and in reducing atherogenesis in mice.

218 humans and if loss of Id3 function modulated atherogenesis in mice.

219 ably influence TC development or function or atherogenesis in mice.

220 tralizing antibodies permitted inhibition of atherogenesis in mice.

221 jective was to delineate the role of Ccr6 in atherogenesis in the apolipoprotein E-deficient (ApoE(-/

222 re, we evaluated the contribution of CD39 to atherogenesis in the apolipoprotein E-deficient (ApoE-de

223 Here, we investigated the role of CSN5 in atherogenesis in vivo by using mice with myeloid-specifi

224 s an ideal human model to study inflammatory atherogenesis in vivo.

225 se cholesterol transport, 2 key mediators of atherogenesis, in SPT subunit 2-haploinsufficient (Sptlc

226 e immune system contributes to all phases of atherogenesis, including well-known inflammatory reactio

227 nstrated that sortilin also directly affects atherogenesis, independent of its regulatory role in lip

228 mune and inflammatory responses can modulate atherogenesis independently of lipid levels.

229 -2 (COX-2), prostacyclin (PGI(2)), restrains atherogenesis, inhibition and deletion of COX-2 have yie

230 ion of macrophages, which play a key role in atherogenesis, inhibits plaque formation.

231 Although atherogenesis is accelerated in global COX-2 knockouts,

232 in endothelial and/or monocytic cells during atherogenesis is counterbalanced by an opposite effect r

233 ole of Th1, Th2, and T-regulatory subsets in atherogenesis is established, the involvement of IL-17A-

234 o date, the role for interleukin (IL)-17A in atherogenesis is not well defined.

235 Atherogenesis is retarded by deletion of the FP, despite

236 A critical event in atherogenesis is the interaction of macrophages with sub

237 O deficiency affects immune responses during atherogenesis is unknown and we explored potential mecha

238 ever, the role of SPT in macrophage-mediated atherogenesis is unknown.

239 e-related miRs in the immune response during atherogenesis is unknown.

240 However, its effect on atherogenesis is unknown.

241 our current understanding of HIV-associated atherogenesis is very limited and has largely been obtai

242 is known to be most closely associated with atherogenesis, is more preferentially glycated in vivo a

243 w EC process LDL and whether this influences atherogenesis, is unclear.

244 activating protein (FLAP) did not influence atherogenesis, it attenuated the proatherogeneic impact

245 idence supporting the vital role of LOX-1 in atherogenesis keeps accumulating, there is growing inter

246 S. pneumoniae infection triggered atherogenesis, led to systemic induction of interleukin

247 anding of the molecular pathways involved in atherogenesis, lesion progression, and the mechanisms un

248 and flow patterns play an essential role in atherogenesis: lesions form only at locations where flui

249 alidation of the association of Adamts7 with atherogenesis, likely through modulation of vascular cel

250 In atherogenesis, macrophage foam cell formation is modulat

251 During the inflammatory response that drives atherogenesis, macrophages accumulate progressively in t

252 ion is at least as important as oxidation in atherogenesis may lead to improvements in our understand

253 nsitive to cigarette smoking and involved in atherogenesis, may be a part of the biological link betw

254 e combined absence of apoE and LRP1 promoted atherogenesis more than did macrophage apoE deletion alo

255 e accumulating lipids in different stages of atherogenesis, notably the spatial segregation of choles

256 clear whether mtDNA damage directly promotes atherogenesis or is a consequence of tissue damage, whic

257 s that may (i) lead to periodontitis-induced atherogenesis, or (ii) result in treatment-induced reduc

258 ocytosis in childhood obesity contributes to atherogenesis over the years.

259 PK)-stimulated inflammation is implicated in atherogenesis, plaque destabilization, and maladaptive p

260 impact the multifactorial steps involved in atherogenesis, plaque progression and instability.

261 d in diverse vascular pathologies, including atherogenesis, plaque stabilization, and neointimal hype

262 lved in immunity and inflammation and impact atherogenesis, primarily by modulating immune and inflam

263 phagy induction and the role of autophagy in atherogenesis remain to be determined.

264 atheroma; however, their functional roles in atherogenesis remain undefined.

265 The role of IL-17 in atherogenesis remains controversial.

266 ted in vascular pathologies, but its role in atherogenesis remains elusive.

267 inflammatory pathologies, but their role in atherogenesis remains elusive.

268 inflammatory response in macrophages during atherogenesis remains unclear.

269 escent cells, but the role of these cells in atherogenesis remains unclear.

270 However, its impact on atherogenesis remains unknown.

271 herapy had protective effects and attenuated atherogenesis, resulting in a decrease of plaque area by

272 These data suggest that during atherogenesis, SAA can amplify the involvement of smooth

273 Key molecular events in atherogenesis such as oxidative modification of lipoprot

274 stablish CD39 as a regionalized regulator of atherogenesis that is driven by shear stress.

275 In view of the role of oxidized lipids in atherogenesis, the adverse effects of lipoxygenase-media

276 altering systemic lipid metabolism such that atherogenesis, the formation of plaque, is curtailed.

277 ough deletion of the PGI(2) receptor fosters atherogenesis, the importance of COX-2 during developmen

278 both innate and adaptive arms of immunity in atherogenesis, their interplay, and the balance of stimu

279 lar and subcellular features associated with atherogenesis, thrombosis and responses to interventiona

280 citrus flavonoids show marked suppression of atherogenesis through improved metabolic parameters as w

281 LA2) has been hypothesized to be involved in atherogenesis through pathways related to inflammation.

282 haematopoietic ANGPTL4 deficiency increases atherogenesis through regulating myeloid progenitor cell

283 methylation of NOS1 has a plausible role in atherogenesis through regulation of NO production, altho

284 Interleukin-18 (IL18) participates in atherogenesis through several putative mechanisms.

285 is increases aortic arch inflammation during atherogenesis through the induction of aortic chemokines

286 mportant mechanism by which EC contribute to atherogenesis under hyperlipidemic conditions.

287 Here we report the effect of Pak1 on atherogenesis using atherosclerosis-prone apolipoprotein

288 icking, metabolism, vascular deposition, and atherogenesis using transgenic mice expressing human alp

289 ngiotensin II (AngII) promotes hypertension, atherogenesis, vascular aneurysm and impairs post-ischem

290 have explored novel mechanisms of ethanol on atherogenesis via effects on HDL composition and functio

291 e cell (VSMC) proliferation is implicated in atherogenesis, VSMCs in advanced plaques and cultured fr

292 Atherogenesis was attenuated when MacKOs were crossed in

293 Unexpectedly, atherogenesis was not changed in mice with ubiquitous Pa

294 peripheral insulin resistance contribute to atherogenesis, we crossed mice deficient for the LDL rec

295 sis and the key role of T cell activation in atherogenesis, we sought to understand the role of TLR s

296 ng evidence that inflammation contributes to atherogenesis, we studied the effect of human neutrophil

297 rthermore, essential mechanisms of IL-17A in atherogenesis were studied in vitro.

298 at MLN4924 may be useful in preventing early atherogenesis, whereas selectively promoting CSN5-mediat

299 post-translational modifications of Cx43 in atherogenesis, which could be of particular importance,

300 pe 2 diabetes is associated with accelerated atherogenesis, which may result from a combination of fa