ライフサイエンスコーパス: atherogenesis

1 tasis, tumor development, wound healing, and atherogenesis.

2 larly abdominal adiposity, dyslipidemia, and atherogenesis.

3 (rRNA) maturation and modulating pathways of atherogenesis.

4 el wall and in the circulation contribute to atherogenesis.

5 nfers hyperpinocytosis to macrophages during atherogenesis.

6 uated mitochondrial dysfunction, and reduced atherogenesis.

7 he causal role that VSMC senescence plays in atherogenesis.

8 ciency in monocytes and macrophages promotes atherogenesis.

9 emokine CC-motif ligand 5 (CCL5) involved in atherogenesis.

10 matory molecule expression, and experimental atherogenesis.

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

12 nduced endothelial cell activation and early atherogenesis.

13 rotic arteries, suggesting its role in human atherogenesis.

14 mpaired mitochondrial function, and enhanced atherogenesis.

15 tributes to the development of plaque during atherogenesis.

16 factor in the initiation and progression of atherogenesis.

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

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

19 FPR2 and its resolving ligand annexin A1 in atherogenesis.

20 nflammation, biological processes central to atherogenesis.

21 flammatory mechanism that may participate in atherogenesis.

22 migration, which is an important process in atherogenesis.

23 both had no detectable phenotypic impact on atherogenesis.

24 NOS uncoupling, endothelial dysfunction, and atherogenesis.

25 oinflammatory cytokine for periodontitis and atherogenesis.

26 rbonyls also contributes to inflammation and atherogenesis.

27 events given its important etiologic role in atherogenesis.

28 endogenous danger signal that contributes to atherogenesis.

29 ports an important role of SMC plasticity in atherogenesis.

30 ophages and the arterial wall contributes to atherogenesis.

31 n factor participates in the acceleration of atherogenesis.

32 own expression and function of C5L2 in human atherogenesis.

33 ascular mitochondrial function to accelerate atherogenesis.

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

35 odontal disease and to promote or exacerbate atherogenesis.

36 phagocytosis, thus possibly contributing to atherogenesis.

37 ols the expression of many genes involved in atherogenesis.

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

39 understanding how adaptive immunity affects atherogenesis.

40 iated with inflammation, hyperlipidemia, and atherogenesis.

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

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

43 arterial system protects arterial wall from atherogenesis.

44 ent, hematopoiesis, vascular remodeling, and atherogenesis.

45 lanine aminotransferase (ALT) and markers of atherogenesis.

46 attenuate Ang II-dependent inflammation and atherogenesis.

47 n atherosclerotic lesions and is involved in atherogenesis.

48 rovides a potential therapeutic strategy for atherogenesis.

49 ulators that control foam cell formation and atherogenesis.

50 med vascular wall and absence of FKN reduces atherogenesis.

51 rns, thus affecting their susceptibility for atherogenesis.

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

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

54 osclerotic plaques, are crucial promoters of atherogenesis.

55 atherosclerotic lesions, the effects promote atherogenesis.

56 hages and bone marrow-derived cells mediates atherogenesis.

57 hages and may be important for regulation of atherogenesis.

58 smooth muscle cells (VSMCs) and superimposed atherogenesis.

59 ant enzyme, the deficiency of which promotes atherogenesis.

60 Wnt pathway proteins occurs in or regulates atherogenesis.

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

62 upporting a link between innate immunity and atherogenesis.

63 t pathways in multiple processes involved in atherogenesis.

64 tion of multiple gene pathways implicated in atherogenesis.

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

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

67 L) causes HDL dysfunction and contributes to atherogenesis.

68 has been developed to study early events of atherogenesis.

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

70 n macrophages, implicating monocytic Nox4 in atherogenesis.

71 ore the induction of hyperlipidemia enhances atherogenesis.

72 c and may be a source of vasa vasorum during atherogenesis.

73 ing a vicious circle to persistently promote atherogenesis.

74 dlr(-/-) mice under high-fat diet and limits atherogenesis.

75 hances systemic inflammation and accelerates atherogenesis.

76 erculosis differ from those operating during atherogenesis.

77 ing pathways that could link risk factors to atherogenesis.

78 diverse roles of immune cells implicated in atherogenesis.

79 phage retention at inflammatory sites during atherogenesis.

80 nsities of CD11d to macrophage arrest during atherogenesis.

81 mechanisms may contribute to HIV-associated atherogenesis.

82 ) macrophages to the aortic wall and trigger atherogenesis.

83 r lipoprotein particles may actively enhance atherogenesis.

84 pidemia and exacerbated Western diet-induced atherogenesis.

85 taxis is a crucial event in inflammation and atherogenesis.

86 and represents a therapeutic target in early atherogenesis.

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

88 nd inflammatory leukocyte recruitment during atherogenesis.

89 gioplasty, vein graft intimal thickening and atherogenesis.

90 vated by SIRT6, and how VSMC SIRT6 regulates atherogenesis.

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

92 RNA miR-100 during vascular inflammation and atherogenesis.

93 clerotic lesions suggests its involvement in atherogenesis.

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

95 may permit further arterial inflammation and atherogenesis.

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

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

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

99 udies investigated the effect of a statin on atherogenesis affected by severe periodontitis.

100 e maintenance and VSMC lifespan and inhibits atherogenesis, all dependent on its deacetylase activity

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

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

103 ential SMILR-targeting intervention to limit atherogenesis and adverse vascular remodeling.

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

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

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

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

108 lvement of neutrophil extracellular traps in atherogenesis and atherothrombosis.

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

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

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

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

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

114 opose P5 peptide as a potential inhibitor of atherogenesis and diabetes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 el, T1317-sHDL showed superior inhibition of atherogenesis and reduced hypertriglyceridemia side effe

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

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

136 ch also contributes to vascular remodelling, atherogenesis and restenosis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

156 spholipase which has a role in inflammation, atherogenesis, and host defense.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

180 in lipid-induced inflammasome activation and atherogenesis by taking advantage of 3 different small m

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

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

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

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

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

189 the role of macrophage-specific FLNA during atherogenesis has not been explored.

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

191 Concepts of atherogenesis have evolved considerably with time.

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 Studies of the cell and molecular biology of atherogenesis have provided considerable insight into th

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

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

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

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

199 ith WT RAGE362-404 restored Ang II-dependent atherogenesis in Ager/Apoe-KO mice, without restoring li

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

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

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

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

204 stigated the effect of rosuvastatin (RSV) on atherogenesis in Apolipoprotein E-deficient mice receivi

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

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

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

208 lncRNA, lncRNA-CCL2, which may contribute to atherogenesis in humans.

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

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

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

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

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

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

215 Caspase1(-/-) ( Casp1(-/-)) mice accelerates atherogenesis in Ldlr(-/-) mice.

216 hat absence of Cav1 significantly suppressed atherogenesis in Ldlr(-/-)eNOS(-/-) mice, demonstrating

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

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

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

220 tralizing antibodies permitted inhibition of atherogenesis in mice.

221 vascular cells does not detectably influence atherogenesis in mice.

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

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

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

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

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

227 r intrinsic factors by which ageing promotes atherogenesis - in particular, the effects on mitochondr

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

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

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

231 lesterol content of TRLs and sdLDL influence atherogenesis independently of low-density lipoprotein c

232 protein particle (HDL-P) subfractions impact atherogenesis, inflammation, and endothelial function, a

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

234 indings challenge the long-held concept that atherogenesis involves passive movement of LDL across a

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

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

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

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

239 However, its effect on atherogenesis is unknown.

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

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

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

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

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

245 ase-3-like protein 1), a protein involved in atherogenesis, is upregulated in human calcific aortic v

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

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

248 macrophages, plays a detrimental role during atherogenesis, leading to the suggestion that autophagy-

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

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

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

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

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

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

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

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

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

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

259 gh-fat diet (HFD) showed ~1.9-fold increased atherogenesis over Cmah wild-type Ldlr (-/-) mice, assoc

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

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

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

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

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

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

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

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

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

269 inflammatory response in macrophages during atherogenesis remains unclear.

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

271 However, its impact on atherogenesis remains unknown.

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

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 CXCL10, a chemokine involved in atherogenesis that predicts non-AIDS events during ART,

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

279 hils contribute to vascular inflammation and atherogenesis through delivery of microvesicles carrying

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 changes prime the vasculature to exacerbate atherogenesis upon acute hyperlipidemia.

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

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

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

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 d with a 10-week western diet and found that atherogenesis was enhanced in aged wild-type mice.

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

295 ic effect of RSV on periodontitis-associated atherogenesis, we investigated the in vitro effect of RS

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

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

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

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

300 TIH accelerated atherogenesis without an increase in plasma cholesterol,