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1 OX-2 expression in COX-1(-/-) macrophages is proatherogenic.
2 te, there is no in vivo evidence that CRP is proatherogenic.
3 induced by NFkappaB might be antirather than proatherogenic.
4 dhesion and proliferation and may thereby be proatherogenic.
5 d with a focus on those that are potentially proatherogenic.
6 at cholesteryl ester transfer protein can be proatherogenic.
7 tivity (cholesteryl ester transfer [CET]) is proatherogenic.
8 usality, and it has been claimed that CRP is proatherogenic.
9 rosis, whereas Cdkn2a appears to be modestly proatherogenic.
10   OSEs are immunogenic, proinflammatory, and proatherogenic.
11 e continued to dissect the potential diverse proatherogenic actions of C-reactive protein on cultured
12  may contribute to vasomotor dysfunction and proatherogenic actions of CRP, respectively.
13 her substrate deficiency plays a role in the proatherogenic actions of iNOS, we administered L-argini
14  from the circulation, (iii) the pleiotropic proatherogenic actions of TRL and remnants at the arteri
15 oliferation of contractile cells, which have proatherogenic actions.
16 s to develop PPARgamma ligands that separate proatherogenic activities from antidiabetic and antiathe
17 s of LDL (glycation and oxidation), monocyte proatherogenic activity, and circulating levels of solub
18 ole propionate (ImP) is a microbiota-derived proatherogenic amino acid metabolite modulating the infl
19 /ApoA-I ratio, which reflects the balance of proatherogenic and antiatherogenic lipoproteins, is a ri
20 yroid hormones have been linked with various proatherogenic and antiatherogenic processes.
21                                To date, both proatherogenic and antiatherogenic properties have been
22 ptor potential vanilloid 4 (TRPV4)-dependent proatherogenic and inflammatory processes in macrophages
23  identifying candidate genes associated with proatherogenic and inflammatory processes.
24       OSEs are immunogenic, proinflammatory, proatherogenic and plaque destabilizing and represent da
25 ting the cardioprotective lipoprotein into a proatherogenic and proapoptotic one.
26  statins affect the nature of lesions in the proatherogenic and proinflammatory environment of low ES
27                     These responses may have proatherogenic and protective effects.
28 l NO and prostacyclin (PGI2) contribute to a proatherogenic and prothrombotic state.
29 ltiple genes and pathways, some of which are proatherogenic and some are protective.
30 lated arsenicals, but not arsenobetaine, are proatherogenic and that As3MT is required for arsenic to
31 icular helper-germinal center B-cell axis is proatherogenic and that CD8(+) regulatory T cells contro
32 en together, our data suggest that IL-17A is proatherogenic and that it plays an important role in bo
33 hether methylated arsenic intermediates were proatherogenic and whether arsenic biotransformation by
34 we demonstrate that HL deficiency raises the proatherogenic apoB-containing lipoprotein levels in pla
35 olesterol, reflecting reduced levels of both proatherogenic apoB-containing lipoproteins as well as H
36 se and atherosclerosis in hyperlipidemic and proatherogenic ApoE(-/-) mice.
37 ed gene disruption and crossed them with the proatherogenic apolipoprotein E-deficient mice (apoE(-/-
38                                         Both proatherogenic as well as atheroprotective roles have be
39                                      Several proatherogenic biological effects have been attributed t
40        The combination of the broad gamut of proatherogenic biological responses triggered by ligatio
41 trated for the first time that inhibition of proatherogenic caspase-1 activation in ECs improves angi
42 (+) T cells have recently been proposed as a proatherogenic cell subset, their full scope of actions
43 failure, and decreased levels of circulating proatherogenic cells in mice fed an atherogenic diet.
44 ion increasing influx of proinflammatory and proatherogenic cellular and noncellular substances into
45  Myeloid cell activation in combination with proatherogenic changes allowing for increased monocyte r
46 ze, we determined if MCMV infection produces proatherogenic changes in aortic gene expression.
47 ution changes, insulin resistance, and other proatherogenic changes in serum lipid levels.
48                  These findings suggest that proatherogenic changes in SVGs may commence early after
49 on in response to hyperglycemia brings about proatherogenic changes in vascular endothelial cell func
50                                        These proatherogenic changes of lipoproteins may contribute to
51 mmunity in macrophages, promoting persistent proatherogenic characteristics.
52 tary components results in the production of proatherogenic circulating factors that act through a me
53  CD36 can be protective even in more extreme proatherogenic circumstances.
54 ining nutrients can lead to formation of the proatherogenic compound TMAO.
55 dized LDL (OxLDL) is enriched with lysoPC, a proatherogenic compound.
56                                        Under proatherogenic conditions, nitric oxide production from
57 h Ldlr(-/-) mice and studied under different proatherogenic conditions.
58 -6 or IFN-gamma did not induce expression of proatherogenic cysteine proteinase cathepsins from vascu
59 results indicate for the first time that the proatherogenic cytokine IL-18 induces human coronary art
60 ated previously that the proinflammatory and proatherogenic cytokine interleukin-18 (IL-18) stimulate
61                                 Furthermore, proatherogenic cytokine interleukin-1beta also induced T
62            GIP induces the expression of the proatherogenic cytokine osteopontin (OPN) in mouse arter
63 ctivated by IFN-gamma, a proinflammatory and proatherogenic cytokine that mediates its downstream eff
64 ired for macrophage migration in response to proatherogenic cytokines (monocyte chemotactic protein-1
65 hyperlipidemia increases serum levels of the proatherogenic cytokines monocyte chemotactic protein (M
66  mechanism for MPO-dependent generation of a proatherogenic dysfunctional form of HDL in vivo.
67 ainst the development of insulin resistance, proatherogenic dyslipidemia, and aortic atherogenesis in
68 event the development of insulin resistance, proatherogenic dyslipidemia, and atherogenesis.
69                                The potential proatherogenic effect of Ang-1 is further supported by t
70 he 2 types of mice, which indicates that the proatherogenic effect of CRP-associated AT1-R overexpres
71 provide a solid explanation for the observed proatherogenic effect of HHcy.
72 nd provide insight into the mechanism of the proatherogenic effect of p21.
73                Another potentially important proatherogenic effect of prolonged ER stress is activati
74 resence of the isoprostane will still have a proatherogenic effect.
75 ear whether NK cells behave as protective or proatherogenic effectors.
76 mediated increases in inflammatory genes and proatherogenic effects in the vasculature are enhanced b
77 ata indicate that CD4(+) NKT cells can exert proatherogenic effects independent of other lymphocytes.
78  we provide experimental evidence that LPS's proatherogenic effects may at least in part reflect alte
79  surprising findings suggest the presence of proatherogenic effects of alcohol in young adults, espec
80     To test this hypothesis, we compared the proatherogenic effects of ambient particles of <0.18 mic
81 ude that ultrafine particles concentrate the proatherogenic effects of ambient PM and may constitute
82 ears to reciprocally modulate and reduce the proatherogenic effects of C. pneumoniae infection.
83 te infection may be necessary to prevent the proatherogenic effects of C. pneumoniae infection.
84 y the host, appear to be responsible for the proatherogenic effects of CMV.
85                              Because several proatherogenic effects of CRP have been documented in en
86 etic littermates but were protected from the proatherogenic effects of diabetes.
87 iated biotransformation was required for the proatherogenic effects of inorganic arsenite.
88 cal antagonism of TP suppresses the vascular proatherogenic effects of iPF2alpha-III.
89                                          The proatherogenic effects of miR-33 are thought to be in la
90 on of ABCA1 is primarily responsible for the proatherogenic effects of miR-33.
91 ta introduce an experimental model of remote proatherogenic effects of renal IR and delineate myeloid
92 of TSP-4 variants that could account for the proatherogenic effects of the (P387)TSP-4 variant.
93 recombinant CD163 was able to neutralize the proatherogenic effects of TWEAK in ApoE/CD163 double-def
94 ate components of the Ath diet have distinct proatherogenic effects on gene expression and suggest a
95 DL but has a markedly altered metabolism and proatherogenic effects on vascular cells.
96 g, and the molecular mechanisms of potential proatherogenic effects remain to be determined.
97 hat B cells have contradictory protective or proatherogenic effects that are also subset and context
98 rosclerosis where Smad1/5 is responsible for proatherogenic effects, whereas Smad2/3 regulate atherop
99  of lipid metabolism, and toxic sterols with proatherogenic effects.
100 ons and could contribute to proinflammatory, proatherogenic effects.
101 enoproteins such as GPx-1 to contribute to a proatherogenic endothelial phenotype.
102 inflammation, leading to an early onset of a proatherogenic environment.
103 LXR primarily in macrophages responding to a proatherogenic environment.
104 e expression and vascular gene activation in proatherogenic environments, and is also a marker of man
105            Evidence suggests that ACAT2 is a proatherogenic enzyme that contributes cholesteryl ester
106 lipase A(2) (sPLA(2)) represents a family of proatherogenic enzymes that hydrolyze lipoprotein phosph
107 ave been previously shown to induce multiple proatherogenic events in endothelial cells and macrophag
108  oxidized LDL (ox-LDL) is implicated in many proatherogenic events, we hypothesized that ox-LDL would
109 results suggest that VSMC-derived SVEP1 is a proatherogenic factor and support the concept that pharm
110 ell formation and has been suggested to be a proatherogenic factor.
111        Experimental and human data show that proatherogenic factors and cells gain direct access to t
112              These findings demonstrate that proatherogenic factors promote the polarization and infl
113 selectively suppressed the production of key proatherogenic factors such as monocyte chemoattractant
114                 However, the contribution of proatherogenic factors to autoimmunity remains unclear.
115  these cells was found to be up-regulated by proatherogenic factors, which enhanced inflammation and
116 eatinine is probably a marker for unmeasured proatherogenic factors.
117 protein transport across the endothelium and proatherogenic fibronectin deposition and disturbed flow
118 e mechanistic insights, especially under the proatherogenic flow condition, remain largely unknown.
119     Given the current evidence that TLRs are proatherogenic, flow suppression of TLR2 expression may
120  genes (STING) in cDC1s was required for the proatherogenic function of cDC1s.
121 promoted proinflammatory gene expression and proatherogenic functional characteristics through glycol
122 t aldosterone activates endogenous EC MR and proatherogenic gene expression in clinically important h
123 otype with lower insulin resistance, reduced proatherogenic gene expression, and preserved vascular f
124 moattractant protein 1 and the expression of proatherogenic genes in peripheral blood mononuclear cel
125 d that IRE1 regulates the expression of many proatherogenic genes, including several important cytoki
126 tch on antiatherogenic genes, and switch off proatherogenic genes.
127 nd Lp(a) was strengthened in the presence of proatherogenic homocysteine and was blocked by plasminog
128     We also tested whether ATG use induces a proatherogenic immune status.
129 ctively modulating such atheroprotective and proatherogenic immunity.
130 these studies demonstrate that NKT cells are proatherogenic in the absence of exogenous stimulation,
131               T lymphocyte responses promote proatherogenic inflammatory events, which are influenced
132                               IL-17A plays a proatherogenic inflammatory role during atherogenesis by
133 s of this study show that ginkgetin inhibits proatherogenic/inflammatory macrophage function in a TRP
134  this cell subset as a critical regulator of proatherogenic innate immune cell responses in atheroscl
135    These uncleared SMCs elicited a series of proatherogenic juxtacrine responses associated with incr
136 flows in the branches and curved regions are proatherogenic, laminar flows in the straight parts are
137 pemia following the SFA-rich fats, increased proatherogenic large triacylglycerol-rich lipoprotein re
138    These results demonstrate that Adamts7 is proatherogenic, lending directionality to the original g
139  aldosterone stimulates transcription of the proatherogenic leukocyte-EC adhesion molecule intercellu
140 ow that macrophage deficiency of ABCA1/G1 is proatherogenic likely by promoting plaque inflammation a
141                 Patients with CKD have major proatherogenic lipid abnormalities that are treatable wi
142 lesions in cx3cr1(-/-)apoE(-/-) mice; and 3) proatherogenic lipids (oxidized low density lipoprotein
143                                              Proatherogenic lipids increase pyroptosis significantly
144                                              Proatherogenic lipids induce higher caspase-1 activation
145 th each other (r=0.51, 95% CI 0.47-0.56) and proatherogenic lipids.
146 l1 establish another functional link between proatherogenic lipoproteins and platelet-mediated thromb
147 hese results provide a critical link between proatherogenic lipoproteins and their metabolic target,
148 ) plasma levels reflect the concentration of proatherogenic lipoproteins very low-density lipoprotein
149 n (PLTP) increases the circulating levels of proatherogenic lipoproteins, accelerates blood coagulati
150 genic high-density lipoproteins (HDL) to the proatherogenic low-density and very low-density lipoprot
151 -KO and ApoE-Stab2-KO mice showed a reverted proatherogenic macrophage activation compared with ApoE-
152 vidence that molecular lipid determinants of proatherogenic macrophage phenotypes are present in larg
153  suggests thrombospondin-1 (TSP-1), a potent proatherogenic matricellular protein, as a putative link
154       However, the molecular details of this proatherogenic mechanism were not known.
155 novel pathway by which IFN-alpha serves as a proatherogenic mediator through repression of eNOS-depen
156 ase or production of the proinflammatory and proatherogenic mediators CD40 ligand (CD40L) and thrombo
157  stress markers, inhibited the expression of proatherogenic mediators, and blocked leukocyte-endothel
158         We determined the association of the proatherogenic metabolite trimethylamine N-oxide (TMAO)
159 s, the atherosclerotic lesion development in proatherogenic mice.
160 ther metabolic abnormalities, is part of the proatherogenic milieu, it is possible that insulin resis
161 erived EV had an increased expression of the proatherogenic miR-223 with respect to healthy subjects
162                       Finally, we found that proatherogenic miR-33 can directly inhibit human OGG1 ex
163 stimulation of the MMP/TIMP balance of three proatherogenic MMPs and increased activities of two MAPK
164 ntion of LDL on cell surfaces may facilitate proatherogenic modifications and support an expanded rol
165           We used the natural prooxidant and proatherogenic molecule oxidized low-density lipoprotein
166 idence suggests that C-reactive protein is a proatherogenic molecule that plays an active role.
167               Trimethylene N-oxide (TMAO), a proatherogenic molecule, is produced from the metabolism
168 metric dimethylarginine may be an endogenous proatherogenic molecule.
169 es, giving rise to dysregulated, obesogenic, proatherogenic monocyte-derived macrophages.
170 ne expression and drives the accumulation of proatherogenic myeloid cells in atherosclerotic aortas.
171 solated from 38 subjects were categorized as proatherogenic or antiatherogenic according to their cap
172 RF-1 or miR-126 expression recapitulated the proatherogenic or antiatherogenic regulation of VCAM-1.
173 protein-associated phospholipase A2, plays a proatherogenic or antiatherogenic role in atherosclerosi
174 t, they suggest a rather complex one, either proatherogenic or antiatherogenic, depending on the cell
175                                              Proatherogenic oxidized low-density lipoprotein (oxLDL)
176 (LDL) by cells in the artery wall leads to a proatherogenic particle that may help initiate early les
177  oxidized phospholipids to yield potentially proatherogenic particles, have been associated with CHD
178 ation, possibly suggesting the activation of proatherogenic pathways at the local level.
179 lting from global Bvra deletion, generates a proatherogenic phenotype and selectively enhances neutro
180 rom vitamin D-deficient subjects will have a proatherogenic phenotype compared with vitamin D-suffici
181         Restoration of miR-204 abolished the proatherogenic phenotype observed in the macrophage-spec
182 e phosphorylation pathway) that underlined a proatherogenic phenotype.
183 induced conversion of blood monocytes into a proatherogenic phenotype.
184 duces EC transition from atheroprotective to proatherogenic phenotypes.
185  TNF-alpha is a master regulator of vascular proatherogenic phenotypic changes, and it has been linke
186                           In addition to the proatherogenic phenotypic switching in areas of low ESS,
187 e first year of life had proinflammatory and proatherogenic plasma metabolomic/lipidomic profiles at
188  and outer adventitial vasa vasorum, deposit proatherogenic plasma molecules, recruit immune cells an
189 atelet activation promotes prothrombotic and proatherogenic platelet/leukocyte aggregate formation.
190 apoA1 levels may serve as a way to monitor a proatherogenic process in the artery wall.
191 didate genes could be classified to distinct proatherogenic processes, including lipid metabolism and
192 in lipoprotein oxidation and other potential proatherogenic processes.
193 ovel chlorinated oxidized lipid species with proatherogenic properties in vivo has not yet been repor
194 cholesterol metabolism may contribute to the proatherogenic properties of LPS.
195                                          The proatherogenic properties of the cholesterol 5,6-secoste
196  maintenance of a stable HDL pool, and other proatherogenic properties such as decreasing clearance o
197 s and unsaturated lysophospholipids, possess proatherogenic properties, as shown by induction of P-se
198  studies indicate that CRP might have direct proatherogenic properties.
199 atherosclerotic development and that SPT has proatherogenic properties.
200                                          The proatherogenic property of Lp(a) can be attributed in pa
201 hrombospondin-1, a potent antiangiogenic and proatherogenic protein involved in development of diabet
202 of STAT3 that controls the expression of the proatherogenic protein profilin-1 in response to 7-ketoc
203                         HHIPL1 is a secreted proatherogenic protein that enhances hedgehog signaling
204         TSP-1 is a potent antiangiogenic and proatherogenic protein that may represent an important l
205 ondin-1 (TSP-1), a potent antiangiogenic and proatherogenic protein, has been implicated in the devel
206 ted proteins in E. limosum might demethylate proatherogenic quaternary amines and contribute to the p
207     We identified TREM-1 as a major upstream proatherogenic receptor.
208  diabetic db/db mice would exhibit increased proatherogenic responses relative to those from control
209 view, therapeutic strategies that target the proatherogenic responses to retained lipoproteins and th
210 ed enhanced inflammatory gene expression and proatherogenic responses.
211 al cells, caveolin-1 and caveolae may play a proatherogenic role by promoting the transcytosis of LDL
212                        These data document a proatherogenic role for CRP in vivo.
213 g literature has led to understanding of the proatherogenic role for IL-6 in cardiovascular disease a
214 , providing genetic evidence in support of a proatherogenic role for macrophage cyclooxygenase-2 expr
215                               Data support a proatherogenic role for oxidized LDL in atherosclerosis
216                        This study supports a proatherogenic role for pDCs in murine atherosclerosis a
217 ints compared with BALB/c mice, supporting a proatherogenic role for Th1 response.
218 ies, our results establish that cDC1s have a proatherogenic role in atherosclerosis by boosting CD4(+
219                           In contrast to its proatherogenic role in macrophages, autophagy disruption
220  and atherosclerotic lesions, suggesting its proatherogenic role in vivo.
221  experiments, in-vivo studies that support a proatherogenic role of C-reactive protein are less likel
222  knowledge, the first in vivo evidence for a proatherogenic role of endothelial TRPC3.
223                     Here, we investigate the proatherogenic role of NKT cells in an adoptive transfer
224  lipopolysaccharide or high-fat diet plays a proatherogenic role.
225 n the mRNA coding sequence of Apob and other proatherogenic secreted proteins, including apolipoprote
226 hepatic cholesterol and triglycerides, and a proatherogenic serum lipoprotein profile.
227 ine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO).
228 e findings extend previous work indicating a proatherogenic state in healthy, nondiabetic subjects wh
229  a number of these processes, resulting in a proatherogenic state.
230 ort, impaired HDL as a marker and a cause of proatherogenic states, and experimental and current appr
231 ase in cholesteryl ester transfer (CET), the proatherogenic step in reverse-cholesterol transport tha
232 tion factor that can be activated by diverse proatherogenic stimuli such as inflammatory cytokines, l
233 be broadly classified as proinflammatory and proatherogenic (such as IL-1, IL-6, and TNF [tumor necro
234 cted antigen presentation by pDCs in driving proatherogenic T cell immunity.
235 hway has an important role in downregulating proatherogenic T cell response and atherosclerosis by li
236 test whether the PD-1/PD-L pathway regulates proatherogenic T cell responses, we compared atheroscler
237  of DC activation and hence the intensity of proatherogenic T cell responses.
238 as associated with significant reductions of proatherogenic T cell-derived interferon-gamma and lesio
239                      CMV infection and these proatherogenic T cells have been independently associate
240  protective Treg response trumps the loss of proatherogenic T effector cell activation.
241 reduced TFH abundance and suppression of the proatherogenic TFH response.
242                                              Proatherogenic TGRL increased expression of VCAM-1, inte
243 plex class II (MHCII) leads to activation of proatherogenic Th1 cells.
244 y provide a means to lower levels of TMA and proatherogenic TMA-N-oxide via precursor competition.
245  trained immunity in monocytes could sustain proatherogenic traits and expedite atherosclerosis.
246 (hi)) monocytes, including downregulation of proatherogenic transcription factor Egr1.
247 uction also facilitates nuclear transport of proatherogenic transcription factors, increases transcri
248 uencing approach was used to distinguish the proatherogenic transcriptional profile in aortic cells i
249 a have been implicated in the progression of proatherogenic vascular endothelial lesions, moreover, o
250 , such as isoprostanes, could still induce a proatherogenic vascular phenotype.
251 n reduced VLDL/CM-P and a reduction in small proatherogenic VLDL-P (r = 0.888, P < 0.001).
252 -33-based therapies because they might raise proatherogenic VLDL-TAG levels.
253 ptake of modified lipoproteins is considered proatherogenic, we found that IL10 also increases choles
254                      PCSK9 overexpression is proatherogenic, whereas its absence is protective.
255 cell subsets identified the Th1 responses as proatherogenic, whereas regulatory T-cell responses exer

 
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