ライフサイエンスコーパス: reverse cholesterol transport

1 's ability to remove cholesterol from cells (reverse cholesterol transport).

2 e of other macrophage proteins implicated in reverse cholesterol transport.

3 glabrata infection, and possibly to enhance reverse cholesterol transport.

4 s in plasma may have an inhibitory effect on reverse cholesterol transport.

5 ed LCAT activation, a critical early step in reverse cholesterol transport.

6 te transporter G1 are involved in macrophage reverse cholesterol transport.

7 ally useful and novel modality for improving reverse cholesterol transport.

8 lipoproteins that are critically involved in reverse cholesterol transport.

9 ceptor agonist markedly increases macrophage reverse cholesterol transport.

10 2) generated by CETP inhibition might impair reverse cholesterol transport.

11 and chylomicron particles and is involved in reverse cholesterol transport.

12 e transporter A1 (ABCA1), a key regulator of reverse cholesterol transport.

13 function of phospholipid transfer protein in reverse cholesterol transport.

14 verexpression to promote macrophage-specific reverse cholesterol transport.

15 rotein, and apoE recycling may be related to reverse cholesterol transport.

16 cation of ABCA1 as playing a pivotal role in reverse cholesterol transport.

17 overexpression promotes macrophage-specific reverse cholesterol transport.

18 ting SR-BI cell surface expression and hence reverse cholesterol transport.

19 ipoprotein regulation and may have a role in reverse cholesterol transport.

20 icle formation, apoA-I integrity, and proper reverse cholesterol transport.

21 kely to amplify the effects of oxysterols on reverse cholesterol transport.

22 ein (HDL)-cholesterol and thereby facilitate reverse cholesterol transport.

23 d function of HDL, as well as the pathway of reverse cholesterol transport.

24 criptional regulation of sequential steps of reverse cholesterol transport.

25 its interactions with SR-BI in facilitating reverse cholesterol transport.

26 ins and appears to play an important role in reverse cholesterol transport.

27 iciency of sterol balancing pathways such as reverse cholesterol transport.

28 , a sialoprotein, plays an important role in reverse cholesterol transport.

29 th HDL-cholesterol level and its function in reverse cholesterol transport.

30 ipid composition will have a large impact on reverse cholesterol transport.

31 to bind to HDL and consequently in defective reverse cholesterol transport.

32 atherogenic states that result from impaired reverse cholesterol transport.

33 consistent with the proposed role of HDL in reverse cholesterol transport.

34 e in high density lipoprotein metabolism and reverse cholesterol transport.

35 properties of HDL are related to its role in reverse cholesterol transport.

36 patic SR-BI reduces HDL levels and increases reverse cholesterol transport.

37 rol from peripheral cells, the first step in reverse cholesterol transport.

38 nd in the liver, where it may participate in reverse cholesterol transport.

39 is consistent with its putative function in reverse cholesterol transport.

40 of HDL phospholipid by HL and, therefore, in reverse cholesterol transport.

41 e-rich lipoproteins and processes related to reverse cholesterol transport.

42 of HDL-cholesterol to the liver and impaired reverse cholesterol transport.

43 proteins and is a key regulated component of reverse cholesterol transport.

44 d appears to be a key regulated component of reverse cholesterol transport.

45 oproteins (HDL) and plays a critical role in reverse cholesterol transport.

46 mitantly promoting ABCA1- and ABCG1-mediated reverse cholesterol transport.

47 of CETP inhibition on cholesterol efflux and reverse cholesterol transport.

48 mphatics to return to the bloodstream during reverse cholesterol transport.

49 rol from macrophages, which is a key step in reverse cholesterol transport.

50 dies indicated the potential of these NPs in reverse cholesterol transport.

51 either carnitine or choline reduced in vivo reverse cholesterol transport.

52 s, which are key acceptors of cholesterol in reverse cholesterol transport.

53 many physiologic functions of HDL, including reverse cholesterol transport.

54 be a promising avenue to increase macrophage reverse cholesterol transport.

55 in arterial macrophages, a critical step in reverse cholesterol transport.

56 either of which would be expected to impede reverse cholesterol transport.

57 ABCG1, which are responsible for initiating reverse cholesterol transport.

58 triggers LXRalpha activation and macrophage reverse cholesterol transport.

59 r risk factors such as glycaemic control and reverse cholesterol transport.

60 ty lipoprotein (HDL) that is responsible for reverse cholesterol transport.

61 oA-I with lipids and ABCA1, two key steps in reverse cholesterol transport.

62 e ability of Nef to suppress ABCA1-dependent reverse cholesterol transport.

63 l wall angiogenesis, and macrophage-mediated reverse cholesterol transport.

64 ression of genes involved in anaplerosis and reverse cholesterol transport.

65 lesteryl ester-rich HDL is a central step in reverse cholesterol transport.

66 l) HDL during the antiatherogenic process of reverse cholesterol transport.

67 alyzed macrophage inflammatory responses and reverse cholesterol transport, 2 key mediators of athero

68 both hypocholesterolemia and an increase in reverse cholesterol transport, a process involving the t

69 Expression of proteins involved in reverse cholesterol transport (ABCA1, ABCG1 and 27-hydro

70 only in the loss of classic atheroprotective reverse cholesterol transport activities of the lipoprot

71 ion correlated with functional impairment in reverse cholesterol transport activity of the isolated l

72 agonists have shown promise as promoters of reverse cholesterol transport and anti-inflammatory agen

73 ogenic protection by mechanisms that include reverse cholesterol transport and antiinflammatory funct

74 ng a potential mechanism leading to impaired reverse cholesterol transport and atherosclerosis in the

75 nti-miR33 oligonucleotide treatment promotes reverse cholesterol transport and atherosclerosis regres

76 DL-C and apoA-I levels, facilitating hepatic reverse cholesterol transport and biliary cholesterol ex

77 clerotic, presumably through acceleration of reverse cholesterol transport and by antioxidant and ant

78 agonists may be effective drugs to increase reverse cholesterol transport and decrease cardiovascula

79 ic role of CETP in facilitating HDL-mediated reverse cholesterol transport and demonstrate that CETP

80 tein mediates its beneficial effects through reverse cholesterol transport and direct anti-inflammato

81 otein of high-density lipoproteins, mediates reverse cholesterol transport and has atheroprotective a

82 rotein cholesterol (HDL-C) by promoting both reverse cholesterol transport and HDL antiinflammatory f

83 atherosclerosis by promoting both macrophage reverse cholesterol transport and HDL antiinflammatory f

84 in A-I with enzymes and proteins involved in reverse cholesterol transport and HDL maturation are med

85 tissue as a potential important regulator of reverse cholesterol transport and high density lipoprote

86 results are also associated with changes in reverse cholesterol transport and inflammation.

87 High-density lipoprotein (HDL) mediates reverse cholesterol transport and is known to be protect

88 SR-BI in the liver plays a critical role in reverse cholesterol transport and it dramatically impact

89 rscore the critical role of prebeta-1 HDL in reverse cholesterol transport and its use as a marker of

90 nosine A2A receptor activation, MTX promotes reverse cholesterol transport and limits foam cell forma

91 only approximately 200 genes associated with reverse cholesterol transport and lipase activity.

92 The dual effects of increased reverse cholesterol transport and lowering of apoB-conta

93 addition, its proposed role in facilitating reverse cholesterol transport and modulating atheroscler

94 ause high-density lipoprotein (HDL) promotes reverse cholesterol transport and other antiatherogenic

95 rotein apoAI prevent atherosclerosis through reverse cholesterol transport and other direct effects.

96 vates RHOA and leads to increased macrophage reverse cholesterol transport and reduced atherosclerosi

97 lso induces an SR-BI-independent increase in reverse cholesterol transport and reduces intestinal cho

98 was accompanied by high levels of macrophage reverse cholesterol transport and slightly reduced plasm

99 rocess for many biological events, including reverse cholesterol transport and sperm capacitation.

100 (HDL) and water is an important component of reverse cholesterol transport and the atheroprotective e

101 ion of dysfunctional HDL leading to impaired reverse cholesterol transport and the development of a p

102 density lipoprotein (sHDL), a key player in reverse cholesterol transport and the most abundant form

103 esterol are considered to indicate efficient reverse cholesterol transport and to protect from athero

104 take, plays a role in murine HDL metabolism, reverse cholesterol transport and whole-body cholesterol

105 via a selective uptake pathway to the liver (reverse cholesterol transport) and steroidogenic tissues

106 metabolism, including chylomicron assembly, reverse cholesterol transport, and appetite regulation.

107 g, lipoprotein uptake by peripheral tissues, reverse cholesterol transport, and bile acid synthesis a

108 zygotes and homozygous individuals, decrease reverse cholesterol transport, and lower glucose levels.

109 1)-mediated cholesterol metabolism, increase reverse cholesterol transport, and provide atheroprotect

110 gh-density lipoprotein (HDL) cholesterol and reverse cholesterol transport are being developed to hal

111 roaches that promote HDL function, including reverse cholesterol transport, are in early-stage clinic

112 t characterizes a key step in the process of reverse cholesterol transport, are limited.

113 lipoproteins (HDL), the primary vehicle for reverse cholesterol transport, are the target of serum o

114 HDL-mediated reverse-cholesterol transport as well as phosphoinositid

115 eral tissues (ovary, aortic wall), and (iii) reverse cholesterol transport, as indicated by the signi

116 transfer protein may also be a key player in reverse cholesterol transport, as it interacts with the

117 apoA-I by ABCA1 increases its potential for reverse cholesterol transport based on the following fin

118 Liver X receptors (LXRs) centrally control reverse cholesterol transport, but also negatively modul

119 -density lipoprotein is not only involved in reverse cholesterol transport, but also prevents endothe

120 One mechanism is believed to be promotion of reverse cholesterol transport, but no direct proof of th

121 ApoE uniquely facilitates reverse cholesterol transport by allowing CE-rich core e

122 s an antiatherogenic enzyme that facilitates reverse cholesterol transport by esterifying free choles

123 st that acrolein might interfere with normal reverse cholesterol transport by HDL by modifying specif

124 up IIa secretory phospholipase A2, may alter reverse cholesterol transport by HDL during inflammation

125 These findings indicate that HHcy inhibits reverse cholesterol transport by reducing circulating HD

126 l acyltransferase (LCAT) plays a key role in reverse cholesterol transport by transferring an acyl gr

127 sma HDLs in APOM Tg mice, in vivo macrophage reverse cholesterol transport capacity was similar to th

128 Our data suggest that impaired reverse cholesterol transport characterizes clinical and

129 of both TMDs on the role of HDL particles on reverse cholesterol transport (cholesterol efflux capaci

130 of LXRalpha in mice substantially decreased reverse cholesterol transport, cholesterol catabolism, a

131 n and suggest that stimulating HDL-dependent reverse cholesterol transport could be beneficial in the

132 of cholesterol transport through HDL (i.e., reverse cholesterol transport) determine the anti-athero

133 ural changes within HDL particles can impede reverse cholesterol transport, enhance oxidation of LDL,

134 3 (miR33) is a key negative regulator of the reverse cholesterol transport factors, ATP-binding casse

135 cipients, suggesting a major requirement for reverse cholesterol transport for the beneficial effects

136 high-density lipoprotein (HDL) synthesis and reverse cholesterol transport, for posttranscriptional r

137 Oral D-4F also promoted reverse cholesterol transport from intraperitoneally inj

138 ory, and HDL-mediated cholesterol efflux and reverse cholesterol transport from macrophages are stimu

139 ovide cardiovascular protection by promoting reverse cholesterol transport from macrophages.

140 By this process, HDL can promote reverse cholesterol transport from peripheral tissues to

141 tors of cholesterol homeostasis by governing reverse cholesterol transport from peripheral tissues, b

142 sidered antiatherogenic because they mediate reverse cholesterol transport from the periphery to the

143 jor protein component of HDL-c that mediates reverse cholesterol transport from tissues to the liver

144 nduction of cellular cholesterol efflux and "reverse cholesterol transport" from peripheral tissues t

145 Best known for triggering "reverse cholesterol transport" gene programs upon their

146 Therapeutically promoting macrophage reverse cholesterol transport has been recognized as one

147 One proposal for boosting reverse cholesterol transport has been to elevate plasma

148 r trafficking of cholesterol, its effect on "reverse cholesterol transport" has not been explored.

149 ies of intestinal cholesterol absorption and reverse cholesterol transport have encouraged the develo

150 protective and an important component of the reverse cholesterol transport HDL system.

151 In addition to its role in reverse cholesterol transport, high-density lipoprotein

152 Because of its role in reverse cholesterol transport, human apolipoprotein A-I

153 These data tend to support the reverse cholesterol transport hypothesis, i.e., that ant

154 L Working Group discusses HDL metabolism and reverse cholesterol transport, impaired HDL as a marker

155 ut that of nascent HDL and how rHDL improves reverse cholesterol transport in an atheroprotective way

156 vidence implicating epigenetic regulation of reverse cholesterol transport in blood in relation to oc

157 physiological with respect to the process of reverse cholesterol transport in heavy drinkers and alco

158 an antiathersclerosis therapy that enhances reverse cholesterol transport in humans and animal model

159 Thus, CETP might not be essential for reverse cholesterol transport in humans, raising hope of

160 oliferator-activated receptor-gamma-mediated reverse cholesterol transport in macrophages, which cont

161 and EL on HDL metabolism but not macrophage reverse cholesterol transport in mice and an unexpected

162 clearance and increases macrophage-to-faeces reverse cholesterol transport in mice.

163 inding cassette transporter G1 in macrophage reverse cholesterol transport in vivo remain unclear.

164 phage-derived cholesterol esterification and reverse cholesterol transport in vivo.

165 ate an important role for PLTP in modulating reverse cholesterol transport in vivo.

166 demonstrated an increased rate of macrophage reverse cholesterol transport in vivo.

167 erent high-density lipoprotein subspecies in reverse cholesterol transport, inflammation, endothelial

168 strategies have been developed that promote reverse cholesterol transport, inhibit inflammatory even

169 decreasing serum LDL levels or accelerating reverse cholesterol transport, inhibition of LDL oxidati

170 the arterial wall as well as later steps of reverse cholesterol transport involving uptake of HDL ch

171 Therapeutically targeting macrophage reverse cholesterol transport is a promising approach to

172 Macrophage reverse cholesterol transport is one of the key mechanis

173 Macrophage reverse cholesterol transport is promoted by apolipoprot

174 omotion of macrophage cholesterol efflux and reverse cholesterol transport is thought to be one of th

175 ferase (LCAT), an important enzyme affecting reverse cholesterol transport, is expressed in liver and

176 acteristics of the HDL particle, and through reverse cholesterol transport it promotes an antiatherog

177 ate that by enhancing cholesterol efflux and reverse cholesterol transport, macrophage-specific overe

178 RECENT FINDINGS: The contribution of HDL to reverse cholesterol transport may not be as great as fir

179 he results suggested that PBLs activated the reverse cholesterol transport mechanism to enhance the m

180 inst atherogenesis through antioxidation and reverse cholesterol transport mechanisms.

181 -kappaB and MAPK pathways, but also enhanced reverse cholesterol transport mediated by ABC transporte

182 HDL has a key role in reverse cholesterol transport, mobilizing cholesterol fr

183 uced expression of hepatic genes involved in reverse cholesterol transport, most notably, that for sc

184 with ABCA1 transporters, thereby initiating reverse cholesterol transport or, alternatively, renal c

185 the liver and thus constitutes a pathway of reverse cholesterol transport parallel to that mediated

186 eraction with cell-surface components of the reverse cholesterol transport pathway and antiatherogeni

187 other pathways of cholesterol efflux in the reverse cholesterol transport pathway and prevents apoA-

188 n development that target other parts of the reverse cholesterol transport pathway and, in addition t

189 load of cholesterol in peripheral cells, the reverse cholesterol transport pathway directs excess cho

190 nificant advance in our understanding of the reverse cholesterol transport pathway occurred in 1999 w

191 t systemic inhibition of the ABCA1-dependent reverse cholesterol transport pathway occurred.

192 tical information that may link ABCG1 to the reverse cholesterol transport pathway or diseases such a

193 x capacity (CEC), which is a key step in the reverse cholesterol transport pathway, is independently

194 ill be the manipulation of components of the reverse cholesterol transport pathway, such as CETP, PLT

195 rol is the last step in the atheroprotective reverse cholesterol transport pathway, to which biliary

196 high-density lipoprotein metabolism and the reverse cholesterol transport pathway.

197 ypothesized to be due to its function in the reverse cholesterol transport pathway.

198 efore, the receptor acts at both ends of the reverse cholesterol transport pathway.

199 and uptake, as well as discrete steps in the reverse cholesterol transport pathway.

200 ein A-I (apoA-I) plays a central role in the reverse cholesterol transport pathway; however, the stru

201 al areas: HDL-cholesterol metabolism and the reverse cholesterol transport pathway; novel therapeutic

202 tion in the expression of genes that promote reverse cholesterol transport (PPAR-gamma, LXR-alpha, an

203 to lipoprotein surfaces is a key step in the reverse cholesterol transport process, as the subsequent

204 n can increase expression of antiatherogenic reverse cholesterol transport proteins and can counterac

205 Message and protein levels of the reverse cholesterol transport proteins cholesterol 27-hy

206 nderpinnings associated with variant HDL and reverse cholesterol transport provides an exceptional op

207 fractional clearance and macrophage to fecal reverse cholesterol transport rates compared with LDLr(-

208 Mechanisms to increase reverse cholesterol transport (RCT) and biliary sterol d

209 Acute inflammation impairs reverse cholesterol transport (RCT) and reduces high-den

210 Serum high-density lipoproteins (HDLs) and reverse cholesterol transport (RCT) are important therap

211 s fecal cholesterol excretion and macrophage reverse cholesterol transport (RCT) dependent on activat

212 Product but not precursor apo A1 promoted reverse cholesterol transport (RCT) from human aortic sm

213 erosis in mice, but their roles in mediating reverse cholesterol transport (RCT) from macrophages in

214 inhibit atherosclerosis through promotion of reverse cholesterol transport (RCT) in vivo, but this ha

215 onditions, SR-BI-mediated SLU contributes to reverse cholesterol transport (RCT) independently of ABC

216 Reverse cholesterol transport (RCT) is considered a sign

217 PURPOSE OF REVIEW: The process of reverse cholesterol transport (RCT) is critical for disp

218 Reverse cholesterol transport (RCT) is the pathway by wh

219 levels is well established, but its role in reverse cholesterol transport (RCT) is unclear.

220 28.1-kDa protein is a major mediator of the reverse cholesterol transport (RCT) pathway, a process t

221 Reverse cholesterol transport (RCT) refers to the mobili

222 er, the role that CETP plays in mediation of reverse cholesterol transport (RCT) remains unclear.

223 Inflammation is proposed to impair reverse cholesterol transport (RCT), a major atheroprote

224 ding cassette A1-dependent (ABCA1-dependent) reverse cholesterol transport (RCT), liver X receptor (L

225 oth of which participate in the HDL-mediated reverse cholesterol transport (RCT), were among the most

226 High-density lipoprotein (HDL) mediates reverse cholesterol transport (RCT), wherein excess chol

227 porters and receptors in a way that enhances reverse cholesterol transport (RCT).

228 is believed to play a role in the process of reverse cholesterol transport (RCT).

229 ified and converted to mature HDL as part of reverse cholesterol transport (RCT).

230 the liver for excretion in a process called reverse cholesterol transport (RCT).

231 and may be antiatherosclerotic by enhancing reverse cholesterol transport (RCT).

232 sease (CVD) risk by mediating the process of reverse cholesterol transport (RCT).

233 s an important role in gallstone disease and reverse cholesterol transport (RCT).

234 t in part, because of its ability to mediate reverse cholesterol transport (RCT).

235 en believed to be critical in the process of reverse cholesterol transport (RCT).

236 acrophages to the liver for excretion [i.e., reverse cholesterol transport (RCT)].

237 les for selective cholesterol uptake/efflux (reverse cholesterol transport, RCT) from peripheral cell

238 y the liver accurately reflects the rate of "reverse cholesterol transport." Receptor dependent HDL c

239 ux from macrophage foam cells, a key step in reverse cholesterol transport, requires trafficking of c

240 sible for lung surfactant catabolism and for reverse cholesterol transport, respectively.

241 crophage foam cells is a method of measuring reverse cholesterol transport specifically from macropha

242 Finally, the reverse cholesterol transport system is the main mechani

243 r transfer (CET), the proatherogenic step in reverse-cholesterol transport that results in the enrich

244 lipoproteins (HDL) are important vehicles in reverse cholesterol transport, the cardioprotective mech

245 Reflecting its role in reverse cholesterol transport, the CETP gene is up-regul

246 terol efflux is an early, obligatory step in reverse cholesterol transport, the putative antiatheroge

247 uclear receptors that play a central role in reverse cholesterol transport through up-regulation of A

248 erol efflux to apolipoprotein A1 and HDL and reverse cholesterol transport to plasma, liver, and fece

249 g by SR-BI does not influence SR-BI-mediated reverse cholesterol transport to the liver in mice.

250 rs of cholesterol from peripheral tissue for reverse cholesterol transport to the liver.

251 rease in circulating HDL levels and enhanced reverse cholesterol transport to the plasma, liver, and

252 Reverse cholesterol transport (transfer of macrophage-ch

253 sity lipoprotein, plays an important role in reverse cholesterol transport via its activity as an ABC

254 w biomarker that characterizes a key step in reverse cholesterol transport, was inversely associated

255 arley-containing meals appeared to stimulate reverse cholesterol transport, which may contribute to t

256 it promotes formation of functional HDL and reverse cholesterol transport, while inhibiting filtrati