ライフサイエンスコーパス: LDL

1 LDL cholesterol is a well established risk factor for at

2 LDL cholesterol reduction was 31.1% with pitavastatin an

3 LDL-C levels <25 or <15 mg/dl on alirocumab were not ass

4 LDL-c rate of change throughout pregnancy was positively

5 LDL-C was lower in both PAH (2.6 +/- 0.8 mmol/l) and CTE

6 LDL-cholesterol concentrations after the cheese diet wer

7 triglycerides (reductions of 33.2 to 63.1%), LDL cholesterol (1.3 to 32.9%), very-low-density lipopro

8 1.02-2.17), MI (OR 1.58, 95% CI 1.06-2.35), LDL-cholesterol (0.21 standard deviations, 95% CI 0.01-0

9 ared with 76.6% in those who did not achieve LDL-C <25 mg/dl.

10 nt association was observed between achieved LDL cholesterol and safety outcomes, either for all seri

11 IER trial, the relationship between achieved LDL-cholesterol concentration at 4 weeks and subsequent

12 outcomes in patients stratified by achieved LDL-C level at 1 month in the Improved Reduction of Outc

13 2669 (10%) of 25 982 patients achieved LDL-cholesterol concentrations of less than 0.5 mmol/L,

14 significant association between the achieved LDL-C level and any of the 9 prespecified safety events.

15 eared to be increased in the group achieving LDL-C levels <25 mg/dl.

16 dverse events occurred in patients achieving LDL-C <25 and <15 mg/dl (72.7% and 71.7%, respectively),

17 Novel adaptable LDL-C estimation performs better in nonfasting samples t

18 nism(s) by which these LDLR mutations affect LDL metabolism and lead to hypercholesterolemia.

19 -Label Study of Long-term Evaluation Against LDL-C (OSLER-1) evaluated the durability of long-term ef

20 ment intensification, 99.3% could achieve an LDL-C level of less than 70 mg/dL, including 67.3% with

21 Only 25.2% achieved an LDL-C level of less than 70 mg/dL.

22 significantly lower in patients achieving an LDL-C level less than 30 mg/dL at 1 month (adjusted haza

23 Patients achieving an LDL-C level less than 30 mg/dL at 1 month had a similar

24 the patients who received the regimen had an LDL cholesterol level below 50 mg per deciliter (1.3 mmo

25 diate-density lipoprotein-apoB (P=0.043) and LDL-apoB (P<0.001), which contributed to the reduction i

26 ight, body mass index (BMI; in kg/m(2)), and LDL cholesterol.

27 The reduction in LDL-apoB and LDL-cholesterol concentrations was significantly greater

28 , intermediate-density lipoprotein-apoB, and LDL-apoB in 81 healthy, normolipidemic, nonobese men.

29 betes mellitus or patients without ASCVD and LDL-C >/=190 mg/dL not due to secondary causes.

30 Alirocumab decreased LDL-C and LDL-apoB by increasing IDL- and LDL-apoB FCRs and decrea

31 d >/=10 mg/dL differences between LDL-CF and LDL-CD compared with 25% and 20% of patients, respective

32 d differences >/=10 mg/dL between LDL-CF and LDL-CD, whereas only 2% and 3% of patients, respectively

33 trategy to help manage total cholesterol and LDL cholesterol.

34 h atherosclerotic cardiovascular disease and LDL cholesterol levels of 70 mg per deciliter (1.8 mmol

35 high- and low-density lipoproteins (HDL and LDL) particles measured by standardized clinical assays.

36 ed LDL-C and LDL-apoB by increasing IDL- and LDL-apoB FCRs and decreasing LDL-apoB PR.

37 importance of elevated circulating LDL, and LDL receptor (LDLR) expression in tumor cells, on the gr

38 ions in intermediate-density lipoprotein and LDL production also contributed to the decrease in LDL p

39 s) significantly reduced levels of PCSK9 and LDL cholesterol for at least 6 months.

40 n had dose-dependent reductions in PCSK9 and LDL cholesterol levels.

41 Reductions in the levels of PCSK9 and LDL cholesterol were maintained at day 180 for doses of

42 sed to stratify patients into quartiles, and LDL-C level was measured at baseline and weeks 10 and 12

43 anced the effect of free sugars on total and LDL cholesterol and triacylglycerols.

44 cohorts in association with serum total and LDL cholesterol, and AT lipidomics.

45 plasma total cholesterol, triglycerides and LDL cholesterol comparable to oral ATV.

46 ds to a greater effect on HbA1c, weight, and LDL cholesterol.

47 bular protein extracts that we identified as LDL receptor-related protein 2 (LRP2), also known as meg

48 Furthermore, AAT3 augments LDL cholesterol-lowering effects of ApoB-ASO.

49 Baseline LDL-C levels were similar across pools, regardless of st

50 Patients were classified by a baseline LDL-C of less than 70 or at least 70 mg/dL and by statin

51 as no difference in the change from baseline LDL-cholesterol concentrations between oral vitamin D3 a

52 < .001) and had significantly lower baseline LDL-C level (123 mg/dL, 124 mg/dL, 128 mg/dL, and 137 mg

53 timibe/simvastatin (85%), had lower baseline LDL-C values, and were more likely older, male, nonwhite

54 Patients with baseline LDL of less than 70 mg/dL either had a final screening L

55 were used to assess the association between LDL-C and mortality.

56 analysis, there were no associations between LDL cholesterol levels and cognitive changes.

57 of absolute and percent differences between LDL-CD and estimated LDL-C (LDL-CN or LDL-CF) was strati

58 patients had >/=10 mg/dL differences between LDL-CF and LDL-CD compared with 25% and 20% of patients,

59 patients had differences >/=10 mg/dL between LDL-CF and LDL-CD, whereas only 2% and 3% of patients, r

60 ighlighting the complex relationship between LDL-C and diabetes.

61 ear regression adjusting for ethnicity, BMI, LDL and duration of T1D, patients with poor glycemic con

62 Mice lacking both LDL receptor (LDLR) and Arhgef1 were protected from high

63 s performed by immobilizing the MREs of both LDL and HDL on the same GDE, which was then used to dete

64 d LDL-C (LDL-CN or LDL-CF) was stratified by LDL-C and triglyceride categories.

65 ascular disease were included, stratified by LDL-C levels into those with LDL-C <190 mg/dL (n=2969; m

66 of LDL-CD falling within an estimated LDL-C (LDL-CN or LDL-CF) category by clinical cut points.

67 ferences between LDL-CD and estimated LDL-C (LDL-CN or LDL-CF) was stratified by LDL-C and triglyceri

68 igh-density lipoprotein cholesterol (HDL-C), LDL-C, and apolipoprotein B (apoB) levels in participant

69 ciated with lower levels of LDL cholesterol (LDL-C) have recently been associated with an increased r

70 ase (CHD), independently of LDL cholesterol (LDL-C) levels.

71 For low-density lipoprotein cholesterol (LDL) of 130-159 mg/dL, AMI rates were 5.44 (4.97, 5.91)

72 mg/dl, low-density lipoprotein cholesterol (LDL-C) <160 mg/dl, and high-density lipoprotein choleste

73 Serum low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C)

74 vels of low-density lipoprotein cholesterol (LDL-C) are an independent risk factor for ASCVD, and cli

75 affect low-density lipoprotein cholesterol (LDL-C) estimation.

76 reduces low-density lipoprotein cholesterol (LDL-C) levels by 55% to 75%.

77 levated low-density lipoprotein cholesterol (LDL-C) levels despite use of statins.

78 s lower low-density lipoprotein cholesterol (LDL-C) levels without reducing cardiovascular events, su

79 reduced low-density lipoprotein cholesterol (LDL-C) on cardiovascular events.

80 reduce low-density lipoprotein cholesterol (LDL-C) to very low levels when added to background lipid

81 HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG).

82 cularly low-density lipoprotein cholesterol (LDL-C), is frequently seen in obese women.

83 gulates low-density lipoprotein cholesterol (LDL-C).

84 plasma low-density lipoprotein cholesterol (LDL-C).

85 tion in low density lipoprotein-cholesterol (LDL-C), an increase in CEC and beneficial changes in pla

86 HDL-C], low-density lipoprotein cholesterol [LDL-C], total cholesterol [TC]) were studied as continuo

87 Low-density lipoprotein cholesterol(LDL-C) is a well established metabolic marker of cardiov

88 re significant increases in HDL cholesterol, LDL cholesterol, and triacylglycerols, although for LDL

89 ent score and lower serum total cholesterol, LDL cholesterol, and albumin concentrations.

90 rmine the importance of elevated circulating LDL, and LDL receptor (LDLR) expression in tumor cells,

91 larger tumors in mice with high circulating LDL-C concentrations than in mice with lower LDL-C.

92 er with the novel method across all clinical LDL-C categories (range, 87%-94%) compared with the Frie

93 In conclusion, LDL-c reduction is positively related to the risk of new

94 patients, 839 (25.1%) achieved 2 consecutive LDL-C values <25 mg/dl, and 314 (9.4%) achieved <15 mg/d

95 ated in patients with at least 2 consecutive LDL-C values <25 or <15 mg/dl in the ODYSSEY program, wi

96 was used to directly measure LDL-C content (LDL-CD).

97 Alirocumab decreased LDL-C and LDL-apoB by increasing IDL- and LDL-apoB FCRs

98 easing IDL- and LDL-apoB FCRs and decreasing LDL-apoB PR.

99 and PCSK9; a secreted protein that degrades LDL receptors in the liver.

100 the same GDE, which was then used to detect LDL and HDL simultaneously in mixed solution.

101 The nano spray dried LDL/CMC/EDC nanogels had relatively poor surface structu

102 apy for at least 6 months and dyslipidaemia (LDL cholesterol 3.4-5.7 mmol/L and triglycerides </=4.5

103 and circulating vitamin D metabolites [i.e., LDL-related protein 2 (LRP2, also known as megalin) with

104 These findings support more effective LDL-C lowering for primordial prevention, even in indivi

105 Electronegative LDL may underlie downregulation of KChIP2 in CKD.

106 for cardiovascular disease who had elevated LDL cholesterol levels.

107 e were used to study the effects of elevated LDL-C in human triple-negative (MDA-MB-231) and mouse He

108 entage of LDL-CD falling within an estimated LDL-C (LDL-CN or LDL-CF) category by clinical cut points

109 ent differences between LDL-CD and estimated LDL-C (LDL-CN or LDL-CF) was stratified by LDL-C and tri

110 Western diet-fed LDL receptor-deficient (Ldlr-/-) mice with myeloid-speci

111 lesterol, and triacylglycerols, although for LDL cholesterol and triacylglycerols there was significa

112 eased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inhibitors, there have been no hum

113 nal trials with different entry criteria for LDL cholesterol levels, we randomly assigned the 27,438

114 ll as examples of trans-mediators (TAGAP for LDL cholesterol).

115 pressure, heart rate, HbA1c, blood glucose, LDL-to-HDL cholesterol ratio, C-reactive protein, angiot

116 lization, provide mechanisms for the greater LDL-cholesterol raising effect.

117 ith the APOE4 allele associated with greater LDL-cholesterol elevation in response to saturated fatty

118 Secondary outcomes were HbA1c, LDL cholesterol, estimated glomerular filtration rate (e

119 and cells have identified increased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inh

120 dvocated in young patients with ACS and high LDL-C levels to allow prompt identification of patients

121 rum lipids in adults with or at risk of high LDL cholesterol.In a randomized, crossover, isocaloric,

122 HR = 0.62; 95% CI = 0.42-0.93), whereas high LDL-C/HDL-C (>/=3.50; HR = 1.50; 95% CI = 1.15-1.96) and

123 PUFAs, particularly in individuals with high LDL cholesterol.

124 Higher LDL-C and TC concentrations at baseline were associated

125 treated with ezetimibe showed a 173% higher LDL-cholesteryl ester plasma disappearance rate (P < 0.0

126 riod compared with patients achieving higher LDL-C concentrations.

127 diabetes) and an unfavorable profile (higher LDL cholesterol and triglycerides).Choline and its metab

128 benefit of lowering LDL-C may depend on how LDL-C is lowered.

129 KJM), a viscous soluble fiber, for improving LDL-cholesterol concentrations.

130 gainst the development of atherosclerosis in LDL-receptor/ApoB48-deficient mice.

131 ry end point was the change from baseline in LDL cholesterol level at 180 days.

132 ed trials had a mean change from baseline in LDL cholesterol levels of -56.0% in the bococizumab grou

133 ly attenuated risk of CHD per unit change in LDL-C level (OR, 0.916 [95% CI, 0.890-0.943] vs 0.831 [9

134 Placebo-controlled percentage change in LDL-C level with evolocumab, 140 mg every 2 weeks and 42

135 oduction also contributed to the decrease in LDL particle concentration with evolocumab by a mechanis

136 The fall in LDL-apoB was caused by an 80.4% increase in LDL-apoB FCR

137 LDL-apoB was caused by an 80.4% increase in LDL-apoB FCR and a 23.9% reduction in LDL-apoB PR.

138 magnitude and durability of the reduction in LDL cholesterol levels.

139 n regimen produced the greatest reduction in LDL cholesterol levels: 48% of the patients who received

140 The reduction in LDL-apoB and LDL-cholesterol concentrations was signific

141 ase in LDL-apoB FCR and a 23.9% reduction in LDL-apoB PR.

142 re was associated with the same reduction in LDL-C levels but an attenuated reduction in apoB levels

143 ay 180, the least-squares mean reductions in LDL cholesterol levels were 27.9 to 41.9% after a single

144 bgroups with 30-40% and 40-50% reductions in LDL-c, respectively, suggesting that LDL-c reduction may

145 alirocumab treatment suggests that increased LDL receptors may also play a role in the reduction of p

146 droxyl and peroxyl radicals), copper-induced LDL-cholesterol peroxidation, as well as alpha-glucosida

147 ary hypertension (PH) reversal can influence LDL-C levels.

148 The group with intensive LDL-c-lowering statin had an 18% increase in the likelih

149 ease in the medium of the bound/internalized LDL, as compared with LDLR-WT.

150 ted that LDLR-R410S recycles loaded with its LDL-cargo.

151 ntrol) after (3)H-cholesteryl oleate-labeled LDL injection.

152 , and pharmacodynamic measures (PCSK9 level, LDL cholesterol level, and exploratory lipid variables)

153 ctor profile [lower low-density lipoprotein (LDL) cholesterol and triglycerides] and lower odds of di

154 -based treatment of low-density lipoprotein (LDL) cholesterol levels.

155 r the low levels of low-density lipoprotein (LDL) cholesterol that result from their use are associat

156 with at least 1 of low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholest

157 for the lowering of low-density lipoprotein (LDL) cholesterol.

158 equence analysis of low-density lipoprotein (LDL) receptor (LDLR) mRNA did not reveal any amino acid

159 To this end, the low-density lipoprotein (LDL) receptor was targeted for degradation via inducible

160 ulating the hepatic low-density lipoprotein (LDL) receptors and increasing the clearance of LDL-chole

161 tive subfraction of low-density lipoprotein (LDL), L5, is correlated with QTc prolongation in patient

162 Egg yolk low density lipoprotein (LDL)/polysaccharide nanogels are newly explored as oral

163 l Trial by reducing low-density-lipoprotein (LDL) cholesterol levels more than statin therapy alone.

164 purified low and high density lipoproteins (LDL and HDL, respectively) were first individually chara

165 ved from uptake of low-density lipoproteins (LDL) and synthesis.

166 Low-density lipoproteins (LDLs) are a class of nanocarriers for the targeted deliv

167 f damaged modified low-density lipoproteins (LDLs), generating macrophage foam cells.

168 tates of high- (HDL) and low-density liquid (LDL) in the metastable part of the phase diagram.

169 icular accuracy advantage in settings of low LDL-C and high triglycerides.

170 people by achieving a lifetime with very low LDL, low blood pressure, low glucose, normal body-mass i

171 The safety of very low LDL-C levels over the long-term is unknown.

172 there were no safety concerns with very low LDL-cholesterol concentrations over a median of 2.2 year

173 in blacks and 13 mg/dL (95% CI, 11-16) lower LDL-C in whites.

174 (95% confidence interval [CI], 32-39) lower LDL-C in blacks and 13 mg/dL (95% CI, 11-16) lower LDL-C

175 ity of postprandial TRL after SFA, and lower LDL binding and hepatocyte internalization, provide mech

176 ssociated with higher levels of HDL-C, lower LDL-C, concordantly lower apoB, and a corresponding lowe

177 el of LDLR expression and dramatically lower LDL uptake.

178 09, and rs11206510) scaled to 1 mmol/L lower LDL cholesterol showed associations with increased fasti

179 17-mmol/L (95% CI: 0.11-, 0.23-mmol/L) lower LDL cholesterol.

180 In PAH patients lower LDL-C significantly predicted death (HR:0.44/1 mmol/l, 9

181 the relationship between progressively lower LDL-cholesterol concentrations achieved at 4 weeks and c

182 TATION: PCSK9 variants associated with lower LDL cholesterol were also associated with circulating hi

183 LDL-C concentrations than in mice with lower LDL-C.

184 t of vitamin D with UVB exposure would lower LDL-cholesterol concentrations compared with the effect

185 KJM significantly lowered LDL cholesterol (MD: -0.35 mmol/L; 95% CI: -0.46, -0.25

186 ab on a background of statin therapy lowered LDL cholesterol levels to a median of 30 mg per decilite

187 ins) have been the main therapy for lowering LDL-C.

188 he short- and long-term benefits of lowering LDL-C for the primary prevention of cardiovascular disea

189 esting that the clinical benefit of lowering LDL-C may depend on how LDL-C is lowered.

190 clinical trial data have shown that lowering LDL-C generally reduces cardiovascular risk.

191 Mean LDL and HDL cholesterol concentrations were 2.35 mmol/L

192 those with LDL-C >/=190 mg/dL (n=2560; mean LDL-C 206+/-12 mg/dL).

193 to those with LDL-C <190 mg/dL (n=2969; mean LDL-C 178+/-6 mg/dL) and those with LDL-C >/=190 mg/dL (

194 sive atorvastatin therapy and who had a mean LDL cholesterol level of 61 mg per deciliter (1.58 mmol

195 s 2 negative LDL receptor mutations had mean LDL-C reductions of 23.5% (p = 0.0044) and 14% (p = 0.03

196 acentrifugation was used to directly measure LDL-C content (LDL-CD).

197 1 men and women (aged 21-73 y) with a median LDL-cholesterol concentration of 159 mg/dL (95% CI: 146,

198 anged from baseline, at week 208, the median LDL-C level reduction was 58%.

199 ocyte-derived macrophages ingesting modified LDL; this was validated by quantitative PCR in human and

200 use macrophages during ingestion of modified LDL.

201 HDL cholesterol but differentially modifies LDL-cholesterol concentrations compared with the effects

202 e resident proteins and an ER-trapped mutant LDL receptor.

203 Patients with 2 defective versus 2 negative LDL receptor mutations had mean LDL-C reductions of 23.5

204 With LDL-C <70 mg/dL, nonfasting LDL-CN accuracy (92%) was superior to LDL-CF accuracy (7

205 t time the impact of fasting status on novel LDL-C accuracy.

206 nce is provided for a tighter association of LDL with LDLR-R410S at acidic pH, a reduced LDL delivery

207 We sought to investigate the associations of LDL cholesterol-lowering PCSK9 variants with type 2 diab

208 We aimed to assess the benefits of LDL-C lowering on cardiovascular outcomes among individu

209 L) receptors and increasing the clearance of LDL-cholesterol.

210 e population with ASCVD and distributions of LDL-C levels under various treatment intensification sce

211 among individuals with primary elevations of LDL-C >/=190 mg/dL without preexisting vascular disease

212 among individuals with primary elevations of LDL-C >/=190 mg/dL.

213 The optimal frequencies of LDL and HDL were found to be 81.38Hz and 5.49Hz, respect

214 ronary heart disease (CHD), independently of LDL cholesterol (LDL-C) levels.

215 Alleles associated with lower levels of LDL cholesterol (LDL-C) have recently been associated wi

216 vascular events per unit change in levels of LDL-C (and apoB).

217 ally occurring discordance between levels of LDL-C and apoB was associated with a similar risk of CHD

218 ociated with concordant changes in levels of LDL-C and apoB.

219 nosis, ALS patients had increasing levels of LDL-C, HDL-C, apoB, and apoA-I, whereas gradually decrea

220 oA-I, whereas gradually decreasing levels of LDL-C/HDL-C and apoB/apoA-I ratios.

221 and significantly attenuated the lowering of LDL cholesterol levels.

222 Accuracy was defined as the percentage of LDL-CD falling within an estimated LDL-C (LDL-CN or LDL-

223 Fluid-phase pinocytosis of LDL by macrophages is regarded as a novel promising targ

224 Whether further reduction of LDL-C beyond these boundaries would be beneficial is unk

225 omising strategy to enhance the stability of LDL-based nanogels in digestive conditions.

226 RP1L-VAP complexes also support transport of LDL-derived cholesterol from endosomes to the endoplasmi

227 d for reconstituting the hydrophobic core of LDLs with a binary fatty acid mixture.

228 were available through day 210, and data on LDL cholesterol and proprotein convertase subtilisin-kex

229 nalysis aimed to assess the effect of KJM on LDL cholesterol, non-HDL cholesterol, and apolipoprotein

230 f >/=3 wk that assessed the effect of KJM on LDL cholesterol, non-HDL cholesterol, or apolipoprotein

231 levels but did not improve VSV attachment or LDL uptake in HPAF-II cells.

232 falling within an estimated LDL-C (LDL-CN or LDL-CF) category by clinical cut points.

233 etween LDL-CD and estimated LDL-C (LDL-CN or LDL-CF) was stratified by LDL-C and triglyceride categor

234 et LDL-c levels </=100 mg/dL (2.6 mmol/L) or LDL-c reductions of at least 30% were extracted separate

235 Ox-LDL may reflect core mechanisms through which MS compone

236 to AMD, such as cholesterol crystals and ox-LDL.

237 ized low-density lipoprotein cholesterol (ox-LDL), plays a crucial role in the uptake of ox-LDL by ce

238 For the second, third, and fourth ox-LDL quartiles versus the first, the odds ratios (95% CI)

239 This study found higher ox-LDL concentrations were associated with MS and its compo

240 ls and oxidized low-density lipoproteins (ox-LDL), potentially by increasing the cellular membrane fl

241 hensive anti-inflammatory effects on LPS, ox-LDL or cholesterol crystal-induced NF-kappaB, c-jun and

242 L), plays a crucial role in the uptake of ox-LDL by cells in the arterial wall.

243 ytes in relation to the lectin-like oxidized LDL receptor (LOX-1).

244 c lipid accumulation and storage of oxidized LDL, cholesteryl esters and triglycerides were abolished

245 on of atherogenic lipoproteins, particularly LDL, by accelerating their catabolism.

246 d hepatic LDLR expression and reduced plasma LDL concentrations in mice.

247 (BMI, systolic and diastolic blood pressure, LDL cholesterol, HDL cholesterol, total cholesterol, tri

248 sorder characterised by substantially raised LDL cholesterol, reduced LDL receptor function, xanthoma

249 tatus, estimated glomerular filtration rate, LDL-cholesterol concentration, and use of lipid-lowering

250 These effects required the WNT receptor LDL receptor-related protein 6 (LRP6).

251 l review on the development of reconstituted LDL (rLDL) particles for theranostic applications.

252 egies have been developed for reconstituting LDL particles, including conjugation to the apolipoprote

253 ls and consistently and substantially reduce LDL-C levels.

254 is an effective additional option to reduce LDL cholesterol in patients with homozygous familial hyp

255 evolocumab as part of the Program to Reduce LDL-C and Cardiovascular Outcomes Following Inhibition o

256 LDL with LDLR-R410S at acidic pH, a reduced LDL delivery to late endosomes/lysosomes, and an increas

257 ubstantially raised LDL cholesterol, reduced LDL receptor function, xanthomas, and cardiovascular dis

258 on in endosomes/lysosomes and showed reduced LDL internalization and degradation relative to LDLR-WT.

259 ansfer protein (CETP) by anacetrapib reduces LDL cholesterol levels and increases high-density lipopr

260 h 0.8% (95% CI: -1.5%, 4.5%), respectively], LDL cholesterol [-4.8% (95% CI: -12.6%, 3.1%) compared w

261 s than 70 mg/dL either had a final screening LDL-C of at least 70 mg/dL or a final screening non-high

262 can potentially be repurposed to lower serum LDL-C.

263 tients with cardiac glycosides reduced serum LDL-C levels.

264 trend) once adjusted for age, sex, smoking, LDL-cholesterol, BMI, waist circumference, and HOMA-insu

265 ial hypercholesterolaemia who were on stable LDL cholesterol-lowering therapy for at least 4 weeks; a

266 In contrast to the synthetic systems, LDL particles are intrinsically biocompatible and biodeg

267 Eight trials with target LDL-c levels </=100 mg/dL (2.6 mmol/L) or LDL-c reductio

268 cedure on the postintervention values of TC, LDL cholesterol, HDL cholesterol, TC:HDL cholesterol, tr

269 We concluded that LDL-C level is low in patients with PAH and is associate

270 lar cholesterol levels; (2) demonstrate that LDL-derived cholesterol travels from lysosomes first to

271 ions in LDL-c, respectively, suggesting that LDL-c reduction may provide a dynamic risk assessment pa

272 The LDL-C response in children and adults was related to und

273 The authors sought to assess the LDL-C efficacy of rosuvastatin versus placebo in HoFH ch

274 es involved in cholesterol biosynthesis, the LDL receptor, and PCSK9; a secreted protein that degrade

275 or degradation via inducible degrader of the LDL receptor (IDOL) overexpression, using liver-targeted

276 eterozygote mutations R410S and G592E of the LDL receptor (LDLR).

277 he gene/variant-dependent specificity of the LDL-C-T2D association.

278 glycemia and highlight the asymmetry of the LDL-C-T2D relationship and/or the gene/variant-dependent

279 ics into aberrant cells that overexpress the LDL receptor.

280 ty in PCSK9 levels and determine whether the LDL-C level reduction achieved with evolocumab differs b

281 In this LDL-C range, 19% of fasting and 30% of nonfasting patien

282 timize cardiovascular risk reduction through LDL-C lowering need to be applied in patients experienci

283 ith a 27.2% decrease in conversion of IDL to LDL.

284 asting LDL-CN accuracy (92%) was superior to LDL-CF accuracy (71%; P<0.001).

285 and total receptor and bound equally well to LDL or extracellular PCSK9, the LDLR-R410S was resistant

286 When LDL-c is reduced by more than 30% during lipid-lowering

287 Therefore we assessed whether LDL-C levels are altered in PAH patients, if they are as

288 With LDL-C <70 mg/dL, nonfasting LDL-CN accuracy (92%) was su

289 n patients with ACS age </=65 years and with LDL-C levels >/=160 mg/dl is high (approximately 9%).

290 vel non-coding rare variants associated with LDL cholesterol (rs17242388 in LDLR) and HDL cholesterol

291 Among individuals with LDL-C >/=190 mg/dL, pravastatin reduced the risk of coro

292 hibitors in primary prevention patients with LDL-C <190 mg/dL with or without diabetes mellitus or pa

293 ate of cataracts was higher in patients with LDL-C <25 mg/dl (2.6%) versus >/=25 mg/dl (0.8%; hazard

294 Patients with LDL-C values less than 30 mg/dL (median, 25 mg/dL; inter

295 25% and 20% of patients, respectively, with LDL-CN.

296 69; mean LDL-C 178+/-6 mg/dL) and those with LDL-C >/=190 mg/dL (n=2560; mean LDL-C 206+/-12 mg/dL).

297 , stratified by LDL-C levels into those with LDL-C <190 mg/dL (n=2969; mean LDL-C 178+/-6 mg/dL) and

298 ent intensification algorithms in those with LDL-C levels of at least 70 mg/dL.

299 associations of PCSK9 genetic variants with LDL cholesterol, fasting blood glucose, HbA1c, fasting i

300 d the association of PCSK9 LOF variants with LDL-C and incident coronary heart disease and stroke thr

301 4) consistently among those with and without LDL-C >/=190 mg/dL (P-interaction >0.9).