ライフサイエンスコーパス: LDL

1 LDL (low-density lipoprotein) that has accumulated in th

2 LDL cholesterol associations were carried out in a sampl

3 LDL cholesterol lowering significantly reduced the risk

4 LDL induced the efflux of radiolabeled UC from cultured

5 LDL-C was corrected (LDL-C(corrected)) for cholesterol c

6 2 randomized treatment arms and by achieved LDL-C at 4 weeks.

7 median follow-up of 3.1 years, the achieved LDL-C concentrations were 64 mg/dL (1.64 mmol/L) in the

8 An LDL-C level of <70 mg/dl was achieved in 73.3% of patien

9 CCE reductions only in those who achieved an LDL-C <70 mg/dl.

10 with ischemic stroke and atherosclerosis, an LDL-C target of <70 mg/dL (1.8 mmol/L) did not reduce th

11 east 4 weeks before screening and who had an LDL cholesterol level of 130 mg per deciliter (3.4 mmol

12 lled trials of cardiovascular outcomes of an LDL cholesterol-lowering drug recommended by the 2018 Am

13 We assessed the influence of an LDL-C polygenic score on levels of LDL-C and risk of ASC

14 egression of carotid atherosclerosis than an LDL-C target of 90 to 110 mg/dL.

15 Study) included 201 patients assigned to an LDL-C concentration of <70 mg/dL and 212 patients assign

16 5.89 mmol/L; CB: 6.11 mmol/L; P = 0.006) and LDL cholesterol (WA: 3.72 mmol/L; CB: 3.86 mmol/L; P = 0

17 nce interval [CI] = 0.85-0.99; p = 0.03) and LDL cholesterol (OR = 0.88; 95% CI = 0.81-0.95; p = 0.00

18 ocumab-induced changes in lipoprotein(a) and LDL-C independently predicted major adverse cardiovascul

19 At baseline, median lipoprotein(a) and LDL-C(corrected) were 21 and 75 mg/dL, respectively; wit

20 statin dosing lowered total cholesterol and LDL-C levels.

21 3.1% for LDL-C between 70 and <100 mg/dl and LDL-C <70 mg/dl, respectively; p = 0.016).

22 quartile range [IQR]: 6.7 to 59.6 mg/dl) and LDL-C [corrected for cholesterol content in lipoprotein(

23 ved that genetically elevated plasma HDL and LDL levels appear to be associated with increased BC ris

24 tage of patients who met all HbA1c, SBP, and LDL cholesterol targets; and mean reductions in SCL-20 s

25 ealth Questionnaire-9 score, HbA1c, SBP, and LDL cholesterol.

26 CAV-1, to regulate both BMP-9 signaling and LDL transcytosis.

27 e relationship of maternal folate and TC and LDL-C concentrations may indicate the importance of fola

28 A 1 SD higher TG and LDL-C level caused a 0.062 (95% CI 0.040, 0.083) and a 0

29 crease of genetically instrumented total and LDL cholesterol were associated with 23% (OR = 0.77; 95%

30 Pericardial fat volumes and LDL (low-density lipoprotein) cholesterol concentrations

31 In multivariable MR analysis including apoB, LDL cholesterol, and triglycerides in the same model, ap

32 accounts for the etiological basis of apoB, LDL cholesterol, and triglycerides in relation to ischem

33 s from the trial, was stratified by baseline LDL-C levels >=100 mg/dl and <100 mg/dl.

34 S relationship was not explained by baseline LDL-C or other established risk factors.

35 The mean baseline LDL cholesterol level in the two groups was 255.1 mg per

36 artery disease, diabetes mellitus, baseline LDL levels, and baseline plaque burden.

37 er-risk individuals, independent of baseline LDL-C and other known risk factors, who might derive gre

38 The overall mean (SD) baseline LDL-C was 91.6 mg/dL (24.0) and geometric mean (95% CI)

39 e, with good value in patients with baseline LDL-C >=100 mg/dl but less economic value with LDL-C <10

40 We assessed the association between LDL-C polygenic score with LDL-C levels and ASCVD risk u

41 10-4) and also found a relationship between LDL and BC risk (OR = 1.03, 95% CI = 1.01-1.07, P = 0.02

42 ations that diminish PCSK9's ability to bind LDL reported here supports the notion that PCSK9-LDL ass

43 daily whole almond consumption lowers blood LDL cholesterol concentrations, but effects on other car

44 phage cholesterol efflux induced in vitro by LDL added to the culture media either alone or together

45 estimates for regional variants weighted by LDL-C on AD risk from 2 large samples (total n = 24,718

46 ation of the LDLR and thus controls cellular LDL uptake.

47 s a key regulator of plasma LDL-cholesterol (LDL-C) and a clinically validated target for the treatme

48 er mean low-density lipoprotein cholesterol (LDL-c) (2.86 vs 2.60 mmol/L; adjusted mean difference, 0

49 vels of low-density lipoprotein cholesterol (LDL-C) and increased risk of premature atherosclerotic c

50 rol and low-density lipoprotein cholesterol (LDL-C) at 6 months or more of follow-up.

51 eting a low-density lipoprotein cholesterol (LDL-C) concentration of <70 mg/dL in terms of reducing t

52 levated low-density lipoprotein cholesterol (LDL-C) is associated with increased cardiovascular event

53 aseline low-density lipoprotein cholesterol (LDL-C) level >=70 mg/dl, non-high-density lipoprotein ch

54 ase and low-density lipoprotein cholesterol (LDL-C) levels >=70 mg/dl or non-high-density cholesterol

55 (a) and low-density lipoprotein cholesterol (LDL-C) levels.

56 but not low-density lipoprotein cholesterol (LDL-C) or HDL-C, were associated with MACEs.

57 vels of low-density lipoprotein cholesterol (LDL-C) predicted greater benefit from alirocumab treatme

58 HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides, for cholesterol and triglycer

59 cluding low density lipoprotein cholesterol (LDL-c), high density lipoprotein cholesterol (HDL-c) and

60 sterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), an

61 (a) and low-density lipoprotein cholesterol (LDL-C).

62 24) in low-density lipoprotein cholesterol (LDL-C); secondary endpoints included achievement of LDL-

63 ncluded low-density lipoprotein cholesterol (LDL-cholesterol), high-density lipoprotein cholesterol (

64 creased low-density lipoprotein-cholesterol (LDL-C) and cholesterol blood levels, and elevated SREBP-

65 4 studies; 121,282 people], LDL-Cholesterol [LDL-C; 61 studies; 86,854 people], and triglycerides [TG

66 17 lipid-related SNPs for total cholesterol, LDL, HDL, and triglycerides, respectively.

67 risk among individuals with low circulating LDL-C and of the underlying mechanisms, including those

68 ltaneously associated with lower circulating LDL-C and increased T2D risk, using data on LDL-C from t

69 Biobank, we found that levels of circulating LDL-C were negatively associated with T2D prevalence (od

70 despite positive associations of circulating LDL-C with HbA(1c) and BMI.

71 nd PCSK9 and genetically proxied circulating LDL cholesterol levels.

72 g/dl or switched to placebo if 2 consecutive LDL-C levels were <15 mg/dl.

73 d reductions of lipoprotein(a) and corrected LDL-C independently predicted lower risk of MACE, after

74 Baseline lipoprotein(a) and corrected LDL-C levels and their reductions by alirocumab predicte

75 5.0 mg/dl (IQR: 0 to 13.5 mg/dl), corrected LDL-C by 51.1 mg/dl (IQR: 33.7 to 67.2 mg/dl), and reduc

76 LDL-C was corrected (LDL-C(corrected)) for cholesterol content in lipoprotein

77 not due to increasing levels of small, dense LDL particles, but rather larger LDL particles, which ar

78 n and silencing of CAV-1 and DNM2 diminishes LDL-mediated ALK-1 internalization.

79 total cholesterol >200 mg/dL, HDL <40 mg/dL, LDL >130 mg/dL, and TGs >150 mg/dL were 1.66 (95% CI: 1.

80 ated ALK-1 internalization strongly re-duces LDL transcytosis to levels seen with ALK-1 deficiency.

81 removed by extracorporeal filtration during LDL apheresis.

82 Additionally, an elevated LDL-C polygenic score (>=80th percentile) was associated

83 ted the hypothesis that genetically elevated LDL is associated with reduced risk of ICH.

84 equivalent (ORION-11 trial) who had elevated LDL cholesterol levels despite receiving statin therapy

85 ials of inclisiran in patients with elevated LDL cholesterol.

86 asis coordinating Rab7 activation, endosomal LDL trafficking and NPC1-dependent lysosomal cholesterol

87 ts in late endosome morphology and endosomal LDL trafficking, resulting in cellular cholesterol defic

88 tensive Lipid Elimination Regimen) evaluated LDL apheresis in nonfamilial hyperlipidemia acute corona

89 L) receptor levels and cleared extracellular LDL.

90 modified diet attenuated the rise in fasting LDL cholesterol observed with the control diet (0.03 +/-

91 r 12 wk showed beneficial effects on fasting LDL cholesterol and endothelial function compared with c

92 For LDL-C and UA, the evidence of G$\times$S is especially n

93 risk of MACCE (17.2% vs. 13.3% vs. 13.1% for LDL-C between 70 and <100 mg/dl and LDL-C <70 mg/dl, res

94 ooled means (mg/dl) were 193 for TC, 120 for LDL-C, 47 for HDL-C, and 139 for TG; no strong trends.

95 (95% confidence interval: 1.09 to 1.26) for LDL-C of 70 to <100 mg/dl, and 1.78 (95% confidence inte

96 RS (odds ratio, 1.26 [95% CI, 1.16-1.38] for LDL-C and 1.24 [95% CI, 1.13-1.36] for TG PRS).

97 ependent SNPs associated at P < 5 x 10-8 for LDL cholesterol (220), apolipoprotein B (n = 255), trigl

98 (95% confidence interval: 1.64 to 1.94) for LDL-C >=100 mg/dl when compared with LDL-C <70 mg/dl.

99 utcome, which persisted after adjustment for LDL-C and other risk factors, with adjusted ORs (95% CI)

100 zation remained stable after adjustments for LDL-C and triglycerides.

101 ained a robust effect, with the estimate for LDL cholesterol (OR 0.85; 95% CI: 0.57-1.27; P = 0.44) r

102 effect (p < 0.05), whereas the estimate for LDL cholesterol was reversed, and that for triglycerides

103 In contrast, the paradox for LDL-C persisted for all primary outcomes after adjustmen

104 in human SV589 cells for genes required for LDL-derived cholesterol to reach the ER.

105 ntrast, a main-effect genetic risk score for LDL cholesterol was not useful for predicting dietary fa

106 Only 1 of these genetic scores, for LDL cholesterol, predicted changes in the associated CRF

107 ores (PRSs) with ~6M variants separately for LDL-C and TG with weights from a UK Biobank-based genome

108 Among 47,884 included patients, 52% had LDL-C measured within 6 months of PCI and 57% had LDL-C

109 measured within 6 months of PCI and 57% had LDL-C <70 mg/dl.

110 within 6 months after PCI, and only 57% had LDL-C <70 mg/dl.

111 One in 2 patients had LDL-C measured within 6 months after PCI, and only 57% h

112 No differences were seen for HDL, LDL and cholesterol.

113 atment targets (HbA1c <7.0%, SBP <130 mm Hg, LDL cholesterol <100 mg/dL [<70 mg/dL if prior cardiovas

114 n cases with low HDL cholesterol level, high LDL cholesterol level, high VLDL cholesterol level, high

115 In 1-sample MR analysis, higher LDL cholesterol was causally associated with higher LV e

116 consumption results in significantly higher LDL-cholesterol than nontropical vegetable oils.

117 However, LDL did not exert a synergistic effect on HDL cholestero

118 VLDL cholesterol explained 50% and IDL + LDL cholesterol 29% of the risk of myocardial infarction

119 systolic blood pressure, smoking, and IDL + LDL cholesterol, whereas VLDL triglycerides did not ente

120 Alirocumab was blindly titrated to 150 mg if LDL-C remained >=50 mg/dl or switched to placebo if 2 co

121 ment groups in mean changes from baseline in LDL cholesterol (-14.6 mg/dL, 95% CI -18.2 to -11.0) and

122 24, the mean percent change from baseline in LDL cholesterol level was -44.5% in the evolocumab group

123 Mean change in LDL-C from baseline to week 12 was -21.2% (-59.8 mg/dl)

124 Changes in LDL among CHC patients who achieved SVR differed by IFNL

125 events; secondary endpoints were changes in LDL-C and other lipids.

126 nts in HbA1c, 5 mm Hg in SBP, or 10 mg/dL in LDL cholesterol.

127 reporter and identify >100 genes involved in LDL-cholesterol import.

128 er patients by 26% per 1 mmol/L reduction in LDL cholesterol (RR 0.74 [95% CI 0.61-0.89]; p=0.0019),

129 Hg reduction in SBP, >=10-mg/dL reduction in LDL cholesterol); percentage of patients who met all HbA

130 t 22% per 38.7 mg/dl (1 mmol/l) reduction in LDL cholesterol, with similar benefit across patient sub

131 revascularisation) per 1 mmol/L reduction in LDL cholesterol.

132 utation in LDLR causing a large reduction in LDL cholesterol.

133 There were robust reductions in LDL cholesterol levels in all genotypes of familial hype

134 Reductions in LDL cholesterol levels of approximately 50% were obtaine

135 s substantial interindividual variability in LDL-C levels and risk of ASCVD.

136 h on cardiometabolic risk markers, including LDL cholesterol, triacylglycerol (TG), fasting glucose (

137 rated fats, full-fat dairy products increase LDL cholesterol.

138 cal studies demonstrating that SFAs increase LDL cholesterol, a major causal factor in the developmen

139 .0%, P = 0.0008, respectively) and increased LDL particle size compared with the milk diet (P = 0.02)

140 n upregulation of LDL receptor and increased LDL uptake in the cells.

141 ce, reduced HDL-cholesterol level, increased LDL-cholesterol level, and decreased insulin sensitivity

142 nterface (R469W, R496W, and F515L) inhibited LDL binding, which was completely abolished in the case

143 We investigated LDL contributions to the m-RCT pathway in hypercholester

144 Electronegative L5 LDL exhibits atherogenic properties in vitro and in vivo

145 ed LDL (low density lipoprotein)'s and large LDL particles, as well as other proinflammatory lipids a

146 mall, dense LDL particles, but rather larger LDL particles, which are much less strongly related to C

147 ases in propionate with increases in leptin, LDL cholesterol, and blood pressure; and increases in bu

148 ated with low- and high-density lipoprotein (LDL and HDL) cholesterol, triglycerides, and apolipoprot

149 78 subjects (5.3%); low-density lipoprotein (LDL) >130 mg/dL, 2,756 subjects (7.0%); and triglyceride

150 n elevated level of low-density lipoprotein (LDL) cholesterol and an increased risk of premature athe

151 ated whether higher low-density lipoprotein (LDL) cholesterol and triglyceride levels and lower high-

152 SK9 associated with low-density lipoprotein (LDL) cholesterol in a genome-wide association study (GWA

153 esterol level, high low-density lipoprotein (LDL) cholesterol level, high very low-density lipoprotei

154 correlation between low-density lipoprotein (LDL) cholesterol levels and risk of intracerebral hemorr

155 ained reductions in low-density lipoprotein (LDL) cholesterol levels with infrequent dosing.

156 and associated with low-density lipoprotein (LDL) cholesterol levels.

157 t patients to lower low-density lipoprotein (LDL) cholesterol levels.

158 nstrated that lower low-density lipoprotein (LDL) cholesterol results in fewer cardiovascular events.

159 hough SFAs increase low-density lipoprotein (LDL) cholesterol, in most individuals, this is not due t

160 Biobank (UKBB) for low-density lipoprotein (LDL) cholesterol, triglycerides, and apolipoprotein B to

161 elevated levels of low-density lipoprotein (LDL) cholesterol.

162 pacity receptor for low-density lipoprotein (LDL) in endothelial cells that mediates its transcytosis

163 Low-density lipoprotein (LDL) is heterogeneous, composed of particles with variab

164 SK9) is a ligand of low-density lipoprotein (LDL) receptor (LDLR) that promotes LDLR degradation in l

165 fficiently restored low-density lipoprotein (LDL) receptor levels and cleared extracellular LDL.

166 mes bind tightly to low-density lipoprotein (LDL) receptor-related protein 1 (LRP1), but the molecula

167 s C (CHC) patients: low-density lipoprotein (LDL), high-density lipoprotein, triglycerides, alanine a

168 -mediated uptake of low-density lipoprotein (LDL), which releases cholesterol in lysosomes.

169 sed first-trimester low-density lipoprotein (LDL-C) concentration has been associated with adverse pr

170 ated with decreased low-density-lipoprotein (LDL) cholesterol (P = 1.3 x 10(-8)) without being associ

171 al domains, exports low-density-lipoprotein (LDL)-derived cholesterol from lysosomes.

172 viation decrease in low-density lipoprotein [LDL] cholesterol 0.76, 95% confidence interval [CI] 0.65

173 th diabetes; median low-density lipoprotein [LDL] cholesterol level, 75.0 mg/dL; median triglycerides

174 r cholesterol from low density lipoproteins (LDL) via expression of LDL receptors (LDLR) at the cell

175 Low-density lipoproteins (LDLs) are removed by extracorporeal filtration during LD

176 oteins (IDLs), and low-density lipoproteins (LDLs).

177 ressure, low- and high-density lipoproteins [LDL and HDL], triglycerides [TGs], and glycated haemoglo

178 ong the 2,338 patients who achieved very low LDL-C levels (<20 mg/dl) compared to the 3,613 patients

179 Lower LDL-c levels were associated with Schistosoma mansoni (2

180 In NSTEMI, a lower LDL-C was paradoxically associated with worse outcomes f

181 Even with statin treatment to lower LDL cholesterol, patients with diabetes have a high resi

182 crose and fructose with starch yielded lower LDL cholesterol.

183 -) mice treated with 2-HOBA have reduced MDA-LDL and MDA-HDL levels, and their HDL display increased

184 ents who carry the IFNL4-DeltaG allele, mean LDL increased during treatment, then decreased at post-S

185 Among Chinese adults, who have low mean LDL-C, CRP, but not fibrinogen, was independently associ

186 The mean LDL increased markedly during DAA therapy (pre-DAA, 86.6

187 In FINRISK, median LDL-C was 3.39 (95% CI, 3.38-3.40) mmol/L, and it ranged

188 Assessed individually using MR, LDL cholesterol (odds ratio [OR] 1.66 per 1-standard-dev

189 ersus standard medical therapy (SMT) with no LDL apheresis and statin therapy alone.

190 e of lipoprotein(a) (P(trend)=0.03), but not LDL-C(corrected) (P(trend)=0.50).

191 e of lipoprotein(a) (P(trend)=0.06), but not LDL-C(corrected) (P(trend)=0.85).

192 seline to Month 4 in lipoprotein(a), but not LDL-C(corrected), was associated with the risk of VTE an

193 vels of triglycerides and remnant-C, but not LDL-C, were associated with cardiovascular outcomes inde

194 ly absent (null-null) or impaired (non-null) LDL-receptor activity.

195 secondary endpoints included achievement of LDL-C <70 mg/dl and percent change in other plasma lipid

196 The clinical benefit of LDL cholesterol lowering treatment in older patients rem

197 However, the capacity of LDL to act as a plasma cholesterol reservoir and its pot

198 e responsible for the diabetogenic effect of LDL-C-lowering medications.

199 analysis, which adjusted for the effects of LDL, TGs, body mass index (BMI), and age at menarche, co

200 We aimed to summarise the evidence of LDL cholesterol lowering therapies in older patients.

201 density lipoproteins (LDL) via expression of LDL receptors (LDLR) at the cell surface.

202 and 47% were men; the mean baseline level of LDL cholesterol was 153 mg per deciliter.

203 Mean level of LDL cholesterol was 74% lower in del2.5 carriers than in

204 mental impact of lifelong very low levels of LDL cholesterol due to del2.5 on health of the carriers.

205 inclisiran had significantly lower levels of LDL cholesterol than those who received placebo, with an

206 nce of an LDL-C polygenic score on levels of LDL-C and risk of ASCVD for individuals with monogenic F

207 Higher levels of LDL-C were associated with an increased incidence of lat

208 lial integrity in preventing permeability of LDL.

209 iculum (ER), where it inhibits production of LDL receptors, completing a feedback loop.

210 ended to associate with baseline quartile of LDL-C(corrected) (P(trend)=0.06); VTE tended to associat

211 lation of LDLR mRNA as a potent regulator of LDL receptor expression in humans.

212 he phenotypic and genotypic relationships of LDL-C with T2D.

213 Transport of LDL-derived cholesterol from lysosomes into the cytoplas

214 0.41 [95% CI 0.39, 0.43] per mmol/L unit of LDL-C), despite positive associations of circulating LDL

215 an hepatoma cells results in upregulation of LDL receptor and increased LDL uptake in the cells.

216 s more sensitive to darapladib when bound on LDL and relatively resistant to darapladib when bound on

217 LDL-C and increased T2D risk, using data on LDL-C from the UK Biobank (n = 431,167) and the Global L

218 variants in LDLR that have a large effect on LDL cholesterol levels.

219 BEIJERINCK (EvolocumaB Effect on LDL-C Lowering in SubJEcts with Human Immunodeficiency V

220 tic events in proportion to their effects on LDL cholesterol and have good safety profiles, though PC

221 Their large estimated effects on LDL cholesterol levels suggest strong impacts on protein

222 (Safety, Tolerability & Efficacy on LDL-C of Evolocumab in Subjects With HIV & Hyperlipidemi

223 s are related to levels of lipoprotein(a) or LDL-C.

224 with both HsCRP (rho=0.27, p < 0.001) and Ox-LDL (rho = 0.24, p < 0.001).

225 Plasma ANGPTL5, HsCRP, and Ox-LDL were measured using ELISA.

226 ovascular disease risk factors, HsCRP and Ox-LDL.

227 RP) and oxidized low-density lipoprotein (Ox-LDL) in adolescents.

228 Oxidized LDL (a LOX-1 ligand) increased angiotensin II-induced va

229 Apolipoprotein E, lipoprotein(a), oxidized LDL (low density lipoprotein)'s and large LDL particles,

230 regnancies with elevated STBEVs and oxidized LDL levels (such as preeclampsia).

231 univariate analyses, lower BMI and oxidized LDL, and higher waist-hip ratio, hsCRP, and zonulin corr

232 gand scavenger receptor Lectin-like Oxidized LDL Receptor-1 (LOX-1) is associated with vascular dysfu

233 dothelial cells through lectin-like oxidized LDL receptor-1 (LOX-1) signaling, and glycosylation remo

234 mmunizing experimental animals with oxidized LDL particles unexpectedly resulted in activation of ath

235 reported here supports the notion that PCSK9-LDL association in the circulation inhibits PCSK9 activi

236 esterol [HDL-C; 84 studies; 121,282 people], LDL-Cholesterol [LDL-C; 61 studies; 86,854 people], and

237 Plasma LDL cholesterol concentrations decreased in the almond g

238 a critical determinant of circulating plasma LDL cholesterol levels and hence development of coronary

239 type 9 (PCSK9) is a key regulator of plasma LDL-cholesterol (LDL-C) and a clinically validated targe

240 ell tolerated and effectively reduced plasma LDL-C levels in patients with HoFH and severe HeFH over

241 Genetically predicted LDL-cholesterol was not associated with overall cancer r

242 nse of 6 CRFs (BMI, systolic blood pressure, LDL cholesterol, HDL cholesterol, triglycerides, and fas

243 xin type 9 (PCSK9) have been shown to reduce LDL cholesterol levels by more than 50% but require admi

244 Evolocumab reduced LDL-C by 56.9% (95% confidence interval: 61.6% to 52.3%)

245 At day 510, inclisiran reduced LDL cholesterol levels by 52.3% (95% confidence interval

246 ctory hypercholesterolemia, with a screening LDL cholesterol level of 70 mg per deciliter or higher w

247 Mean (+/-SD) LDL cholesterol levels at baseline were 104.7+/-38.3 mg

248 Mean +/- SEM LDL-cholesterol concentrations (109.9 +/- 4.5 compared w

249 The cheese diet increased serum LDL-cholesterol concentrations compared with the control

250 and merged with available measures of serum LDL cholesterol and HDL cholesterol concentrations.

251 id-lowering therapy (ILLT) comprising single LDL apheresis and statins versus standard medical therap

252 c testing; risk restratification strategies; LDL-cholesterol treatment targets; management protocols

253 sitively associated with serum levels of TC, LDL-C, and TG, but inversely associated with serum level

254 osphate (PLP), and total B-12 with serum TC, LDL-C, HDL-C, and TG concentrations across trimesters.

255 3) do dietary SFAs affect factors other than LDL cholesterol that may impact CVD risk, and 4) is ther

256 We conclude that LDL cholesterol normally moves from lysosomes to the PM.

257 MR analysis demonstrates that LDL cholesterol and triglycerides are associated with ad

258 Early studies established that LDL (low-density lipoprotein) particles could act as eff

259 from both datasets consistently showed that LDL-c was strongly associated with increased risk for CA

260 These findings suggest that LDL cholesterol and triglycerides may have a causal effe

261 events were 55.2/1,000 person-years for the LDL-C <70 mg/dl group, 60.3/1,000 person-years for 70 to

262 s ratio was 1.36 (95% CI, 1.24-1.49) for the LDL-C PRS and 1.31 (95% CI, 1.19-1.43) for the TG PRS.

263 was the percent change from baseline in the LDL cholesterol level at week 16 with evinacumab as comp

264 was the percent change from baseline in the LDL cholesterol level at week 24.

265 The time-averaged percent change in the LDL cholesterol level between day 90 and day 540 was a r

266 adjusted percent change from baseline in the LDL cholesterol level between day 90 and day 540.

267 ast-squares mean change from baseline in the LDL cholesterol level between the groups assigned to rec

268 ad a relative reduction from baseline in the LDL cholesterol level of 47.1%, as compared with an incr

269 were the percent change from baseline in the LDL cholesterol level on day 510 and the time-adjusted p

270 east-squares mean absolute difference in the LDL cholesterol level was -132.1 mg per deciliter (95% C

271 The absolute change in the LDL cholesterol level was -77.5 mg per deciliter (-2.0 m

272 At day 510, the percent change in the LDL cholesterol level was a reduction of 39.7% (95% conf

273 y SFAs lower the incidence of CVD, 2) is the LDL-cholesterol reduction with lower SFA intake predicti

274 y inducing liver-specific degradation of the LDL (low-density lipoprotein) receptor combined with a 1

275 l/L between the lowest and highest 5% of the LDL-C PRS distribution.

276 Area under the LDL-C versus age curve is a possible risk parameter.

277 PCSK9 required for high-affinity binding to LDL particles.

278 In human plasma, 30-40% of PCSK9 is bound to LDL particles; however, the physiological significance o

279 Polygenic contributions to LDL-C explain some of the heterogeneity in clinical pres

280 transfer of the radiolabeled UC from HDL to LDL occurred.

281 tein-related protein ORP1L, which transports LDL-derived cholesterol at membrane contacts between the

282 ce reduced total cholesterol, triglycerides, LDL-cholesterol, and the atherogenic index of plasma (AI

283 mansoni infection with lower triglycerides, LDL-c, and diastolic blood pressure.

284 , we assessed the relationship of area under LDL-C versus age curve to incident CVD event risk and mo

285 esterol concentrations due to increased VLDL/LDL fractions.

286 We constructed a weighted LDL-C polygenic score, composed of 28 single-nucleotide

287 tandard deviation) lipid concentrations were LDL cholesterol 3.57 (0.87) mmol/L and HDL cholesterol 1

288 CETP-independent m-RCT path exists, in which LDL mediates the transfer of cholesterol from macrophage

289 r due to pleiotropic effects associated with LDL-c and HDL-c SNPs.

290 Ss discriminate genetic risk associated with LDL-C from risk associated with reciprocal genetic effec

291 milarly, treatment of endothelial cells with LDL reduces BMP-9-induced SMAD1/5 phosphorylation and ge

292 94) for LDL-C >=100 mg/dl when compared with LDL-C <70 mg/dl.

293 0 mg/dl) compared to the 3,613 patients with LDL-C >=100 mg/dl (3.8% vs. 4.5%, p = 0.57).

294 Among patients with LDL-C >=100 mg/dl, incremental cost-effectiveness ratios

295 sociation between LDL-C polygenic score with LDL-C levels and ASCVD risk using linear regression and

296 L-C >=100 mg/dl but less economic value with LDL-C <100 mg/dl.

297 Adults >=18 years with LDL cholesterol >3 mmol/L (n = 113) were recruited from

298 (95% CI: 0.09, 11.9) of the variance in 1-y LDL cholesterol changes in the intervention arm but was

299 Patients whose 1-year LDL-C remained >=100 mg/dl experienced higher 4-year cum

300 ted with improved outcomes across all 1-year LDL-C strata.

301 experienced a MACCE reduction only if 1-year LDL-C was <70 mg/dl (hazard ratio: 0.61; 95% confidence