ライフサイエンスコーパス: Lp(a)

1 Lp(a) and other lipid parameters were measured at baseli

2 Lp(a) concentrations (median [25th-75th percentile], in

3 Lp(a) concentrations were measured in plasma using an im

4 Lp(a) internalization was also dependent on clathrin-coa

5 Lp(a) internalization was reduced 0.35-fold in HAP1 and

6 Lp(a) is an independent predictor of CVD in men and wome

7 Lp(a) is composed of apolipoprotein B-100 and apolipopro

8 Lp(a) is considered a cardiovascular risk factor.

9 Lp(a) levels were elevated among carriers of rs10455872

10 Lp(a) levels were higher with wider interindividual vari

11 Lp(a) levels were positively associated with CVD events.

12 Lp(a) may be atherothrombotic through its low-density li

13 Lp(a) reductions were significantly correlated with perc

14 Lp(a) remains the last major lipoprotein disorder withou

15 Lp(a) transports oxidized phospholipids with a high cont

16 Lp(a) was associated with increased CV risk in both trea

17 Lp(a) was maximally internalized by 2 hours and was dete

18 Lp(a) was measured using a standardized isoform-independ

19 Lp(a) was similarly associated with risk of PAD (pooled

20 Lp(a), a low-density lipoprotein (LDL) particle linked t

21 Lp(a)-bound PCSK9 may be pursued as a biomarker for card

22 In 1995, Lp(a) was measured in 826 men and women (age range, 45 t

23 R-B1 is also a receptor for lipoprotein (a) (Lp(a)), mediating cellular uptake of Lp(a) in vitro and

24 Elevated levels of lipoprotein(a) (Lp(a)) have been identified as an independent risk facto

25 Lipoprotein(a) (Lp(a)) hyperlipoproteinemia is a major risk factor for c

26 Lipoprotein(a) (Lp(a)) is associated with cardiovascular disease risk.

27 oB, ApoAI, ApoAII, ApoE and lipoprotein (a) (Lpa) levels were measured in serum samples obtained prio

28 made in agreeing a role for lipoprotein (a) [Lp(a)] in clinical practice and developing therapies wit

29 studies have suggested that lipoprotein (a) [Lp(a)] is a causal mediator of cardiovascular disease (C

30 Lipoprotein (a) [Lp(a)] is an independent risk factor for atherosclerosis

31 ipoproteins (OxPL/apoB) and lipoprotein (a) [Lp(a)], and risk of peripheral artery disease (PAD).

32 gen, which is homologous to lipoprotein (a) [Lp(a)], contains proinflammatory oxidized phospholipids

33 ine the relationship between lipoprotein(a) [Lp(a)] and cardiovascular disease (CVD) in a large cohor

34 Recent studies showed that lipoprotein(a) [Lp(a)] is a causal risk factor for cardiovascular diseas

35 Lipoprotein(a) [Lp(a)] is a highly atherogenic low-density lipoprotein-l

36 RATIONALE: Lipoprotein(a) [Lp(a)] is a low-density lipoprotein-like lipoprotein and

37 Lipoprotein(a) [Lp(a)] is a low-density lipoprotein-like lipoprotein and

38 Lipoprotein(a) [Lp(a)] is a low-density lipoprotein-like particle largel

39 Elevated lipoprotein(a) [Lp(a)] is a prevalent, independent cardiovascular risk f

40 Lipoprotein(a) [Lp(a)] is a risk factor for cardiovascular disease (CVD)

41 Lipoprotein(a) [Lp(a)] is an atherogenic lipoprotein.

42 Lipoprotein(a) [Lp(a)] is an emerging risk factor for cardiovascular dis

43 Lipoprotein(a) [Lp(a)] is an independent risk factor for cardiovascular

44 h limited statistical power, lipoprotein(a) [Lp(a)] is not considered a risk factor for cardiovascula

45 d causal association between lipoprotein(a) [Lp(a)] levels and coronary risk, but the nature of the a

46 proteins (apo) A-1 and B and lipoprotein(a) [Lp(a)] levels and the development of subsequent cardiova

47 tudies have highlighted that lipoprotein(a) [Lp(a)] was associated with calcific aortic valve disease

48 ave acquired a great deal of knowledge about Lp(a), but this has not yet led to reductions in CVD.

49 s in HDL level, no SCARB1 variants affecting Lp(a) have been reported.

50 k of CVD is higher in those patients with an Lp(a) level >50 mg/dl and carrying a receptor-negative m

51 On multivariate analysis, Lp(a) was an independent predictor of cardiovascular dis

52 cant for OxPL/apoB (OR: 1.99; p = 0.004) and Lp(a) (OR: 1.96; p < 0.001) in the IL-1(+) group versus

53 -1.04 mmol.L(-1) (99.0+/-40.1 mg.dL(-1)) and Lp(a) 3.74+/-1.63 micromol.L(-1) (104.9+/-45.7 mg.dL(-1)

54 body-mass index less than 32.0 kg/m(2), and Lp(a) concentration of 25 nmol/L (100 mg/L) or more.

55 .62; 95% confidence interval, 0.43-0.90) and Lp(a) less than the median (hazard ratio, 0.46; 95% conf

56 flects the biological activity of Lp(a), and Lp(a) levels were measured in 220 patients with mild-to-

57 Niacin has been reported to lower apoB and Lp(a) and to raise apoA-1.

58 xPL on apolipoprotein B-100 (OxPL/apoB), and Lp(a) levels were measured in 499 patients undergoing co

59 tionship between levels of apoA-1, apoB, and Lp(a), and CV events in each treatment group.

60 Interaction between ATX and Lp(a) was confirmed by in situ proximity ligation assay.

61 re screened for combined HDL cholesterol and Lp(a) elevations.

62 mean low-density lipoprotein cholesterol and Lp(a) were 2.56+/-1.04 mmol.L(-1) (99.0+/-40.1 mg.dL(-1)

63 ject with high levels of HDL cholesterol and Lp(a), SCARB1 was sequenced and demonstrated a missense

64 d by high levels of both HDL cholesterol and Lp(a).

65 ith the extreme phenotype (HDL >80 mg/dL and Lp(a) >100 nmol/L in GeneSTAR, n=8, and >100 mg/dL in CC

66 minogen-independent cytokine inhibition, and Lp(a)/apo(a) inhibits plasminogen activation and regulat

67 n the understanding of Lp(a) metabolism, and Lp(a) levels, rather than apolipoprotein (a) isoform siz

68 Patients carrying null mutations and Lp(a) levels >50 mg/dl showed the highest cardiovascular

69 ith patients carrying the same mutations and Lp(a) levels <50 mg/dl.

70 Characterize the association of PCSK9 and Lp(a) in 39 subjects with high Lp(a) levels (range 39-32

71 also dependent on clathrin-coated pits, and Lp(a) was targeted for lysosomal and not proteasomal deg

72 ed with Lp(a) purified from human plasma and Lp(a) uptake studied using Western blot analysis and int

73 ed with Lp(a) purified from human plasma and Lp(a) uptake studied using Western blot analysis and int

74 rs, high-sensitivity C-reactive protein, and Lp(a), OxPL/apoB remained an independent predictor of CA

75 in the plasminogen-deficient background and Lp(a)tg mice were resistant to inhibition of macrophage

76 ivation was markedly reduced in apo(a)tg and Lp(a)tg mice in both peritonitis and vascular injury inf

77 transgenic mice were generated, apo(a)tg and Lp(a)tg mice, to determine whether Lp(a)/apo(a) modifies

78 ApoAI, ApoAII, ApoE and Lpa were not associated with T2 lesions.

79 into account the limited number of available Lp(a)-targeted drugs, L-carnitine might be an effective

80 Baseline Lp(a) concentrations were associated with incident cardi

81 G145 compared with those with lower baseline Lp(a) values.

82 lar disease among participants with baseline Lp(a) greater than or equal to the median (hazard ratio,

83 ntly greater in those patients with baseline Lp(a) of </=125 nmol/l, the absolute reduction was subst

84 Because Lp(a) is the prominent carrier of proinflammatory oxidiz

85 Because Lp(a)/apo(a) is expressed only in primates, transgenic m

86 k, but the nature of the association between Lp(a) levels and risk of type 2 diabetes (T2D) is unclea

87 ment to test whether the association between Lp(a) levels and T2D is causal.

88 ere used to estimate the association between Lp(a) levels and T2D.

89 es, there was an inverse association between Lp(a) levels and T2D: hazard ratio was 0.63 (95% CI 0.49

90 We evaluated associations between Lp(a) and incident CVD events in blacks and whites in th

91 to PCSK9, on Lp(a), the relationship between Lp(a) and lowering of low-density lipoprotein cholestero

92 net reclassification improvement afforded by Lp(a) was 22.5% for noncases, 17.1% for cases, and 39.6%

93 ication in valvular cells and are carried by Lp(a).

94 etic variation in the LPA locus, mediated by Lp(a) levels, is associated with aortic-valve calcificat

95 thophysiology of atherosclerosis mediated by Lp(a).

96 OxPL circulate in plasma, are transported by Lp(a), and deposit in the vascular wall and induce local

97 ATX is transported in the aortic valve by Lp(a) and is also secreted by valve interstitial cells.

98 amilial hypercholesterolemia; in both cases, Lp(a) internalization was not affected by PCSK9.

99 Circulating Lp(a) levels are primarily influenced by the LPA gene wi

100 Conversely, Lp(a) internalization was enhanced 2-fold in HAP1 and 1.

101 Currently, Lp(a) pathophysiology is not fully understood, and speci

102 f ISIS-APO(a)Rx (50-400 mg) did not decrease Lp(a) concentrations at day 30, six doses of ISIS-APO(a)

103 d the ApoB/ApoA-1 ratio (19%), and decreased Lp(a) 21%, but did not reduce CV events.

104 A dedicated Lp(a)-lowering trial has not been performed to date.

105 Genetically determined Lp(a) levels, as predicted by LPA genotype, were also as

106 Elevated Lp(a) and OxPL-apoB levels are associated with faster AS

107 Elevated Lp(a) levels and corresponding genotypes were associated

108 Elevated Lp(a) levels were associated with multivariable adjusted

109 Elevated Lp(a) predicts 15-year CVD outcomes and improves CVD ris

110 After multivariable adjustment, elevated Lp(a) or OxPL-apoB levels remained independent predictor

111 shed CVD whose major risk factor is elevated Lp(a) levels and propose clinical studies and trials to

112 ecently, new data have emerged that elevated Lp(a) is causally associated with calcific aortic valve

113 d with risk of T2D, suggesting that elevated Lp(a) levels are not causally associated with a lower ri

114 However, a genetic variant that elevated Lp(a) levels was not associated with risk of T2D, sugges

115 We show that subjects with elevated Lp(a) (108 mg/dL [50-195 mg/dL]; n=30) have increased ar

116 tic valve stenosis in patients with elevated Lp(a) concentration.

117 Participants with elevated Lp(a) concentrations (125-437 nmol/L in cohort A; >/=438

118 s being developed for patients with elevated Lp(a) concentrations with existing cardiovascular diseas

119 nocytes isolated from subjects with elevated Lp(a) remain in a long-lasting primed state, as evidence

120 may offset the risk associated with elevated Lp(a), but it is unknown whether Lp(a) is a determinant

121 Emerging Lp(a)-lowering therapies with specific and potent loweri

122 athophysiological insights, have established Lp(a) as an independent, genetic, and likely causal risk

123 There is now interest in evaluating Lp(a) as a therapeutic target.

124 Finally, Lp(a)-associated PCSK9 levels directly correlated with p

125 VS of 1.6 (95% CI: 1.2 to 2.1) for a 10-fold Lp(a) increase, comparable to the observational hazard r

126 ultiple independent genetic determinants for Lp(a)-cholesterol.

127 ne the intracellular trafficking pathway for Lp(a) and the receptor responsible for its uptake in liv

128 tic studies have supported a causal role for Lp(a) in accelerated atherosclerosis, independent of oth

129 calcification, supporting a causal role for Lp(a).

130 etion, indicating a proinflammatory role for Lp(a).

131 known locus on chromosome 6q25-26 and found Lp(a) levels also to be significantly associated with a

132 old increase) was seen in subjects with high Lp(a) and normal low-density lipoprotein.

133 of PCSK9 and Lp(a) in 39 subjects with high Lp(a) levels (range 39-320 mg/dL) and in transgenic mice

134 ion with Lp(a) particles in humans with high Lp(a) levels and in mice carrying human Lp(a).

135 th FH, especially those with CVD, had higher Lp(a) plasma levels compared with their unaffected relat

136 R) for incident CVD was 1.37 per 1-SD higher Lp(a) level (SD = 32 mg/dl) and 2.37 when comparing the

137 We review recent studies that highlight Lp(a) in CVD and calcific aortic valve stenosis and prop

138 high Lp(a) levels and in mice carrying human Lp(a).

139 expressing either human apo(a) only or human Lp(a) (via coexpression of human apo(a) and human apolip

140 t was the percentage change from baseline in Lp(a) concentration at 30 days in the single-dose cohort

141 Although the median change in Lp(a) with rosuvastatin and placebo was zero, rosuvastat

142 A significant difference in Lp(a) levels was observed when the most frequent null an

143 5% CI: 1.2 to 1.7) for a 10-fold increase in Lp(a) plasma levels.

144 e role of a specific plasminogen receptor in Lp(a) uptake.

145 The reduction in Lp(a) correlated with the reduction in low-density lipop

146 fidence interval) dose-related reductions in Lp(a) compared to control: 29.5% (23.3% to 35.7%) and 24

147 xpected, consistent and robust reductions in Lp(a) have also been reported.

148 IS-APO(a)-LRx resulted in mean reductions in Lp(a) of 66% (SD 21.8) in the 10 mg group, 80% (SD 13.7%

149 comparatively smaller percent reductions in Lp(a) with AMG145 compared with those with lower baselin

150 ed in significant dose-related reductions in Lp(a).

151 trong evidence that the LDLR plays a role in Lp(a) catabolism and that this process can be modulated

152 poB100 production plays an important role in Lp(a) levels.

153 which explained 26.8% of the variability in Lp(a) levels, was not associated with risk of T2D (OR 1.

154 Statins tend to increase Lp(a) levels, possibly contributing to the "residual ris

155 These data indicate that, in inflammation, Lp(a)/apo(a) suppresses neutrophil recruitment by plasmi

156 factor axis and interleukin-6 also influence Lp(a) levels and may be targets of therapy.

157 , the apo(a) component from the internalized Lp(a) was resecreted back into the cellular media, where

158 These findings provide new insights into Lp(a) regulation.

159 justed hazard ratio per 1-SD increment in Ln[Lp(a)], 1.18; 95% confidence interval, 1.03-1.34; P=0.02

160 similar among participants with high or low Lp(a).

161 kexin-type 9 inhibitors and mipomersen lower Lp(a) 20% to 30%, and emerging RNA-targeted therapies lo

162 are no approved drugs to specifically lower Lp(a).

163 ecific therapy exists to substantially lower Lp(a) concentrations.

164 %, and emerging RNA-targeted therapies lower Lp(a) >80%.

165 and specifically targeted therapies to lower Lp(a) are not available.

166 antisense oligonucleotides designed to lower Lp(a) concentrations.

167 , there are few available therapies to lower Lp(a).

168 esis is the most efficacious method to lower Lp(a).

169 mmarize emerging therapeutic agents to lower Lp(a).

170 c potential of PCSK9 in effectively lowering Lp(a) levels.

171 dies and trials to demonstrate that lowering Lp(a) levels will effectively reduce the risk of calcifi

172 a tool to test the hypothesis that lowering Lp(a) plasma levels will lead to clinical benefit.

173 icipants assigned to IONIS-APO(a)Rx had mean Lp(a) reductions of 66.8% (SD 20.6) in cohort A and 71.6

174 ignificant dose-dependent reductions in mean Lp(a) concentrations were noted in all single-dose IONIS

175 IONIS-APO(a)-LRx might mitigate Lp(a)-mediated cardiovascular risk and is being develope

176 validation of biological pathways modulating Lp(a) metabolism are lacking.

177 rial wall compared with subjects with normal Lp(a) (7 mg/dL [2-28 mg/dL]; n=30).

178 This may be attributable to the ability of Lp(a) to elicit endothelial dysfunction.

179 ), which reflects the biological activity of Lp(a), and Lp(a) levels were measured in 220 patients wi

180 The addition of Lp(a) to the RRS increased the C-index by 0.016.

181 sing 3 different approaches: (1) analysis of Lp(a) fractions isolated by ultracentrifugation; (2) imm

182 otein [apo(a)], the unique apolipoprotein of Lp(a), and a mimic of plasminogen.

183 n this study, we assessed the association of Lp(a) levels with risk of incident T2D and tested whethe

184 demonstrate a strong inverse association of Lp(a) levels with risk of T2D.

185 On 6q locus, we detected associations of Lp(a)-cholesterol with 118 common variants (P = 5 x 10(-

186 ere investigated who commenced LA because of Lp(a)-hyperlipoproteinemia and progressive cardiovascula

187 of Lp(a) in vitro and promoting clearance of Lp(a) in vivo.

188 he role of LDL receptors in the clearance of Lp(a), is poorly defined, and no mechanistic studies of

189 stinguishing kringle-containing component of Lp(a)) elicits cytoskeletal rearrangements in vascular e

190 ther than the apolipoprotein(a) component of Lp(a).

191 been known that the plasma concentration of Lp(a) is highly heritable, with its genetic determinants

192 f both the lipid and protein constituents of Lp(a) from plasma.

193 lications for the catabolism and function of Lp(a).

194 Internalization of Lp(a) was markedly reduced following treatment of HepG2

195 ramatically increased the internalization of Lp(a).

196 s review summarizes the current landscape of Lp(a), discusses controversies, and reviews emerging the

197 Patients with higher levels of Lp(a) at baseline had larger absolute reductions but com

198 t analysis and intracellular localization of Lp(a) by confocal microscopy.

199 t analysis and intracellular localization of Lp(a) by confocal microscopy.

200 erapies with specific and potent lowering of Lp(a) are in phase II clinical trials and provide a tool

201 However, the mechanism of Lp(a) catabolism in vivo and the role of PCSK9 in this p

202 Although the major site and mode of Lp(a) clearance remain unidentified, a recent cell and a

203 In vitro studies of the pathophysiology of Lp(a) on monocytes were performed with an in vitro model

204 ction of apo(a); (3) ELISA quantification of Lp(a)-associated PCSK9.

205 comparing the top versus bottom quintile of Lp(a).

206 e at least as strong, with a larger range of Lp(a) concentrations, in blacks compared with whites.

207 and specific treatments for the reduction of Lp(a) levels and the associated risk of cardiovascular d

208 a-analysis showed a significant reduction of Lp(a) levels following L-carnitine supplementation (WMD:

209 propose pathways to clinical registration of Lp(a)-lowering agents.

210 The pathogenic risk of Lp(a) is associated with elevated plasma concentration,

211 Nevertheless, the role of Lp(a) as a predictor of CVD in patients with FH has been

212 AS severity, patients in the top tertile of Lp(a) or OxPL-apoB had increased risk of aortic valve re

213 as faster in patients in the top tertiles of Lp(a) (peak aortic jet velocity: +0.26 +/- 0.26 vs. +0.1

214 a reduced binding/intracellular transport of Lp(a).

215 provide a rationale for randomized trials of Lp(a)-lowering and OxPL-apoB-lowering therapies in AS.

216 Progress in the understanding of Lp(a) metabolism has the potential to lead to the develo

217 continues to be made in the understanding of Lp(a) metabolism, and Lp(a) levels, rather than apolipop

218 First, a detailed understanding of Lp(a) synthesis and clearance has not been realized.

219 in (a) (Lp(a)), mediating cellular uptake of Lp(a) in vitro and promoting clearance of Lp(a) in vivo.

220 imilar results were obtained with the use of Lp(a) cutoffs of </=10 mg/dL, >10 to </=20 mg/dL, >20 to

221 rationale for the potential clinical use of Lp(a)-lowering therapies in high-risk patients or patien

222 The effect of AMG145 on Lp(a) was consistent regardless of age, sex, race, histo

223 OxPLs are pro-inflammatory, circulate on Lp(a), and mediate CAD.

224 markedly attenuated by inactivating OxPL on Lp(a) or removing OxPL on apolipoprotein(a).

225 00 (OxPL/apoB), primarily reflecting OxPL on Lp(a), independently predict cardiovascular disease (CVD

226 nvertase subtilisin kexin type 9 (PCSK9), on Lp(a).

227 fully human monoclonal antibody to PCSK9, on Lp(a), the relationship between Lp(a) and lowering of lo

228 Optimal Lp(a) internalization in both hepatic and primary human

229 at least partially due to disagreement over Lp(a) measurement methodologies, its physiological role

230 ly significant positive shift in the overall Lp(a) distribution (P<0.0001).

231 The major lipoprotein carrier of OxPL, Lp(a), was also associated with risk of PAD, reinforcing

232 y IL-1 genotype, oxidation of phospholipids, Lp(a), and genetic predisposition to CAD and cardiovascu

233 Plasma Lp(a) levels are reduced by monoclonal antibodies target

234 Plasma Lp(a) was measured in blacks (n=3467) and whites (n=9851

235 DL-C by 55.1%, LDL-apoB by 56.3%, and plasma Lp(a) by 18.7%.

236 ere mean percentage change in fasting plasma Lp(a) concentration at day 85 or 99 in the per-protocol

237 ere mean percentage change in fasting plasma Lp(a) concentration, safety, and tolerability at day 30

238 pendent, mean percentage decreases in plasma Lp(a) concentration of 39.6% from baseline in the 100 mg

239 istration, a significant reduction in plasma Lp(a) concentration was observed with oral (WMD: -9.00 m

240 No effective therapies to lower plasma Lp(a) concentrations exist.

241 The regulation of plasma Lp(a) levels, including the role of LDL receptors in the

242 also play a role in the reduction of plasma Lp(a).

243 se-dependent, selective reductions of plasma Lp(a).

244 o assess the impact of L-carnitine on plasma Lp(a) concentrations through systematic review and meta-

245 reviews emerging therapies to reduce plasma Lp(a) levels to decrease risk of CVD and CAVS.

246 PCSK9 levels directly correlated with plasma Lp(a) levels but not with total plasma PCSK9 levels.

247 effective alternative to effectively reduce Lp(a).

248 ale exists to develop novel agents to reduce Lp(a) and test the hypothesis that this will lead to red

249 Current therapeutic options to reduce Lp(a) are limited.

250 a novel, tolerable, potent therapy to reduce Lp(a) concentrations.

251 mg, 105 mg, and 140 mg every 2 weeks reduced Lp(a) at 12 weeks by 18%, 32%, and 32%, respectively (P<

252 mg, 350 mg, and 420 mg every 4 weeks reduced Lp(a) by 18%, 23%, and 23%, respectively (P<0.001 for ea

253 AMG145 significantly reduces Lp(a), by up to 32%, among subjects with hypercholestero

254 pathophysiology and assess whether reducing Lp(a) levels minimizes CVD risk.

255 Selective Lp(a) apheresis has offered some evidence that Lp(a)-low

256 on, the meta-analysis suggests a significant Lp(a) lowering by oral L-carnitine supplementation.

257 Allele-specific Lp(a) levels did not add to the predictive ability of th

258 ctice and developing therapies with specific Lp(a)-lowering activity.

259 Similarly, on-statin Lp(a) concentrations were associated with residual risk

260 Baseline and on-study Lp(a) were predictive of CV events in both simvastatin p

261 st irrefutable evidence has accumulated that Lp(a) is a causal, independent, genetic risk factor for

262 These findings demonstrate that Lp(a) induces monocyte trafficking to the arterial wall

263 However, recent data has demonstrated that Lp(a) can be significantly lowered, along with reduction

264 (a) apheresis has offered some evidence that Lp(a)-lowering can improve cardiovascular end-points.

265 The novel findings that Lp(a) is internalized by the plasminogen receptor, plasm

266 These findings support the hypothesis that Lp(a) mediates AS progression through its associated OxP

267 We report that Lp(a) internalization by hepatic HepG2 cells and primary

268 In vitro studies show that Lp(a) contains OxPL and augments the proinflammatory res

269 These findings suggest that Lp(a) levels may be used in risk assessment of subjects

270 detected a high level of ATX activity in the Lp(a) fraction in circulation.

271 y defined, and no mechanistic studies of the Lp(a) lowering by alirocumab in humans have been publish

272 These approaches will allow testing of the "Lp(a) hypothesis" in clinical trials.

273 icipants treated with potent statin therapy, Lp(a) was a significant determinant of residual risk.

274 e predictive ability of the FRS or RRS or to Lp(a).

275 r race-specific 1-SD-greater log-transformed Lp(a) were 1.13 (1.04-1.23) for incident CVD, 1.11 (1.00

276 Baseline and on-treatment Lp(a) concentrations were assessed in 9612 multiethnic p

277 nvestigational efforts to further understand Lp(a) pathophysiology and assess whether reducing Lp(a)

278 This study sought to determine whether Lp(a) and OxPL are associated with hemodynamic progressi

279 his study was conducted to determine whether Lp(a) improves CVD risk prediction.

280 (a)tg and Lp(a)tg mice, to determine whether Lp(a)/apo(a) modifies plasminogen-dependent leukocyte re

281 However, whether Lp(a) modifies clinical risk assessment was not establis

282 with risk of incident T2D and tested whether Lp(a) levels are causally linked to T2D.

283 th elevated Lp(a), but it is unknown whether Lp(a) is a determinant of residual risk in the setting o

284 findings provide a novel mechanism by which Lp(a) mediates cardiovascular disease.

285 mpany new classes of therapeutic agents with Lp(a)-lowering effects.

286 thesized that it can also be associated with Lp(a) in plasma.

287 how that PCSK9 is physically associated with Lp(a) in vivo using 3 different approaches: (1) analysis

288 enetic variant (rs10455872), associated with Lp(a) levels, in calcific AVS.

289 2 numbers were significantly associated with Lp(a)-cholesterol (P = 2.28 x 10(-9)).

290 to identify genetic variants associated with Lp(a)-cholesterol levels in the Old Order Amish.

291 s3798220 and rs10455872 were associated with Lp(a)-cholesterol levels independent of each other and K

292 d two variants most strongly associated with Lp(a)-cholesterol, rs3798220 (P = 1.07 x 10(-14)) and rs

293 at plasma PCSK9 is found in association with Lp(a) particles in humans with high Lp(a) levels and in

294 Plasma PCSK9 levels correlated with Lp(a) levels, but not with the number of kringle IV-2 re

295 g subjects and also strongly correlated with Lp(a) levels.

296 In patients with Lp(a)-hyperlipoproteinemia, progressive cardiovascular d

297 Preferential association of PCSK9 with Lp(a) versus low-density lipoprotein (1.7-fold increase)

298 o(a) only, and the association of PCSK9 with Lp(a) was not affected by the loss of the apo(a) region

299 Human hepatoma cells were treated with Lp(a) purified from human plasma and Lp(a) uptake studie

300 S AND Human hepatoma cells were treated with Lp(a) purified from human plasma and Lp(a) uptake studie