Differentiation of the roles of the apolipoprotein(a) and LDL moiety in the binding of lipoprotein(a) to limited plasmin digested des AA fibrin

1996 ◽  
Vol 10 (5-6) ◽  
pp. 317-324 ◽  
Author(s):  
J. Prins ◽  
F.R. Leus ◽  
B.N. Bouma ◽  
H.J.M. van Rijn
Keyword(s):  
Lipoprotein A ◽  
Apolipoprotein A

Lp(a): der akzeptierte unabhängige Risikofaktor

2019 ◽  
Vol 23 (09) ◽  
pp. 388-391
Author(s):  
Volker Schettler
Keyword(s):  
Lipoprotein A ◽  
Apolipoprotein A ◽  
Apolipoprotein B100

Lipoprotein(a) (Lp(a)) besteht aus einem LDL-Partikel, an dem über das Apolipoprotein B100 des Partikels eine Disulfidbrücke zu einem Apolipoprotein(a) besteht ( Abb. 1 ). Obwohl Lp(a) bereits 1963 von Berg et al. erstmals als „lipoprotein associated antigen“ entdeckt 1 und schon früh ein Zusammenhang mit kardiovaskulären Ereignissen diskutiert wurde 2, konnten diese Annahmen der klinischen Eigenschaften erst deutlich später im Rahmen von epidemiologischen Evaluationen bestätigt werden 3, 4. Ab einer Lp(a)-Konzentration von über 30 mg/dl (> 75 nmol/l) besteht ein nahezu linearer Zusammenhang zwischen dem Anstieg der Lp(a)-Konzentration und kardiovaskulären Ereignissen wie Myokardinfarkt und das Risiko für eine Aortenklappenstenose 3, 4.

Effects of NIDDM on lipoprotein(a) concentration and apolipoprotein(a) size

Diabetes ◽  
1994 ◽  
Vol 43 (7) ◽  
pp. 942-946 ◽  
Author(s):  
D. L. Rainwater ◽  
J. W. MacCluer ◽  
M. P. Stern ◽  
J. L. VandeBerg ◽  
S. M. Haffner
Keyword(s):  
Lipoprotein A ◽  
Apolipoprotein A

scholarly journals Functional and metabolic differences between elastase-generated fragments of human lipoprotein[a] and apolipoprotein[a]

1996 ◽  
Vol 37 (8) ◽  
pp. 1786-1801
Author(s):  
C Edelstein ◽  
J A Italia ◽  
O Klezovitch ◽  
A M Scanu
Keyword(s):  
Lipoprotein A ◽  
Apolipoprotein A

Evidence for increased synthesis of lipoprotein(a) in the nephrotic syndrome.

1998 ◽  
Vol 9 (8) ◽  
pp. 1474-1481
Author(s):  
M G De Sain-Van Der Velden ◽  
D J Reijngoud ◽  
G A Kaysen ◽  
M M Gadellaa ◽  
H Voorbij ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Synthesis Rate ◽  
Fractional Synthesis Rate ◽  
Lipoprotein A ◽  
Control Subjects ◽  
Apolipoprotein A ◽  
Catabolic Rate ◽  
Fractional Synthesis ◽  
The Mean

In patients with the nephrotic syndrome, markedly increased levels of lipoprotein(a) (Lp(a)) concentration have been frequently reported, and it has been suggested that this may contribute to the increased cardiovascular risk in these patients. The mechanism, however, is not clear. In the present study, in vivo fractional synthesis rate of Lp(a) was measured using incorporation of the stable isotope 13C valine. Under steady-state conditions, fractional synthesis rate equals fractional catabolic rate (FCR). FCR of Lp(a) was estimated in five patients with the nephrotic syndrome and compared with five control subjects. The mean plasma Lp(a) concentration in the patients (1749+/-612 mg/L) was higher than in control subjects (553+/-96 mg/L). Two patients were heterozygous for apolipoprotein(a) (range, 19 to 30 kringle IV domains), whereas all control subjects were each homozygous with regard to apolipoprotein(a) phenotype (range, 18 to 28 kringle IV domains). The FCR of Lp(a) was comparable between control subjects (0.072+/-0.032 pools/d) and patients (0.064+/-0.029 pools/d) despite the wide variance in plasma concentration. This suggests that differences in Lp(a) levels are caused by differences in synthesis rate. Indeed, the absolute synthetic rate of Lp(a) correlated directly with plasma Lp(a) concentration (P < 0.0001) in all subjects. The present results demonstrate that increased synthesis, rather than decreased catabolism, causes elevated plasma Lp(a) concentrations in the nephrotic syndrome.

scholarly journals Cys4057 of apolipoprotein(a) is essential for lipoprotein(a) assembly.

1993 ◽  
Vol 90 (24) ◽  
pp. 11643-11647 ◽  
Author(s):  
C. Brunner ◽  
H. G. Kraft ◽  
G. Utermann ◽  
H. J. Muller
Keyword(s):  
Lipoprotein A ◽  
Apolipoprotein A
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