Polymorphisms in human apolipoprotein(a) kringle IV-10 and coronary artery disease: relationship to allele size, plasma lipoprotein(a) concentration, and lysine binding site activity

2001 ◽  
Vol 79 (5-6) ◽  
pp. 294-299 ◽  
Author(s):  
Josep M. Simó ◽  
Jorge Joven ◽  
Elisabet Vilella ◽  
Montserrat Ribas ◽  
Lídia Figuera ◽  
...  
1995 ◽  
Vol 307 (1) ◽  
pp. 17-22 ◽  
Author(s):  
V N Trieu ◽  
U Olsson ◽  
W J McConathy

Lipoprotein (a) [Lp(a)] is a risk factor for coronary artery disease. It is characterized by apolipoprotein (a) [apo(a)] disulphide linked to apolipoprotein B (apoB), by Cys4057 of apo(a) and possibly Cys3734 of apoB. We call this the covalent apo(a):apoB-Lp interaction, to distinguish it from the non-covalent Lp(a):apoB-Lp interaction, mediated by the proline-binding kringle-4-like domain(s) of Lp(a). The Lp(a):apoB-Lp interaction was inhibited by an apoB peptide spanning residues 3304-3317. This peptide was found by a computerized search for sites on apoB similar to the plasminogen's kringle-4-binding site of alpha 2-antiplasmin. It probably constitutes part of the Lp(a)-binding site on apoB because: (1) it corresponds to the alpha 2-antiplasmin minimum binding domain for plasminogen's kringle-4; (2) the competitive nature of inhibition [KI = (1.5 +/- 0.7) x 10(-4) M, n = 5] suggested that it and apoB-Lp bound to Lp(a) by the same mechanism at the same site; and (3) it specifically bound Lp(a) and not apoB-Lp, and the bound Lp(a) was dissociated by inhibitors of the Lp(a):apoB-Lp interaction, 6-aminohexanoic acid and L-proline. Inhibition was independent of its proline residue, suggesting that proline in the context of a peptide is not a ligand for the kringle(s) which mediated the binding of Lp(a) to apoB-Lp.


2008 ◽  
Vol 9 (1) ◽  
pp. 113-114
Author(s):  
N. Bogavac-Stanojevic ◽  
Z. Jelic-Ivanovic ◽  
V. Spasojevic-Kalimanovska ◽  
S. Spasic ◽  
L. Memon

2008 ◽  
Vol 2 (3) ◽  
Author(s):  
M E Farah ◽  
K Eltahir ◽  
HHM A Elhassan ◽  
MOEH Gadour ◽  
M S Alkhaleefa

Diabetes Care ◽  
1995 ◽  
Vol 18 (2) ◽  
pp. 234-236 ◽  
Author(s):  
G. F. Watts ◽  
R. M. A. Gwilym ◽  
J. Mazurkiewicz ◽  
J. Coltart

2021 ◽  
Vol 8 ◽  
Author(s):  
Jin Liu ◽  
Liwei Liu ◽  
Bo Wang ◽  
Shiqun Chen ◽  
Buyun Liu ◽  
...  

Background: A high level of lipoprotein(a) can lead to a high risk of cardiovascular events or mortality. However, the association of moderately elevated lipoprotein(a) levels (≥15 mg/dL) with long-term prognosis among patients with coronary artery disease (CAD) is still uncertain. Hence, we aim to systematically analyzed the relevance of baseline plasma lipoprotein(a) levels to long-term mortality in a large cohort of CAD patients.Methods: We obtained data from 43,647 patients who were diagnosed with CAD and had follow-up information from January 2007 to December 2018. The patients were divided into two groups (<15 and ≥15 mg/dL). The primary endpoint was long-term all-cause death. Kaplan–Meier curve analysis and Cox proportional hazards models were used to investigate the association between moderately elevated baseline lipoprotein(a) levels (≥15 mg/dL) and long-term all-cause mortality.Results: During a median follow-up of 5.04 years, 3,941 (18.1%) patients died. We observed a linear association between lipoprotein(a) levels and long-term all-cause mortality. Compared with lipoprotein(a) concentrations <15 mg/dL, lipoprotein(a) ≥15 mg/dL was associated with a significantly higher risk of all-cause mortality [adjusted hazard ratio (aHR) 1.10, 95%CI: 1.04–1.16, P-values = 0.001). Similar results were found for the subgroup analysis of non-acute myocardial infarction, non-percutaneous coronary intervention, chronic heart failure, diabetes mellitus, or non-chronic kidney diseases.Conclusion: Moderately elevated baseline plasma lipoprotein(a) levels (≥15 mg/dL) are significantly associated with higher all-cause mortality in patients with CAD. Our finding provides a rationale for testing the lipoprotein(a)-reducing hypothesis with lower targets (even <15 mg/dL) in CAD outcome trials.


2001 ◽  
Vol 34 (8) ◽  
pp. 1169-1173
Author(s):  
Hiroshige Ohashi ◽  
Hiroshi Oda ◽  
Michiya Ohno ◽  
Sachirow Watanabe ◽  
Yasunori Kotoo ◽  
...  

2017 ◽  
Vol 5 (7) ◽  
pp. 524-533 ◽  
Author(s):  
Danish Saleheen ◽  
Philip C Haycock ◽  
Wei Zhao ◽  
Asif Rasheed ◽  
Adam Taleb ◽  
...  

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