For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
35
views
44
references
 Top references
cited by
164
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      3,670
      similar
       All similar
      • Record: found
      • Abstract: not found
      • Article: not found

      Apolipoprotein B Particles and Cardiovascular Disease : A Narrative Review

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The conventional model of atherosclerosis presumes that the mass of cholesterol within very low-density lipoprotein particles, low-density lipoprotein particles, chylomicron, and lipoprotein (a) particles in plasma is the principal determinant of the mass of cholesterol that will be deposited within the arterial wall and will drive atherogenesis. However, each of these particles contains one molecule of apolipoprotein B (apoB) and there is now substantial evidence that apoB more accurately measures the atherogenic risk owing to the apoB lipoproteins than does low-density lipoprotein cholesterol or non-high-density lipoprotein cholesterol.

          Related collections

          Most cited references44

          • Record: found
          • Abstract: found
          • Article: not found

          Genetic associations with valvular calcification and aortic stenosis.

          George Thanassoulis, Catherine Y Campbell, David S Owens … (2013)
          Limited information is available regarding genetic contributions to valvular calcification, which is an important precursor of clinical valve disease. We determined genomewide associations with the presence of aortic-valve calcification (among 6942 participants) and mitral annular calcification (among 3795 participants), as detected by computed tomographic (CT) scanning; the study population for this analysis included persons of white European ancestry from three cohorts participating in the Cohorts for Heart and Aging Research in Genomic Epidemiology consortium (discovery population). Findings were replicated in independent cohorts of persons with either CT-detected valvular calcification or clinical aortic stenosis. One SNP in the lipoprotein(a) (LPA) locus (rs10455872) reached genomewide significance for the presence of aortic-valve calcification (odds ratio per allele, 2.05; P=9.0×10(-10)), a finding that was replicated in additional white European, African-American, and Hispanic-American cohorts (P<0.05 for all comparisons). Genetically determined Lp(a) levels, as predicted by LPA genotype, were also associated with aortic-valve calcification, supporting a causal role for Lp(a). In prospective analyses, LPA genotype was associated with incident aortic stenosis (hazard ratio per allele, 1.68; 95% confidence interval [CI], 1.32 to 2.15) and aortic-valve replacement (hazard ratio, 1.54; 95% CI, 1.05 to 2.27) in a large Swedish cohort; the association with incident aortic stenosis was also replicated in an independent Danish cohort. Two SNPs (rs17659543 and rs13415097) near the proinflammatory gene IL1F9 achieved genomewide significance for mitral annular calcification (P=1.5×10(-8) and P=1.8×10(-8), respectively), but the findings were not replicated consistently. Genetic variation in the LPA locus, mediated by Lp(a) levels, is associated with aortic-valve calcification across multiple ethnic groups and with incident clinical aortic stenosis. (Funded by the National Heart, Lung, and Blood Institute and others.).
          Article 0 comments Cited 269 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The central role of arterial retention of cholesterol-rich apolipoprotein-B-containing lipoproteins in the pathogenesis of atherosclerosis: a triumph of simplicity.

            Jan Borén, Kevin Jon Williams (2016)
            Today, it is no longer a hypothesis, but an established fact, that increased plasma concentrations of cholesterol-rich apolipoprotein-B (apoB)-containing lipoproteins are causatively linked to atherosclerotic cardiovascular disease (ASCVD) and that lowering plasma LDL concentrations reduces cardiovascular events in humans. Here, we review evidence behind this assertion, with an emphasis on recent studies supporting the 'response-to-retention' model - namely, that the key initiating event in atherogenesis is the retention, or trapping, of cholesterol-rich apoB-containing lipoproteins within the arterial wall.
            Article 0 comments Cited 163 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: not found
              • Article: not found

              Baseline and on-statin treatment lipoprotein(a) levels for prediction of cardiovascular events: individual patient-data meta-analysis of statin outcome trials

              Peter Willeit, Paul Ridker, Paul Nestel … (2018)
              Article 0 comments Cited 151 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Title: JAMA Cardiology
                Abbreviated Title: JAMA Cardiol
                Publisher: American Medical Association (AMA)
                ISSN (Print): 2380-6583
                Publication date (Electronic): October 23 2019
                Affiliations
                [1 ]Mike and Valeria Rosenbloom Centre for Cardiovascular Prevention, Department of Medicine, McGill University Health Centre, Montreal, Quebec, Canada
                [2 ]Monash Health Centre, Victoria, Australia
                [3 ]Duke Clinical Research Institute, Durham, North Carolina
                [4 ]Associate Editor, JAMA Cardiology
                [5 ]Duke University School of Medicine, Durham, North Carolina
                [6 ]Deputy Editor for Statistics, JAMA Cardiology
                [7 ]Department of Pharmacological and Biomolecular Sciences, University of Milan, Multimedica IRCCS, Milano, Italy
                [8 ]Centre for Naturally Randomized Trials, University of Cambridge, Cambridge, United Kingdom
                [9 ]Institute for Advanced Studies, University of Bristol, Bristol, United Kingdom
                [10 ]MRC/BHF Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom
                Article
                DOI: 10.1001/jamacardio.2019.3780
                PMC ID: 7369156
                PubMed ID: 31642874
                SO-VID: b64a2d31-2ce2-43fa-bd59-6b6008012a46
                Copyright © © 2019
                History

                Data availability:

                Comments

                Comment on this article

                scite_

                Similar content3,670

                See all similar

                Cited by160

                See all cited by

                Most referenced authors1,238

                See all reference authors