Evidence map›Paper›PMID 25197325›Full record

ReviewBiomolecular concepts2013

Aggregation and fusion of low-density lipoproteins in vivo and in vitro.

Mengxiao Lu, Olga Gursky

Open access · bronzeAbstract readReview
In one paragraph

Review in Biomolecular concepts, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 68 citations in OpenAlex.

  1. Effect ofCancer science · 2023
    Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Can Electronegative LDL Act as a Multienzymatic Complex?International journal of molecular sciences · 2023
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Pathophysiology of Atherosclerosis.International journal of molecular sciences · 2022
    Review
  19. Cholesterol Transport Dysfunction and Its Involvement in Atherogenesis.International journal of molecular sciences · 2022
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Mengxiao LuDepartment of Physiology and Biophysics, Boston University School of Medicine, W321, 700 Albany Street, Boston, MA 02118, USA. mxlu@bu.edu
Olga Gursky
Boston University · US

Funding

Structural Thermodynamics of Human Apolipoprotein C-1R01GM067260 · NIGMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GURSKY, OLGA · 2003 to 2024
$7.4M
NHLBI NIH HHS HL026355NIGMS NIH HHS GM067260NIGMS NIH HHS R01 GM067260
6 · The paper itself

Abstract

Low-density lipoproteins (LDLs, also known as 'bad cholesterol') are the major carriers of circulating cholesterol and the main causative risk factor of atherosclerosis. Plasma LDLs are 20- to 25-nm nanoparticles containing a core of cholesterol esters surrounded by a phospholipid monolayer and a single copy of apolipoprotein B (550 kDa). An early sign of atherosclerosis is the accumulation of LDL-derived lipid droplets in the arterial wall. According to the widely accepted 'response-to-retention hypothesis', LDL binding to the extracellular matrix proteoglycans in the arterial intima induces hydrolytic and oxidative modifications that promote LDL aggregation and fusion. This enhances LDL uptake by the arterial macrophages and triggers a cascade of pathogenic responses that culminate in the development of atherosclerotic lesions. Hence, LDL aggregation, fusion, and lipid droplet formation are important early steps in atherogenesis. In vitro, a variety of enzymatic and nonenzymatic modifications of LDL can induce these reactions and thereby provide useful models for their detailed analysis. Here, we summarize current knowledge of the in vivo and in vitro modifications of LDLs leading to their aggregation, fusion, and lipid droplet formation; outline the techniques used to study these reactions; and propose a molecular mechanism that underlies these pro-atherogenic processes. Such knowledge is essential in identifying endogenous and exogenous factors that can promote or prevent LDL aggregation and fusion in vivo and to help establish new potential therapeutic targets to decelerate or even block these pathogenic reactions.

Indexed as

Apolipoproteins BAtherosclerosisCeramidesEstradiolFatty Acids, NonesterifiedHumansLipoproteinsLipoproteins, LDLSerum AlbuminStress, MechanicalApolipoproteins BCeramidesEstradiolFatty Acids, NonesterifiedLipoproteinsLipoproteins, LDLSerum Albumin

Identifiers

PMID25197325
PMCPMC4154560
OpenAlexW2066702789

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.