Evidence map›Paper›PMID 21400045›Full record

ReviewProtein & cell2011

Apolipoproteins and amyloid fibril formation in atherosclerosis.

Chai Lean Teoh, Michael D W Griffin, Geoffrey J Howlett

Open access · bronzeAbstract readReview
In one paragraph

Review in Protein & cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 59 citations in OpenAlex.

  1. Trial
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  8. Review
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  15. Review
  16. Renal ApoA-1 amyloidosis with Glu34Lys mutation and intra-amyloid lipid accumulation.Journal of the American Society of Nephrology : JASN · 2014
    Article
  17. Conformational and aggregation properties of the 1-93 fragment of apolipoprotein A-I.Protein science : a publication of the Protein Society · 2014
    Article
  18. Article
  19. Pharmaceutical amyloidosis associated with subcutaneous insulin and enfuvirtide administration.Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis · 2014
    Article
  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

3 authors at 1 institution in 1 country.

Chai Lean TeohDepartment of Biochemistry and Molecular Biology, University of Melbourne, Parkville, Victoria 3010, Australia.
Michael D W Griffin
Geoffrey J Howlett
University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyloid fibrils arise from the aggregation of misfolded proteins into highly-ordered structures. The accumulation of these fibrils along with some non-fibrillar constituents within amyloid plaques is associated with the pathogenesis of several human degenerative diseases. A number of plasma apolipoproteins, including apolipoprotein (apo) A-I, apoA-II, apoC-II and apoE are implicated in amyloid formation or influence amyloid formation by other proteins. We review present knowledge of amyloid formation by apolipoproteins in disease, with particular focus on atherosclerosis. Further insights into the molecular mechanisms underlying their amyloidogenic propensity are obtained from in vitro studies which describe factors affecting apolipoprotein amyloid fibril formation and interactions. Additionally, we outline the evidence that amyloid fibril formation by apolipoproteins might play a role in the development and progression of atherosclerosis, and highlight possible molecular mechanisms that could contribute to the pathogenesis of this disease.

Indexed as

AmyloidApolipoproteinsAtherosclerosisHumansMolecular ChaperonesPhospholipidsAmyloidApolipoproteinsMolecular ChaperonesPhospholipids

Identifiers

PMID21400045
PMCPMC4723368
OpenAlexW1977353914

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.