Evidence map›Paper›PMID 21445663›Full record

ReviewAnalytical and bioanalytical chemistry2011

Secreted phospholipase A2, lipoprotein hydrolysis, and atherosclerosis: integration with lipidomics.

Kei Yamamoto, Yuki Isogai, Hiroyasu Sato, Yoshitaka Taketomi, Makoto Murakami

Open access · hybridAbstract readReview
In one paragraph

Review in Analytical and bioanalytical chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.5field-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

14 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Group IID, IIE, IIF and III secreted phospholipase ABiochimica et biophysica acta. Molecular and cell biology of lipids · 2019
    Review
  8. Metabolic regulation by secreted phospholipase AInflammation and regeneration · 2016
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

5 authors at 1 institution in 1 country.

Kei YamamotoLipid Metabolism Project, The Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo, 156-8506, Japan.
Yuki Isogai
Hiroyasu Sato
Yoshitaka Taketomi
Makoto Murakami
Tokyo Metropolitan Institute of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phospholipase A(2) (PLA(2)) is a group of enzymes that hydrolyze the sn-2 position of glycerophospholipids to yield fatty acids and lysophospholipids. Of many PLA(2)s or related enzymes identified to date, secreted PLA(2)s (sPLA(2)s) comprise the largest family that contains 10 catalytically active isozymes. Besides arachidonic acid released from cellular membranes for eicosanoid synthesis, several if not all sPLA(2)s have recently been implicated in hydrolysis of phospholipids in lipoprotein particles. The sPLA(2)-processed low-density lipoprotein (LDL) particles contain a large amount of lysophospholipids and exhibit the property of "small-dense" or "modified" LDL, which facilitates foam cell formation from macrophages. Transgenic overexpression of these sPLA(2)s leads to development of atherosclerosis in mice. More importantly, genetic deletion or pharmacological inhibition of particular sPLA(2)s significantly attenuates atherosclerosis and aneurysm. In this article, we will give an overview of current understanding of the role of sPLA(2)s in atherosclerosis, with recent lipidomics data showing the action of a subset of sPLA(2)s on lipoprotein phospholipids.

Indexed as

AnimalsAtherosclerosisHumansHydrolysisLipidsLipoproteinsMicePhospholipases A2, SecretorySpectrometry, Mass, Electrospray IonizationLipidsLipoproteinsPhospholipases A2, Secretory

Identifiers

PMID21445663
PMCPMC3098357
OpenAlexW2033247700

What OpenQuestion holds

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LicenceCC BY-NC
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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.