Evidence map›Paper›PMID 25646365›Full record

ArticleJournal of lipid research2015

Source and role of intestinally derived lysophosphatidic acid in dyslipidemia and atherosclerosis.

Mohamad Navab, Arnab Chattopadhyay, Greg Hough, David Meriwether, Spencer I Fogelman, Alan C Wagner, Victor Grijalva, Feng Su, G M Anantharamaiah, Lin H Hwang and 3 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of lipid research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Frontiers in cardiovascular medicine · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Article
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  11. Review
  12. Coronary Artery Disease Risk-AssociatedArteriosclerosis, thrombosis, and vascular biology · 2019
    Article
  13. Review
  14. Article
  15. An Updated Review of Lysophosphatidylcholine Metabolism in Human Diseases.International journal of molecular sciences · 2019
    Review
  16. Article
  17. Article
  18. Review
  19. 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

13 authors at 2 institutions in 1 country.

Mohamad NavabDepartment of Medicine, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095-1736.
Arnab ChattopadhyayDepartment of Medicine, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095-1736.
Greg HoughDepartment of Medicine, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095-1736.
David MeriwetherDepartment of Medicine, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095-1736 Department of Molecular and Medical Pharmacology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095-1736.
Spencer I FogelmanDepartment of Medicine, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095-1736.
Alan C WagnerDepartment of Medicine, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095-1736.
Victor GrijalvaDepartment of Medicine, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095-1736.
Feng SuDepartment of Obstetrics and Gynecology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095-1736.
G M AnantharamaiahDepartment of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294.
Lin H HwangSemel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095-1736.
Kym F FaullSemel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095-1736.
Srinivasa T ReddyDepartment of Medicine, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095-1736 Department of Molecular and Medical Pharmacology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095-1736 Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095-1736.
Alan M FogelmanDepartment of Medicine, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095-1736.
University of California, Los Angeles · USUniversity of Alabama at Birmingham · US

Funding

ULTRASTRUCTURE OF THE INTIMA IN EARLY LESION FORMATIONP01HL030568 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FOGELMAN, ALAN M · 1985 to 2019
$55.2M
SYNTHETIC PEPTIDE STUDIES OF THE AMPHIPATHIC HELIXP01HL034343 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SEGREST, JERE P · 1985 to 2012
$18.8M
NHLBI NIH HHS HL-30568NHLBI NIH HHS HL-34343NHLBI NIH HHS P01 HL030568NHLBI NIH HHS P01 HL034343
6 · The paper itself

Abstract

We previously reported that i) a Western diet increased levels of unsaturated lysophosphatidic acid (LPA) in small intestine and plasma of LDL receptor null (LDLR(-/-)) mice, and ii) supplementing standard mouse chow with unsaturated (but not saturated) LPA produced dyslipidemia and inflammation. Here we report that supplementing chow with unsaturated (but not saturated) LPA resulted in aortic atherosclerosis, which was ameliorated by adding transgenic 6F tomatoes. Supplementing chow with lysophosphatidylcholine (LysoPC) 18:1 (but not LysoPC 18:0) resulted in dyslipidemia similar to that seen on adding LPA 18:1 to chow. PF8380 (a specific inhibitor of autotaxin) significantly ameliorated the LysoPC 18:1-induced dyslipidemia. Supplementing chow with LysoPC 18:1 dramatically increased the levels of unsaturated LPA species in small intestine, liver, and plasma, and the increase was significantly ameliorated by PF8380 indicating that the conversion of LysoPC 18:1 to LPA 18:1 was autotaxin dependent. Adding LysoPC 18:0 to chow increased levels of LPA 18:0 in small intestine, liver, and plasma but was not altered by PF8380 indicating that conversion of LysoPC 18:0 to LPA 18:0 was autotaxin independent. We conclude that i) intestinally derived unsaturated (but not saturated) LPA can cause atherosclerosis in LDLR(-/-) mice, and ii) autotaxin mediates the conversion of unsaturated (but not saturated) LysoPC to LPA.

Indexed as

AnimalsAortaAtherosclerosisBenzoxazolesDietary FatsDyslipidemiasFemaleGroup IB Phospholipases A2Intestinal AbsorptionIntestinal MucosaIntestinesJejunumLiverLysophosphatidylcholinesLysophospholipase DLysophospholipids6-(3-(piperazin-1-yl)propanoyl)benzo(d)oxazol-2(3H)-oneBenzoxazolesDietary FatsGroup IB Phospholipases A2lysophosphatidic acidLysophosphatidylcholinesLysophospholipase DLysophospholipidsPhosphoric Diester HydrolasesPiperazinesPla2g1b protein, mouseReceptors, LDL6F peptideapolipoprotein A-I mimetic peptidesgenetically engineered tomato plantslysophosphatidylcholine

Identifiers

PMID25646365
PMCPMC4373744
OpenAlexW2121323318

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.