Evidence map›Paper›PMID 16467150›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Peroxisome proliferator-activated receptor delta promotes very low-density lipoprotein-derived fatty acid catabolism in the macrophage.

Chih-Hao Lee, Kihwa Kang, Isaac R Mehl, Russell Nofsinger, William A Alaynick, Ling-Wa Chong, John M Rosenfeld, Ronald M Evans

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. Article
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  4. Nutritional immunomodulation of Atlantic salmon response toFrontiers in molecular biosciences · 2022
    Article
  5. Article
  6. Article
  7. Article
  8. Role of LpL (Lipoprotein Lipase) in Macrophage Polarization In Vitro and In Vivo.Arteriosclerosis, thrombosis, and vascular biology · 2019
    Article
  9. Article
  10. Exercise in a Pill: The Latest on Exercise-Mimetics.Brain plasticity (Amsterdam, Netherlands) · 2017
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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  20. Review
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

8 authors at 4 institutions in 1 country.

Chih-Hao LeeDepartment of Genetics and Complex Diseases, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA.
Kihwa Kang
Isaac R Mehl
Russell Nofsinger
William A Alaynick
Ling-Wa Chong
John M Rosenfeld
Ronald M Evans
Howard Hughes Medical Institute · USHarvard University · USSalk Institute for Biological Studies · USUniversity of California, San Diego · US

Funding

HORMONAL REGULATION OF MAMMALIAN GENE EXPRESSIONR37DK057978 · NIDDK · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI EVANS, RONALD M · 2000 to 2019
$16.0M
Hormonal Regulation of Mammalian Gene ExpressionR01DK057978 · NIDDK · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI EVANS, RONALD M · 2021 to 2024
$2.6M
NHLBI NIH HHS P50 HL56898NIDDK NIH HHS DK57978NIDDK NIH HHS R01 DK057978NIDDK NIH HHS R37 DK057978
6 · The paper itself

Abstract

Significant attention has focused on the role of low-density lipoprotein (LDL) in the pathogenesis of atherosclerosis. However, recent advances have identified triglyceride-rich lipoproteins [e.g., very LDL (VLDL)] as independent risk predictors for this disease. We have previously demonstrated peroxisome proliferator-activated receptor (PPAR)delta, but not PPARgamma, is the major nuclear VLDL sensor in the macrophage, which is a crucial component of the atherosclerotic lesion. Here, we show that, in addition to beta-oxidation and energy dissipation, activation of PPARdelta by VLDL particles induces key genes involved in carnitine biosynthesis and lipid mobilization mediated by a recently identified TG lipase, transport secretion protein 2 (also named desnutrin, iPLA2zeta, and adipose triglyceride lipase), resulting in increased fatty acid catabolism. Unexpectedly, deletion of PPARdelta results in derepression of target gene expression, a phenotype similar to that of ligand activation, suggesting that unliganded PPARdelta suppresses fatty acid utilization through active repression, which is reversed upon ligand binding. This unique transcriptional mechanism assures a tight control of the homeostasis of VLDL-derived fatty acid and provides a therapeutic target for other lipid-related disorders, including dyslipidemia and diabetes, in addition to coronary artery disease.

Indexed as

Gene Expression RegulationAcyltransferasesAnimalsCarboxylic Ester HydrolasesCarnitineFatty AcidsGene DeletionLipaseLipid MetabolismLipoproteins, VLDLMacrophagesMiceOxidation-ReductionPPAR deltaAcyltransferasesCarboxylic Ester HydrolasesCarnitineFatty AcidsLipaseLipoproteins, VLDLPNPLA2 protein, mousePPAR delta

Identifiers

PMID16467150
PMCPMC1413732
OpenAlexW2000251574

What Socratic 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 Socratic graph.