Evidence map›Paper›PMID 21474962›Full record

ArticleJournal of nutrigenetics and nutrigenomics2011

Nutrigenetic disruption of inflammation-resolution homeostasis and atherogenesis.

Aksam J Merched, Charles N Serhan, Lawrence Chan

Open access · goldAbstract read
In one paragraph

Article in Journal of nutrigenetics and nutrigenomics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Review
  3. Inverse Association between Omega-3 Index and Severity of COVID-19: A Case-Control Study.International journal of environmental research and public health · 2022
    Article
  4. Review
  5. Review
  6. Mediterranean Diet: Lipids, Inflammation, and Malaria Infection.International journal of molecular sciences · 2020
    Review
  7. Review
  8. Review
  9. Pro-resolving lipid mediators in vascular disease.The Journal of clinical investigation · 2018
    Review
  10. The role of non-resolving inflammation in atherosclerosis.The Journal of clinical investigation · 2018
    Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
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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

3 authors at 2 institutions in 1 country.

Aksam J MerchedDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA. amerched@bcm.edu
Charles N Serhan
Lawrence Chan
Baylor College of Medicine · USBrigham and Women's Hospital · US

Funding

MODELS FOR ATHEROSCLEROSIS RESEARCHR01HL051586 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI CHAN, LAWRENCE · 1994 to 2014
$5.5M
BLOOD CELL LIPOXYGENASE PRODUCTS: FORMATION AND ACTIONR01GM038765 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI SERHAN, CHARLES NICHOLAS · 1992 to 2020
$4.9M
NHLBI NIH HHS HL-51586NHLBI NIH HHS R01 HL051586NIGMS NIH HHS GM03865NIGMS NIH HHS R01 GM038765
6 · The paper itself

Abstract

BACKGROUND/

aimPro-resolving and anti-inflammatory mediator products of murine 12/15-lipoxygenase (LOX) exhibit potent actions on vascular inflammation and protect against the progression of atherosclerosis. The present study was designed to determine whether augmenting dietary lipids modulates the body's endogenous anti-inflammatory pro-resolving mechanisms and promotes atherosclerosis. METHODS/

resultsWe investigated the biometabolic consequences of variations in lipid mediator biosynthesis using genetic knockout and overexpression models of 12/15-LOX mice fed the commonly used 'Western diet'. Unexpectedly, this high-fat diet annulled the protective actions of 12/15-LOX, and the combination of a Western diet and 12/15-LOX overexpression paradoxically promoted inflammation leading to production of diet-related and 12/15-LOX-dependent blood mediators that differentially activated endothelial cells via expression of ICAM-1. Hyperlipidemia not only affected the biosynthesis of lipoxin A4, a key pro-resolving mediator, but also disrupted the protective pro-resolving function of 12/15-LOX products, and the enzyme pathway no longer protected against atherosclerosis in vivo.

conclusionWe uncovered a novel mechanism whereby a high-fat diet as well as hyperlipidemia disrupt the homeostasis of inflammation resolution. These findings underscore the importance of dietary essential PUFAs and LOX-derived lipid mediators in combination with lipid-lowering agents in the prevention and treatment of atherosclerotic cardiovascular diseases.

Indexed as

Nutritional Physiological PhenomenaAnimalsAnti-Inflammatory AgentsApolipoproteins EAtherosclerosisCells, CulturedExtracellular Matrix ProteinsFemaleHomeostasisHumansHypolipidemic AgentsInflammationMaleMiceMice, Inbred C57BLMice, KnockoutAnti-Inflammatory AgentsApolipoproteins EExtracellular Matrix ProteinsHypolipidemic AgentsLox protein, mouseProtein-Lysine 6-Oxidase

Identifiers

PMID21474962
PMCPMC3080581
OpenAlexW2011975289

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.