Evidence map›Paper›PMID 27185859›Full record

ArticleJournal of lipid research2016

Endothelial HO-1 induction by model TG-rich lipoproteins is regulated through a NOX4-Nrf2 pathway.

Sally H Latham Birt, Robert Purcell, Kathleen M Botham, Caroline P D Wheeler-Jones

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 32% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. New insight into dyslipidemia-induced cellular senescence in atherosclerosis.Biological reviews of the Cambridge Philosophical Society · 2022
    Review
  2. Article
  3. 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

4 authors at 1 institution in 1 country.

Sally H Latham BirtDepartment of Comparative Biomedical Sciences, Royal Veterinary College, London NW1 0TU, United Kingdom.
Robert PurcellDepartment of Comparative Biomedical Sciences, Royal Veterinary College, London NW1 0TU, United Kingdom.
Kathleen M BothamDepartment of Comparative Biomedical Sciences, Royal Veterinary College, London NW1 0TU, United Kingdom.
Caroline P D Wheeler-JonesDepartment of Comparative Biomedical Sciences, Royal Veterinary College, London NW1 0TU, United Kingdom cwheeler@rvc.ac.uk.
Royal Veterinary College · GB

Funding

BBSRC BB/I005862/1BBSRC BB/J50015X/1
6 · The paper itself

Abstract

Circulating levels of chylomicron remnants (CMRs) increase postprandially and their composition directly reflects dietary lipid intake. These TG-rich lipoproteins likely contribute to the development of endothelial dysfunction, albeit via unknown mechanisms. Here, we investigated how the FA composition of CMRs influences their actions on human aortic endothelial cells (HAECs) by comparing the effects of model CMRs-artificial TG-rich CMR-like particles (A-CRLPs)-containing TGs extracted from fish, DHA-rich algal, corn, or palm oils. HAECs responded with distinct transcriptional programs according to A-CRLP TG content and oxidation status, with genes involved in antioxidant defense and cytoprotection most prominently affected by n-3 PUFA-containing A-CRLPs. These particles were significantly more efficacious inducers of heme oxygenase-1 (HO-1) than n-6 PUFA corn or saturated FA-rich palm CRLPs. Mechanistically, HO-1 induction by all CRLPs requires NADPH oxidase 4, with PUFA-containing particles additionally dependent upon mitochondrial reactive oxygen species. Activation of both p38 MAPK and PPARβ/δ culminates in increased nuclear factor erythroid 2-related factor 2 (Nrf2) expression/nuclear translocation and HO-1 induction. These studies define new molecular pathways coupling endothelial cell activation by model CMRs with adaptive regulation of Nrf2-dependent HO-1 expression and may represent key mechanisms through which dietary FAs differentially impact progression of endothelial dysfunction.

Indexed as

AnimalsAntioxidantsChylomicron RemnantsEndothelial CellsFatty Acids, Omega-3Gene Expression RegulationHeme Oxygenase-1HumansLipid MetabolismLipoproteinsNADPH Oxidase 4NADPH OxidasesNF-E2-Related Factor 2Oxidative StressReactive Oxygen SpeciesTriglyceridesAntioxidantsChylomicron RemnantsFatty Acids, Omega-3Heme Oxygenase-1HMOX1 protein, humanLipoproteinsNADPH Oxidase 4NADPH OxidasesNFE2L2 protein, humanNF-E2-Related Factor 2NOX4 protein, humanReactive Oxygen SpeciesTriglyceridesartificial chylomicron remnant-like particlescell signalingendothelial cellsfatty acidheme oxygenase-1lipids/oxidationnuclear factor erythroid 2-related factor 2omega-3 fatty acidsreduced nicotinamide adenine dinucleotide phosphate oxidase 4triglyceride

Identifiers

PMID27185859
PMCPMC4918850
OpenAlexW2405700589

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.