Evidence map›Paper›PMID 27581680›Full record

Trial reportJournal of lipid research2016

Statin action enriches HDL3 in polyunsaturated phospholipids and plasmalogens and reduces LDL-derived phospholipid hydroperoxides in atherogenic mixed dyslipidemia.

Alexina Orsoni, Patrice Thérond, Ricardo Tan, Philippe Giral, Paul Robillard, Anatol Kontush, Peter J Meikle, M John Chapman

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report 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 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Deciphering Acute Coronary Syndromes Pathobiology Through Proteomics.Journal of cardiovascular development and disease · 2025
    Review
  3. Review
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  8. Exploring the Role of a Novel Peptide fromInternational journal of molecular sciences · 2020
    Article
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  10. Review
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  15. 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

8 authors at 5 institutions in 2 countries.

Alexina OrsoniClinical Biochemistry Service, APHP, HUPS, Bicêtre University Hospital, Le Kremlin Bicêtre, France.ORCID 0000-0003-4250-6280
Patrice ThérondClinical Biochemistry Service, APHP, HUPS, Bicêtre University Hospital, Le Kremlin Bicêtre, France.ORCID 0000-0002-7655-2229
Ricardo TanBaker IDI Heart and Diabetes Institute, Melbourne, Australia.
Philippe GiralService of Endocrinology-Metabolism and Cardiovascular Disease Prevention, Pitié-Salpêtrière University Hospital, Paris, France.
Paul RobillardINSERM UMR-S939, Dyslipidemia and Atherosclerosis, and University of Pierre and Marie Curie, Pitié-Salpêtrière University Hospital, Paris, France.
Anatol KontushINSERM UMR-S1166 and University of Pierre and Marie Curie, Pitié-Salpêtrière University Hospital, Paris, France.
Peter J MeikleBaker IDI Heart and Diabetes Institute, Melbourne, Australia.ORCID 0000-0002-2593-4665
M John ChapmanClinical Biochemistry Service, APHP, HUPS, Bicêtre University Hospital, Le Kremlin Bicêtre, France john.chapman@upmc.fr.
Baker Heart and Diabetes Institute · AUBicêtre Hospital · FRSorbonne Université · FRInserm · FRPitié-Salpêtrière Hospital · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherogenic mixed dyslipidemia associates with oxidative stress and defective HDL antioxidative function in metabolic syndrome (MetS). The impact of statin treatment on the capacity of HDL to inactivate LDL-derived, redox-active phospholipid hydroperoxides (PCOOHs) in MetS is indeterminate. Insulin-resistant, hypertriglyceridemic, hypertensive, obese males were treated with pitavastatin (4 mg/day) for 180 days, resulting in marked reduction in plasma TGs (-41%) and LDL-cholesterol (-38%), with minor effects on HDL-cholesterol and apoAI. Native plasma LDL (baseline vs. 180 days) was oxidized by aqueous free radicals under mild conditions in vitro either alone or in the presence of the corresponding pre- or poststatin HDL2 or HDL3 at authentic plasma mass ratios. Lipidomic analyses revealed that statin treatment i) reduced the content of oxidizable polyunsaturated phosphatidylcholine (PUPC) species containing DHA and linoleic acid in LDL; ii) preferentially increased the content of PUPC species containing arachidonic acid (AA) in small, dense HDL3; iii) induced significant elevation in the content of phosphatidylcholine and phosphatidylethanolamine (PE) plasmalogens containing AA and DHA in HDL3; and iv) induced formation of HDL3 particles with increased capacity to inactivate PCOOH with formation of redox-inactive phospholipid hydroxide. Statin action attenuated LDL oxidability Concomitantly, the capacity of HDL3 to inactivate redox-active PCOOH was enhanced relative to HDL2, consistent with preferential enrichment of PE plasmalogens and PUPC in HDL3.

Indexed as

AdultAgedAntioxidantsApolipoprotein A-ICholesterol, HDLCholesterol, LDLDyslipidemiasFemaleHumansMaleMiddle AgedOxidative StressQuinolinesAntioxidantsAPOA1 protein, humanApolipoprotein A-ICholesterol, HDLCholesterol, LDLpitavastatinQuinolinesantioxidative activityhigh density lipoprotein 3lipidomicslow density lipoproteinmetabolic syndrome diseaseoxidative stressphospholipid hydroxidespitavastatin

Identifiers

PMID27581680
PMCPMC5087874
OpenAlexW2514952024

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.