Evidence map›Paper›PMID 29378164›Full record

ReviewArchives of biochemistry and biophysics2018

The chlorinated lipidome originating from myeloperoxidase-derived HOCl targeting plasmalogens: Metabolism, clearance, and biological properties.

Elisa N D Palladino, Celine L Hartman, Carolyn J Albert, David A Ford

Abstract readReview
In one paragraph

Review in Archives of biochemistry and biophysics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. NETosis as a Pathogenic Factor for Heart Failure.Oxidative medicine and cellular longevity · 2021
    Review
  6. Looking Back at the Early Stages of Redox Biology.Antioxidants (Basel, Switzerland) · 2020
    Review
  7. Article
  8. Article
  9. Review
  10. S1P and plasmalogen derived fatty aldehydes in cellular signaling and functions.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020
    Review
  11. Article
  12. Review
  13. 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

4 authors at 1 institution in 1 country.

Elisa N D PalladinoEdward A. Doisy Department of Biochemistry and Molecular Biology and the Center for Cardiovascular Research, Saint Louis University School of Medicine, St. Louis, MO, United States.
Celine L HartmanEdward A. Doisy Department of Biochemistry and Molecular Biology and the Center for Cardiovascular Research, Saint Louis University School of Medicine, St. Louis, MO, United States.
Carolyn J AlbertEdward A. Doisy Department of Biochemistry and Molecular Biology and the Center for Cardiovascular Research, Saint Louis University School of Medicine, St. Louis, MO, United States.
David A FordEdward A. Doisy Department of Biochemistry and Molecular Biology and the Center for Cardiovascular Research, Saint Louis University School of Medicine, St. Louis, MO, United States. Electronic address: david.ford@health.slu.edu.
Saint Louis University · US

Funding

Chlorinated lipids in sepsisR01GM115553 · NIGMS · SAINT LOUIS UNIVERSITY · PI FORD, DAVID A., MCHOWAT, JANE · 2015 to 2021
$3.0M
NIGMS NIH HHS R01 GM115553
6 · The paper itself

Abstract

Myeloperoxidase produces the two-electron oxidant HOCl, which targets plasmalogen phospholipids liberating 2-chlorofatty aldehyde. 2-Chlorofatty aldehyde has four known fates: 1) oxidation to 2-chlorofatty acid; 2) reduction to 2-chlorofatty alcohol; 3) Schiff base adduct formation with proteins and amines; and 4) reactivity with glutathione through nucleophilic attack of the α-chlorinated carbon. 2-Chlorofatty acid does not undergo conventional fatty acid β-oxidation due to the presence of the α-chlorinated carbon; however, 2-chlorofatty acid does undergo sequential ω-oxidation and β-oxidation from the ω-end, ultimately resulting in 2-chloroadipic acid urinary excretion. Recent studies have demonstrated that 2-chlorofatty acid clearance is increased by treatment with the PPAR-α agonist WY14643, which increases the enzymatic machinery responsible for hepatic ω-oxidation. Furthermore, 2-chlorofatty acid has been shown to be a PPAR-α agonist, and thus accelerates its own clearance. The roles of 2-chlorofatty aldehyde and 2-chlorofatty acid on leukocyte and endothelial function have been explored by several groups, suggesting that chlorinated lipids induce endothelial cell dysfunction, neutrophil chemotaxis, monocyte apoptosis, and alterations in vascular tone. Thus, the chlorinated lipidome, produced in response to leukocyte activation, is a potential biomarker and therapeutic target to modulate host response in inflammatory diseases.

Indexed as

Lipid MetabolismAldehydesAnimalsBiomarkersChlorineDiseaseEsterificationFatty Acids, NonesterifiedHalogenationHumansHypochlorous AcidNeutrophilsOxidation-ReductionPeroxidasePlasmalogensPPAR alphaAldehydesBiomarkersChlorineFatty Acids, NonesterifiedHypochlorous AcidPeroxidasePlasmalogensPPAR alphaChlorinated lipidomeInflammationNeutrophil activationPlasmalogens

Identifiers

PMID29378164
PMCPMC5817035
OpenAlexW2791532299

What OpenQuestion holds

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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.