Evidence map›Paper›PMID 25038992›Full record

ReviewAdvances in experimental medicine and biology2014

Inflammation, infection, cancer and all that…the role of paraoxonases.

Asokan Devarajan, Diana Shih, Srinivasa T Reddy

Open access · greenAbstract readReview
In one paragraph

Review in Advances in experimental medicine and biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
18.6field-weighted citation impact, top 1% 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

32 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Review
  3. Paraoxonase 3 regulates the pore-forming α subunit of the large-conductance KBiochimica et biophysica acta. Molecular cell research · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Paraoxonase 2 is an ER chaperone that regulates the epithelial NaAmerican journal of physiology. Cell physiology · 2022
    Article
  14. Review
  15. Association of M55L and Q192R polymorphisms of paraoxonase 1 geneInternational journal of reproductive biomedicine · 2021
    Article
  16. Review
  17. Article
  18. Article
  19. Review
  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 1 institution in 1 country.

Asokan DevarajanDepartment of Obstetrics and Gynecology, David Geffen School of Medicine at UCLA, 90095, Los Angeles, CA, USA, ADevarajan@mednet.ucla.edu.
Diana Shih
Srinivasa T Reddy
University of California, Los Angeles · US

Funding

The role of PON2 and PON3 proteins in AtherosclerosisR01HL071776 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI REDDY, SRINIVASA T. · 2003 to 2017
$4.8M
NHLBI NIH HHS R01 HL071776
6 · The paper itself

Abstract

The paraoxonase (PON) gene family consists of three members, PON1, PON2 and PON3. All PON proteins possess antioxidant properties and lipo-lactonase activities, and are implicated in the pathogenesis of several inflammatory diseases including atherosclerosis, Alzheimer's, Parkinson's, diabetes and cancer. Despite the role of PON proteins in critical cellular functions and associated pathologies, the physiological substrates and molecular mechanisms by which PON proteins function as anti-inflammatory proteins remain largely unknown. PON1 is found exclusively extracellular and associated solely with high-density lipoprotein (HDL) particles in the circulation, and, in part, confers the anti-oxidant and anti-inflammatory properties associated with HDL. Recent studies demonstrated that the intracellular PON proteins; PON2 and PON3 (i) are associated with mitochondria and mitochondria-associated membranes, (ii) modulate mitochondria-dependent superoxide production, and (iii) prevent apoptosis. Overexpression of PON2 and PON3 genes protected (i) mitochondria from antimycin or oligomycin mediated mitochondrial dysfunction and (ii) ER stress and ER stress mediated mitochondrial dysfunction. These studies illustrate that the anti-inflammatory effects of PON2 and PON3 may, in part, be mediated by their role in mitochondrial and associated organelle function. Since oxidative stress as a result of mitochondrial dysfunction is implicated in the development of inflammatory diseases including atherosclerosis and cancer, these recent studies on PON2 and PON3 proteins may provide a mechanism for the scores of epidemiological studies that show a link between PON genes and numerous inflammatory diseases. Understanding such mechanisms will provide novel routes of intervention in the treatment of diseases associated with pro-inflammatory oxidative stress.

Indexed as

Oxidative StressAnimalsApoptosisAryldialkylphosphataseAtherosclerosisHumansInfectionsInflammationLipoproteins, HDLMitochondriaMitochondrial MembranesNeoplasm ProteinsNeoplasmsSuperoxidesAryldialkylphosphataseLipoproteins, HDLNeoplasm ProteinsSuperoxides

Identifiers

PMID25038992
PMCPMC4405152
OpenAlexW1920729648

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.