Evidence map›Paper›PMID 29729330›Full record

ArticleFree radical biology & medicine2018

Paraoxonase 2 prevents the development of heart failure.

Wei Li, David Kennedy, Zhili Shao, Xi Wang, Andre Klaassen Kamdar, Malory Weber, Kayla Mislick, Kathryn Kiefer, Rommel Morales, Brendan Agatisa-Boyle and 4 more

Abstract read
In one paragraph

Article in Free radical biology & medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. A Case-Control Study Supports Genetic Contribution of theAntioxidants (Basel, Switzerland) · 2024
    Article
  3. Article
  4. Article
  5. Paraoxonases at the Heart of Neurological Disorders.International journal of molecular sciences · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Human Paraoxonase-2 (PON2): Protein Functions and Modulation.Antioxidants (Basel, Switzerland) · 2021
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

14 authors at 7 institutions in 1 country.

Wei LiDepartment of Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, WV, United States.
David KennedyDepartment of Medicine, University of Toledo, OH, United States.
Zhili ShaoDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, OH, United States.
Xi WangDepartment of Medicine, Stanford University School of Medicine, CA, United States.
Andre Klaassen KamdarDepartment of Medicine, University of Minnesota, MN, United States.
Malory WeberDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, OH, United States.
Kayla MislickDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, OH, United States.
Kathryn KieferDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, OH, United States.
Rommel MoralesDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, OH, United States.
Brendan Agatisa-BoyleDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, OH, United States.
Diana M ShihDepartment of Medicine, Division of Cardiology, University of California at Los Angeles, Los Angeles, CA, United States.
Srinivasa T ReddyDepartment of Medicine, Division of Cardiology, University of California at Los Angeles, Los Angeles, CA, United States.
Christine S MoravecDepartment of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, OH, United States.
W H Wilson TangDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, OH, United States; Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, OH, United States; Center for Clinical Genomics, Cleveland Clinic, OH, United States. Electronic address: tangw@ccf.org.
Cleveland Clinic Lerner College of Medicine · USUniversity of California, Los Angeles · USCleveland Clinic · USMarshall University · USStanford University · USUniversity of Minnesota · USUniversity of Toledo · US

Funding

Clinical and Translational Science Collaborative of ClevelandUL1TR000439 · NCATS · CASE WESTERN RESERVE UNIVERSITY · PI KONSTAN, MICHAEL W. · 2012 to 2016
$50.0M
The role of PON2 and PON3 proteins in AtherosclerosisR01HL071776 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI REDDY, SRINIVASA T. · 2003 to 2017
$4.8M
Functional Cardio-MetabolomicsP20HL113452 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI HAZEN, STANLEY L, TANG, WAI HONG WILSON · 2012 to 2016
$4.8M
Nitrative stress in heart failureR01HL103931 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI TANG, WAI HONG WILSON · 2010 to 2014
$3.8M
Diet, Gut Microbiota, and Heart FailureR01HL126827 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI HAZEN, STANLEY L, TANG, WAI HONG WILSON · 2016 to 2019
$3.1M
Dietary Choline, Gut Microbiota, and Susceptibility for Chronic Kidney DiseaseR01DK106000 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI HAZEN, STANLEY L, TANG, WAI HONG WILSON · 2015 to 2018
$2.8M
NCATS NIH HHS UL1 TR000439NHLBI NIH HHS P20 HL113452NHLBI NIH HHS R01 HL071776NHLBI NIH HHS R01 HL103931NHLBI NIH HHS R01 HL126827NIDDK NIH HHS R01 DK106000
6 · The paper itself

Abstract

backgroundMitochondrial oxidation is a major source of reactive oxygen species (ROS) and mitochondrial dysfunction plays a central role in development of heart failure (HF). Paraoxonase 2 deficient (PON2-def) mitochondria are impaired in function. In this study, we tested whether PON2-def aggravates HF progression. METHODS AND

resultsUsing qPCR, immunoblotting and lactonase activity assay, we demonstrate that PON2 activity was significantly decreased in failing hearts despite increased PON2 expression. To determine the cardiac-specific function of PON2, we performed heart transplantations in which PON2-def and wild type (WT) donor hearts were implanted into WT recipient mice. Beating scores of the donor hearts, assessed at 4 weeks post-transplantation, were significantly decreased in PON2-def hearts when compared to WT donor hearts. By using a transverse aortic constriction (TAC) model, we found PON2 deficiency significantly exacerbated left ventricular remodeling and cardiac fibrosis post-TAC. We further demonstrated PON2 deficiency significantly enhanced ROS generation in heart tissues post-TAC. ROS generation was measured through dihydroethidium (DHE) using high-pressure liquid chromatography (HPLC) with a fluorescent detector. By using neonatal cardiomyocytes treated with CoCl

conclusionOur study suggests a cardioprotective role for PON2 in both experimental and human heart failure, which may be associated with the ability of PON2 to improve mitochondrial function and diminish ROS generation.

Indexed as

Oxidative StressAnimalsAryldialkylphosphataseHeart FailureHeart TransplantationHumansMaleMiceMice, KnockoutMyocytes, CardiacOxidation-ReductionReactive Oxygen SpeciesAryldialkylphosphatasePON2 protein, humanPON2 protein, mouseReactive Oxygen SpeciesCardiomyopathyHeart failureParaoxonase 2

Identifiers

PMID29729330
PMCPMC5971153
OpenAlexW2800265223

What OpenQuestion holds

Textmetadata
LicenceTDM
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.