Evidence map›Paper›PMID 23493561›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Unique mechanistic insights into the beneficial effects of soluble epoxide hydrolase inhibitors in the prevention of cardiac fibrosis.

Padmini Sirish, Ning Li, Jun-Yan Liu, Kin Sing Stephen Lee, Sung Hee Hwang, Hong Qiu, Cuifen Zhao, Siu Mei Ma, Javier E López, Bruce D Hammock and 1 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
–field-weighted citation impact
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

60 citing papers in PubMed.

  1. The Roles of EETs in Neurological Disorders.CNS neuroscience & therapeutics · 2026
    Review
  2. Soluble Epoxide Hydrolase Inhibitors Improve Cornea Alkali Wound Healing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Annexin A1 attenuates cardiac diastolic dysfunction in mice with inflammatory arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Review
  15. Article
  16. Review
  17. Article
  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

11 authors.

Padmini SirishDivision of Cardiovascular Medicine, University of California, Davis, CA 95616, USA.
Ning Li
Jun-Yan Liu
Kin Sing Stephen Lee
Sung Hee Hwang
Hong Qiu
Cuifen Zhao
Siu Mei Ma
Javier E López
Bruce D Hammock
Nipavan Chiamvimonvat

Funding

Workshop on Environmental Technology Transfer and EntrepreneurshipP42ES004699 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1987 to 2021
$50.1M
UC Davis Center for Children's Environmental Health (CCEH)P01ES011269 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI VAN DE WATER, JUDY A. · 2001 to 2018
$12.5M
Functional Interactions of Cardiac Ion ChannelsR01HL085844 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN · 2007 to 2025
$7.3M
Training Program In Basic & Translational Cardiovascular ScienceT32HL086350 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Martin Cadeiras, David A. Liem · 2008 to 2026
$7.1M
Translational Study of Cardiac DysfunctionR01HL085727 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN, SIRISH, PADMINI · 2008 to 2022
$5.7M
HYDROLYTIC ENZYMES IN THE METABOLISM OF TOXINSR01ES002710 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1985 to 2018
$4.0M
HYDROLYTIC ENZYMES IN THE METABOLISM OF TOXINSR37ES002710 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1998 to 2007
$3.0M
Regulation of ion channels in the heartI01BX000576 · VA · VA NORTHERN CALIFORNIA HEALTH CARE SYS · PI CHIAMVIMONVAT, NIPAVAN · 2009 to 2019
–
BLRD VA I01 BX000576Howard Hughes Medical InstituteNHLBI NIH HHS HL85727NHLBI NIH HHS HL85844NHLBI NIH HHS R01 HL085727NHLBI NIH HHS R01 HL085844NHLBI NIH HHS T32 HL086350NHLBI NIH HHS T32 HL86350NIEHS NIH HHS P01 ES011269NIEHS NIH HHS P01 ES11269NIEHS NIH HHS P42 ES004699NIEHS NIH HHS P42 ES04699NIEHS NIH HHS R01 ES002710NIEHS NIH HHS R37 ES002710NIEHS NIH HHS R37 ES02710
6 · The paper itself

Abstract

Tissue fibrosis represents one of the largest groups of diseases for which there are very few effective therapies. In the heart, myocardial infarction (MI) resulting in the loss of cardiac myocytes can culminate in adverse cardiac remodeling leading to eventual heart failure. Adverse cardiac remodeling includes myocyte hypertrophy, fibrosis, and electrical remodeling. We have previously demonstrated the beneficial effects of several potent soluble epoxide hydrolase inhibitors (sEHIs) in different models of cardiac hypertrophy and failure. Here, we directly determine the molecular mechanisms underlying the beneficial effects of sEHIs in cardiac remodeling post-MI. Treatment with a potent sEHI, 1-trifluoromethoxyphenyl-3-(1-propionylpiperidine-4-yl)urea (TPPU), which was started 1 wk post-MI in a murine model, results in a significant improvement in cardiac function. Importantly, treatment with TPPU results in a decrease in cardiac fibrosis as quantified using histological and immunostaining techniques. Moreover, single-cell-based assays demonstrate that treatment with TPPU results in a significant decrease not only in the percentages but also the proliferative capacity of different populations of cardiac fibroblasts as well as a reduction in the migration of fibroblasts into the heart from the bone marrow. Our study provides evidence for a possible unique therapeutic strategy to reduce cardiac fibrosis and improve cardiac function post-MI.

Indexed as

AnimalsCell MovementCell ProliferationCytokinesEchocardiographyEpoxide HydrolasesFibrosisFlow CytometryMiceMyocardial InfarctionOxylipinsPhenylurea CompoundsPiperidinesVentricular Remodeling1-trifluoromethoxyphenyl-3-(1-propionylpiperidine-4-yl)ureaCytokinesEpoxide HydrolasesOxylipinsPhenylurea CompoundsPiperidines

Identifiers

PMID23493561
PMCPMC3619365

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.