Evidence map›Paper›PMID 23898174›Full record

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

Epoxyeicosanoids promote organ and tissue regeneration.

Dipak Panigrahy, Brian T Kalish, Sui Huang, Diane R Bielenberg, Hau D Le, Jun Yang, Matthew L Edin, Craig R Lee, Ofra Benny, Dayna K Mudge and 18 more

Open access · bronzeAbstract 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 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
9.7field-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

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 153 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Soluble Epoxide Hydrolase Inhibitors Improve Cornea Alkali Wound Healing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
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  14. Article
  15. Article
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  17. Article
  18. Targeting Angiogenesis via Resolution of Inflammation.Cold Spring Harbor perspectives in medicine · 2023
    Review
  19. Article
  20. Article

26 more citing papers are in PubMed but not listed here.

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

28 authors at 12 institutions in 1 country.

Dipak PanigrahyVascular Biology Program and Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA. dpanigra@bidmc.harvard.edu
Brian T Kalish
Sui Huang
Diane R Bielenberg
Hau D Le
Jun Yang
Matthew L Edin
Craig R Lee
Ofra Benny
Dayna K Mudge
Catherine E Butterfield
Akiko Mammoto
Tadanori Mammoto
Bora Inceoglu
Roger L Jenkins
Mary A Simpson
Tomoshige Akino
Fred B Lih
Kenneth B Tomer
Donald E Ingber
Bruce D Hammock
John R Falck
Vijaya L Manthati
Arja Kaipainen
Patricia A D'Amore
Mark Puder
Darryl C Zeldin
Mark W Kieran
Center for Vascular Biology Research · USNational Institutes of Health · USUniversity of California, Davis · USHarvard University · USLahey Hospital and Medical Center · USThe University of Texas Southwestern Medical Center · USBoston Children's Hospital · USFred Hutch Cancer Center · USInstitute for Systems Biology · USNational Institute of Environmental Health Sciences · USSmith-Kettlewell Eye Research Institute · USUniversity of North Carolina at Chapel Hill · US

Funding

Workshop on Environmental Technology Transfer and EntrepreneurshipP42ES004699 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1987 to 2021
$50.1M
TUMOR DORMANCY INDUCED BY BLOCKED ANGIOGENESISP01CA045548 · NCI · CHILDREN'S HOSPITAL BOSTON · PI KLAGSBRUN, MICHAEL · 1987 to 2011
$22.6M
Novel Eicosanoids: Synthesis and FunctionR01GM031278 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI FALCK, JOHN R. · 1985 to 2012
$4.7M
HYDROLYTIC ENZYMES IN THE METABOLISM OF TOXINSR01ES002710 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1985 to 2018
$4.0M
Quantitative Mass SpectrometryZIAES050167 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI TOMER, KENNETH · 2009 to 2013
$1.7M
Cytochrome P450 Derived Eicosanoids and InflammationR01GM088199 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LEE, CRAIG R · 2009 to 2013
$1.6M
Metabolomic study of ozone and nitronaphthalene toxicityR01ES013933 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 2005 to 2009
$1.5M
Control of cancer and metastasis by endothelial-derived epoxyeicosatrienoic acidsR01CA148633 · NCI · BOSTON CHILDREN'S HOSPITAL · PI PANIGRAHY, DIPAK · 2010 to 2014
$1.4M
Howard Hughes Medical InstituteIntramural NIH HHSNCI NIH HHS CA045548NCI NIH HHS P01 CA045548NCI NIH HHS R01 CA148633NCI NIH HHS R01CA148633-01A4NIEHS NIH HHS P42 ES004699NIEHS NIH HHS R01 ES002710NIEHS NIH HHS R01 ES013933NIGMS NIH HHS GM31278NIGMS NIH HHS R01 GM031278NIGMS NIH HHS R01 GM088199PHS HHS NIEHS Z01 025034PHS HHS NIEHS Z01 050167
6 · The paper itself

Abstract

Epoxyeicosatrienoic acids (EETs), lipid mediators produced by cytochrome P450 epoxygenases, regulate inflammation, angiogenesis, and vascular tone. Despite pleiotropic effects on cells, the role of these epoxyeicosanoids in normal organ and tissue regeneration remains unknown. EETs are produced predominantly in the endothelium. Normal organ and tissue regeneration require an active paracrine role of the microvascular endothelium, which in turn depends on angiogenic growth factors. Thus, we hypothesize that endothelial cells stimulate organ and tissue regeneration via production of bioactive EETs. To determine whether endothelial-derived EETs affect physiologic tissue growth in vivo, we used genetic and pharmacological tools to manipulate endogenous EET levels. We show that endothelial-derived EETs play a critical role in accelerating tissue growth in vivo, including liver regeneration, kidney compensatory growth, lung compensatory growth, wound healing, corneal neovascularization, and retinal vascularization. Administration of synthetic EETs recapitulated these results, whereas lowering EET levels, either genetically or pharmacologically, delayed tissue regeneration, demonstrating that pharmacological modulation of EETs can affect normal organ and tissue growth. We also show that soluble epoxide hydrolase inhibitors, which elevate endogenous EET levels, promote liver and lung regeneration. Thus, our observations indicate a central role for EETs in organ and tissue regeneration and their contribution to tissue homeostasis.

Indexed as

AnimalsChromatography, LiquidEicosanoidsEndothelial CellsEpoxide HydrolasesEpoxy CompoundsEyeImmunohistochemistryKidneyLiverLungMiceMice, TransgenicNeovascularization, PhysiologicReceptor, TIE-2RegenerationEicosanoidsEpoxide HydrolasesEpoxy CompoundsReceptor, TIE-2angiocrineautacoidorgan regenerationsmall molecule mediatorVEGF

Identifiers

PMID23898174
PMCPMC3746918
OpenAlexW2154439651

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.