Evidence map›Paper›PMID 25726384›Full record

ReviewTrends in endocrinology and metabolism: TEM2015

Biliverdin reductase isozymes in metabolism.

Luke O'Brien, Peter A Hosick, Kezia John, David E Stec, Terry D Hinds

Open access · greenAbstract readReview
In one paragraph

Review in Trends in endocrinology and metabolism: TEM, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

94 citing papers in PubMed, 141 citations in OpenAlex.

  1. Article
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  12. Biliverdin reductase A is a major determinant of protective NRF2 signaling.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  13. Review
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  16. Modeling the Interactions Between Chemicals and Proteins to Predict the Health Consequences of Air Pollution.International journal of environmental research and public health · 2025
    Article
  17. Article
  18. Article
  19. Article
  20. Review

34 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

5 authors at 2 institutions in 1 country.

Luke O'BrienCenter for Hypertension and Personalized Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine, Toledo, OH 43614, USA.
Peter A HosickDepartment of Exercise Science and Physical Education, Montclair State University, Montclair, NJ 07043, USA.
Kezia JohnCenter for Hypertension and Personalized Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine, Toledo, OH 43614, USA.
David E StecCenter for Excellence in Cardiovascular-Renal Research, Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216, USA.
Terry D HindsCenter for Hypertension and Personalized Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine, Toledo, OH 43614, USA. Electronic address: Terry.Hinds@utoledo.edu.
University of Toledo · USMontclair State University · US

Funding

STRUCTURAL VASCULAR ADAPTATION OF THE MICROCIRCULATIONP01HL051971 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI HALL, JOHN E · 1993 to 2018
$39.4M
The role of leptin in autoimmune-associated hypertensionP20GM104357 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI TAYLOR, ERIN BASSFORD · 2013 to 2022
$23.4M
Hypertension and Cardiorenal Research Training ProgramT32HL105324 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI Joey P. Granger · 2010 to 2026
$7.8M
PRIDE: Functional and Translational Genomics of Blood DisordersR25HL106365 · NHLBI · AUGUSTA UNIVERSITY · PI PACE, BETTY SUE · 2010 to 2024
$5.2M
The Renal Medulla and HypertensionR01HL088421 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI STEC, DAVID E · 2008 to 2012
$1.9M
Antioxidant-PPARalpha interaction and hypertensionK01HL125445 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI HINDS, TERRY D · 2015 to 2019
$779k
NHLBI NIH HHS 1T32HL105324NHLBI NIH HHS HL088421NHLBI NIH HHS HL106365NHLBI NIH HHS K01 HL125445NHLBI NIH HHS K01HL-125445NHLBI NIH HHS P01 HL051971NHLBI NIH HHS P01HL-051971NHLBI NIH HHS R01 HL088421NHLBI NIH HHS R25 HL106365NHLBI NIH HHS T32 HL105324NIGMS NIH HHS P20 GM104357NIGMS NIH HHS P20GM-104357NIMHD NIH HHS L32 MD009154
6 · The paper itself

Abstract

The biliverdin reductase (BVR) isozymes BVRA and BVRB are cell surface membrane receptors with pleiotropic functions. This review compares, for the first time, the structural and functional differences between the isozymes. They reduce biliverdin, a byproduct of heme catabolism, to bilirubin, display kinase activity, and BVRA, but not BVRB, can act as a transcription factor. The binding motifs present in the BVR isozymes allow a wide range of interactions with components of metabolically important signaling pathways such as the insulin receptor kinase cascades, protein kinases (PKs), and inflammatory mediators. In addition, serum bilirubin levels have been negatively associated with abdominal obesity and hypertriglyceridemia. We discuss the roles of the BVR isozymes in metabolism and their potential as therapeutic targets.

Indexed as

Energy MetabolismModels, BiologicalSignal TransductionAdipokinesAdipose TissueAnimalsBilirubinBinding SitesHumansHypertriglyceridemiaInsulin ResistanceIsoenzymesObesity, AbdominalOxidoreductases Acting on CH-CH Group DonorsProtein ConformationAdipokinesBilirubinbiliverdin reductaseIsoenzymesOxidoreductases Acting on CH-CH Group Donorsbilirubinbiliverdin reductaseBVRABVRBdiabetesheme oxygenaseobesity

Identifiers

PMID25726384
PMCPMC4380527
OpenAlexW2042703845

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.