Evidence map›Paper›PMID 26347662›Full record

ReviewFrontiers in psychiatry2015

Kynurenine 3-Monooxygenase: An Influential Mediator of Neuropathology.

Jennifer M Parrott, Jason C O'Connor

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.

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  10. Subclinical Hepatic Injury and Dysfunction Following Surgery: Evidence From a Young and Aged Laparotomy Murine Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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17 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

2 authors at 1 institution in 1 country.

Jennifer M ParrottDepartment of Pharmacology, School of Medicine, University of Texas Health Science Center at San Antonio , San Antonio, TX , USA ; Center for Biomedical Neuroscience, University of Texas Health Science Center at San Antonio , San Antonio, TX , USA.
Jason C O'ConnorDepartment of Pharmacology, School of Medicine, University of Texas Health Science Center at San Antonio , San Antonio, TX , USA ; Center for Biomedical Neuroscience, University of Texas Health Science Center at San Antonio , San Antonio, TX , USA ; Mood Disorders Translational Research Core, University of Texas Health Science Center at San Antonio , San Antonio, TX , USA ; Audie L. Murphy Memorial VA Hospital, South Texas Veterans Health System , San Antonio, TX , USA.
The University of Texas Health Science Center at San Antonio · US

Funding

Institute for Integration of Medicine & Science: A Partnership to Improve HealthUL1TR001120 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A, HARGREAVES, KENNETH M · 2013 to 2017
$16.5M
Biobehavioral Role of Brain Kynurenine Metabolism in Mental IllnessR01MH090127 · NIMH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI O'CONNOR, JASON C · 2010 to 2014
$1.8M
Integrated Graduate Training Program in Neuroscience, UTHSCSAT32NS082145 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI David A Morilak · 2013 to 2026
$1.5M
Impact of BDNF expression on neuroimmune activation and depressive-like behaviorsF31MH102070 · NIMH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI PARROTT, JENNIFER MICHELLE · 2014 to 2015
$44k
NCATS NIH HHS UL1 TR001120NIMH NIH HHS F31 MH102070NIMH NIH HHS R01 MH090127NINDS NIH HHS T32 NS082145
6 · The paper itself

Abstract

Mounting evidence demonstrates that kynurenine metabolism may play an important pathogenic role in the development of multiple neurological and neuropsychiatric disorders. The kynurenine pathway consists of two functionally distinct branches that generate both neuroactive and oxidatively reactive metabolites. In the brain, the rate-limiting enzyme for one of these branches, kynurenine 3-monooxygenase (KMO), is predominantly expressed in microglia and has emerged as a pivotal point of metabolic regulation. KMO substrate and expression levels are upregulated by pro-inflammatory cytokines and altered by functional genetic mutations. Increased KMO metabolism results in the formation of metabolites that activate glutamate receptors and elevate oxidative stress, while recent evidence has revealed neurodevelopmental consequences of reduced KMO activity. Together, the evidence suggests that KMO is positioned at a critical metabolic junction to influence the development or trajectory of a myriad of neurological diseases. Understanding the mechanism(s) by which alterations in KMO activity are able to impair neuronal function, and viability will enhance our knowledge of related disease pathology and provide insight into novel therapeutic opportunities. This review will discuss the influence of KMO on brain kynurenine metabolism and the current understanding of molecular mechanisms by which altered KMO activity may contribute to neurodevelopment, neurodegenerative, and neuropsychiatric diseases.

Indexed as

kynurenine 3-monooxygenasekynurenine pathwaymicroglianeurodegenerative diseasesneurodevelopmental disordersneuroinflammationneuropsychiatric disorders

Identifiers

PMID26347662
PMCPMC4542134
OpenAlexW1800932169

What OpenQuestion holds

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LicenceCC BY
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.