Evidence map›Paper›PMID 29977455›Full record

ReviewOxidative medicine and cellular longevity2018

Relevance of Alternative Routes of Kynurenic Acid Production in the Brain.

L A Ramos-Chávez, R Lugo Huitrón, D González Esquivel, B Pineda, C Ríos, D Silva-Adaya, L Sánchez-Chapul, G Roldán-Roldán, V Pérez de la Cruz

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.5field-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

49 citing papers in PubMed, 68 citations in OpenAlex.

  1. Gut-Brain Signaling in Parkinson's Disease: A Narrative Review.International journal of molecular sciences · 2026
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  16. Kynurenic acid promotes osteogenesis via the Wnt/β-catenin signaling.In vitro cellular & developmental biology. Animal · 2023
    Article
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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

9 authors at 3 institutions in 1 country.

L A Ramos-ChávezLaboratorio de Neurobiología de la Conducta, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico.
R Lugo HuitrónDepartamento de Neuroquímica, SSA, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City 14269, Mexico.
D González EsquivelDepartamento de Neuroquímica, SSA, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City 14269, Mexico.ORCID 0000-0001-8262-3399
B PinedaLaboratorio de Neuroinmunología, SSA, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City 14269, Mexico.ORCID 0000-0002-1455-312X
C RíosDepartamento de Neuroquímica, SSA, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City 14269, Mexico.
D Silva-AdayaLaboratorio Experimental de Enfermedades Neurodegenerativas, SSA, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City 14269, Mexico.ORCID 0000-0002-4679-5182
L Sánchez-ChapulDivisión de Neurociencias, SSA, Instituto Nacional de Rehabilitación, Mexico City 14389, Mexico.
G Roldán-RoldánLaboratorio de Neurobiología de la Conducta, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico.ORCID 0000-0003-1356-6428
V Pérez de la CruzDepartamento de Neuroquímica, SSA, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City 14269, Mexico.ORCID 0000-0002-1451-8754
Instituto Nacional de Neurología y Neurocirugía · MXInstituto Nacional de Rehabilitación · MXUniversidad Nacional Autónoma de México · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The catabolism of tryptophan has gained great importance in recent years due to the fact that the metabolites produced during this process, with neuroactive and redox properties, are involved in physiological and pathological events. One of these metabolites is kynurenic acid (KYNA), which is considered as a neuromodulator since it can interact with NMDA, nicotinic, and GPR35 receptors among others, modulating the release of neurotransmitters as glutamate, dopamine, and acetylcholine. Kynureninate production is attributed to kynurenine aminotransferases. However, in some physiological and pathological conditions, its high production cannot be explained just with kynurenine aminotransferases. This review focuses on the alternative mechanism whereby KYNA can be produced, either from D-amino acids or by means of other enzymes as D-amino acid oxidase or by the participation of free radicals. It is important to mention that an increase in KYNA levels in processes as brain development, aging, neurodegenerative diseases, and psychiatric disorders, which share common factors as oxidative stress, inflammation, immune response activation, and participation of gut microbiota that can also be related with the alternative routes of KYNA production, has been observed.

Indexed as

AnimalsBrainHumansKynurenic AcidKynurenic Acid

Identifiers

PMID29977455
PMCPMC5994304
OpenAlexW2803960895

What OpenQuestion holds

Textmetadata
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.