Evidence map›Paper›PMID 39204088›Full record

ReviewPharmaceuticals (Basel, Switzerland)2024

Kynurenines and Inflammation: A Remarkable Axis for Multiple Sclerosis Treatment.

Paul Carrillo-Mora, Carlos Landa-Solís, David Valle-Garcia, Alexandra Luna-Angulo, Hamlet Avilés-Arnaut, Benjamín Robles-Bañuelos, Laura Sánchez-Chapul, Edgar Rangel-López

Abstract readReview
In one paragraph

Review in Pharmaceuticals (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Review
  2. A guide to uraemic toxicity.Nature reviews. Nephrology · 2026
    Review
  3. Review
  4. Review
  5. Kynurenines and Mitochondrial Disturbances in Multiple Sclerosis.International journal of molecular sciences · 2025
    Review
  6. Review
  7. 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

8 authors.

Paul Carrillo-MoraClinical Neurosciences Division, National Institute of Rehabilitation "Luis Guillermo Ibarra Ibarra", Mexico City 14389, Mexico.
Carlos Landa-SolísTissue Engineering, Cell Therapy, and Regenerative Medicine Unit, National Institute of Rehabilitation "Luis Guillermo Ibarra Ibarra", Mexico City 14389, Mexico.
David Valle-GarciaNeuroimmunology Laboratory, National Institute of Neurology and Neurosurgery "Manuel Velasco Suárez", Mexico City 14269, Mexico.ORCID 0000-0002-3397-3103
Alexandra Luna-AnguloNeuromuscular Diseases Laboratory, Clinical Neurosciences Division, National Institute of Rehabilitation "Luis Guillermo Ibarra Ibarra", Mexico City 14389, Mexico.
Hamlet Avilés-ArnautFaculty of Biological Sciences, Institute of Biotechnology, National Autonomous University of Nuevo Leon, Nuevo León 66455, Mexico.ORCID 0000-0001-6813-6869
Benjamín Robles-BañuelosCell Reprogramming Laboratory, National Institute of Neurology and Neurosurgery "Manuel Velasco Suárez", Mexico City 14269, Mexico.ORCID 0000-0001-5692-4067
Laura Sánchez-ChapulNeuromuscular Diseases Laboratory, Clinical Neurosciences Division, National Institute of Rehabilitation "Luis Guillermo Ibarra Ibarra", Mexico City 14389, Mexico.ORCID 0000-0002-4268-2279
Edgar Rangel-LópezCell Reprogramming Laboratory, National Institute of Neurology and Neurosurgery "Manuel Velasco Suárez", Mexico City 14269, Mexico.ORCID 0000-0002-4741-1793

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic inflammatory autoimmune neurological disease characterized by the recurrent appearance of demyelinating lesions and progressive disability. Currently, there are multiple disease-modifying treatments, however, there is a significant need to develop new therapeutic targets, especially for the progressive forms of the disease. This review article provides an overview of the most recent studies aimed at understanding the inflammatory processes that are activated in response to the accumulation of kynurenine pathway (KP) metabolites, which exacerbate an imbalance between immune system cells (e.g., Th1, Th2, and T reg) and promote the release of pro-inflammatory interleukins that modulate different mechanisms: membrane-receptors function; nuclear factors expression; and cellular signals. Together, these alterations trigger cell death mechanisms in brain cells and promote neuron loss and axon demyelination. This hypothesis could represent a remarkable approach for disease-modifying therapies for MS. Here, we also provide a perspective on the repositioning of some already approved drugs involved in other signaling pathways, which could represent new therapeutic strategies for MS treatment.

Indexed as

inflammationkynurenine metaboliteskynurenines pathwaymultiple sclerosisquinolinic acidtreatment

Identifiers

PMID39204088
PMCPMC11356993

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.