Evidence map›Paper›PMID 40883288›Full record

ArticleCell death & disease2025

Retrograde transport of neurotrophin receptor TrkB-FL induced by excitotoxicity regulates Golgi stability and is a target for stroke neuroprotection.

Gema María Esteban-Ortega, Elena Torres-Campos, Margarita Díaz-Guerra

Erratum issuedAbstract read
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
–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 synthesis or guideline pooled it.

  1. Pooled it
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  4. Review
  5. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Gema María Esteban-OrtegaInstituto de Investigaciones Biomédicas Sols-Morreale (IIBM), Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, Madrid, 28029, Spain.
Elena Torres-CamposInstituto de Investigaciones Biomédicas Sols-Morreale (IIBM), Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, Madrid, 28029, Spain.
Margarita Díaz-GuerraInstituto de Investigaciones Biomédicas Sols-Morreale (IIBM), Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, Madrid, 28029, Spain. mdiazguerra@iib.uam.es.ORCID http://orcid.org/0000-0002-4478-0956

Funding

Ministry of Economy and Competitiveness | Agencia Estatal de Investigación (Spanish Agencia Estatal de Investigación) PID2019-105784RB-100Ministry of Economy and Competitiveness | Agencia Estatal de Investigación (Spanish Agencia Estatal de Investigación) PID2022-137710OB-I00
6 · The paper itself

Abstract

Excitotoxicity, aberrant function of survival pathways dependent on brain-derived neurotrophic factor (BDNF), and disruption of the Golgi complex are shared pathological hallmarks in relevant neurological diseases, including stroke. However, the precise interdependence among these mechanisms is not completely defined, knowledge essential for developing neuroprotective strategies. For ischemic stroke, a leading cause of death, disability, and dementia, interfering with excitotoxicity-the major mechanism of neuronal death in the penumbra area-has shown promising results. We are exploring neuroprotection by promoting survival cascades dependent on the BDNF receptor, full-length tropomyosin-related kinase B (TrkB-FL), as these pathways become aberrant after excitotoxicity. We previously developed MTFL

Indexed as

Golgi ApparatusNeuroprotectionNeuroprotective AgentsReceptor, trkBStrokeAnimalsBrain-Derived Neurotrophic FactorEndocytosisHumansMaleMiceMice, Inbred C57BLProtein TransportRatsBrain-Derived Neurotrophic FactorNeuroprotective AgentsReceptor, trkB

Identifiers

PMID40883288
PMCPMC12397353

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Registered trials

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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.