Evidence map›Paper›PMID 41276654›Full record

ArticleMolecular neurobiology2025

Anandamide-Induced Neuroprotection of Cortical Neurons Relies on Metabolic/Redox Regulation and Mitochondrial Dynamics.

Ana Laura Torres-Román, Tània Gavaldà-Vives, Samuel Simón-Sánchez, Omar Emiliano Aparicio-Trejo, José Pedraza-Chaverri, Tessy López-Goerne, Alette Ortega Gómez, Alexey A Tinkov, Michael Aschner, Ismael Galve-Roperh and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

11 authors.

Ana Laura Torres-RománPrograma de Posgrado (Doctorado) en Ciencias Biológicas, Universidad Nacional Autónoma de México, 04510, Mexico City, Mexico.
Tània Gavaldà-VivesDepartamento de Bioquímica y Biología Molecular, Instituto Universitario de Investigación en Neuroquímica (IUIN), Universidad Complutense, 28040, Madrid, Spain.
Samuel Simón-SánchezDepartamento de Bioquímica y Biología Molecular, Instituto Universitario de Investigación en Neuroquímica (IUIN), Universidad Complutense, 28040, Madrid, Spain.
Omar Emiliano Aparicio-TrejoDepartment of Cardio-Renal Physiopathology, Instituto de Cardiología Ignacio Chávez, 14080, Mexico City, Mexico.
José Pedraza-ChaverriLaboratorio F-315, Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México, 04510, Mexico City, Mexico.
Tessy López-GoerneLaboratorio de Nanotecnología y Nanomedicina, Departamento de Atención a La Salud, Universidad Autónoma Metropolitana-Xochimilco, 04960, Mexico City, Mexico.
Alette Ortega GómezSubdirección de Oncología y Hematología, Instituto Nacional de Cancerología, 14080, Mexico City, Mexico.
Alexey A TinkovDepartment of Medical Elementology, Peoples Friendship University of Russia, RUDN University), Moscow, 117198, Russia.
Michael AschnerDepartment of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY, 10461, USA.
Ismael Galve-RoperhDepartamento de Bioquímica y Biología Molecular, Instituto Universitario de Investigación en Neuroquímica (IUIN), Universidad Complutense, 28040, Madrid, Spain. igalvero@ucm.es.
Abel SantamaríaLaboratorio de Nanotecnología y Nanomedicina, Departamento de Atención a La Salud, Universidad Autónoma Metropolitana-Xochimilco, 04960, Mexico City, Mexico. absada@yahoo.com.

Funding

CannaLatan Network CYTED #220RT0002Consejo Nacional de Humanidades, Ciencias y Tecnologías 809272Instituto de Salud Carlos III PI21/0938
6 · The paper itself

Abstract

Mitochondrial disruption is a key mechanism in the etiology of neurodegenerative diseases. Promoting mitochondrial dynamics and renewal of the mitochondrial network can restore its function and sustain neuronal viability. Although a growing body of evidence implicates endocannabinoid signaling in the regulation of mitochondrial function, its neuroprotective role in neurodegenerative diseases remains largely unexplored. Clarifying this relationship is crucial for understanding the therapeutic efficacy of the endocannabinoid system. This study aimed to evaluate whether endocannabinoid signaling via PPARγ and CB

Indexed as

Arachidonic AcidsCerebral CortexEndocannabinoidsMitochondrial DynamicsNeuronsNeuroprotectionNeuroprotective AgentsPolyunsaturated AlkamidesAnimalsCalciumCells, CulturedCell SurvivalLipid PeroxidationMitochondriaNitro CompoundsOxidation-Reduction3-nitropropionic acidanandamideArachidonic AcidsCalciumEndocannabinoidsNeuroprotective AgentsNitro CompoundsPolyunsaturated AlkamidesPPAR gammaPropionatesQuinolinic AcidReceptor, Cannabinoid, CB1AnandamideCannabinoid receptorsEndocannabinoid SystemEnergy metabolismMitochondrial dynamicsPPARγ receptor

Identifiers

PMID41276654
PMCPMC12641045

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.