Evidence map›Paper›PMID 40410878›Full record

ArticleJournal of translational medicine2025

Chronic mild stress disrupts mitophagy and mitochondrial status in rat frontal cortex.

Cristina Ulecia-Morón, Álvaro G Bris, Karina S MacDowell, José L M Madrigal, Borja García-Bueno, Juan C Leza, Javier R Caso

Abstract read
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Ferroptosis in depression: mechanisms, association, and therapeutic strategies.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  4. Review
  5. Metabolic Reprogramming of Microglia in Neuroinflammation and Depression.International journal of molecular sciences · 2026
    Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. 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

7 authors.

Cristina Ulecia-MorónDepartamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Centro de Investigación Biomédica en Red de Salud Mental, Instituto de Salud Carlos III (CIBERSAM, ISCIII), Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Instituto Universitario de Investigación Neuroquímica (IUIN-UCM), Plaza Ramón y Cajal s/n, Madrid, 28040, Spain.
Álvaro G BrisDepartamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Centro de Investigación Biomédica en Red de Salud Mental, Instituto de Salud Carlos III (CIBERSAM, ISCIII), Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Instituto Universitario de Investigación Neuroquímica (IUIN-UCM), Plaza Ramón y Cajal s/n, Madrid, 28040, Spain.
Karina S MacDowellDepartamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Centro de Investigación Biomédica en Red de Salud Mental, Instituto de Salud Carlos III (CIBERSAM, ISCIII), Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Instituto Universitario de Investigación Neuroquímica (IUIN-UCM), Plaza Ramón y Cajal s/n, Madrid, 28040, Spain.
José L M MadrigalDepartamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Centro de Investigación Biomédica en Red de Salud Mental, Instituto de Salud Carlos III (CIBERSAM, ISCIII), Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Instituto Universitario de Investigación Neuroquímica (IUIN-UCM), Plaza Ramón y Cajal s/n, Madrid, 28040, Spain.
Borja García-BuenoDepartamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Centro de Investigación Biomédica en Red de Salud Mental, Instituto de Salud Carlos III (CIBERSAM, ISCIII), Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Instituto Universitario de Investigación Neuroquímica (IUIN-UCM), Plaza Ramón y Cajal s/n, Madrid, 28040, Spain.
Juan C LezaDepartamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Centro de Investigación Biomédica en Red de Salud Mental, Instituto de Salud Carlos III (CIBERSAM, ISCIII), Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Instituto Universitario de Investigación Neuroquímica (IUIN-UCM), Plaza Ramón y Cajal s/n, Madrid, 28040, Spain.
Javier R CasoDepartamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Centro de Investigación Biomédica en Red de Salud Mental, Instituto de Salud Carlos III (CIBERSAM, ISCIII), Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Instituto Universitario de Investigación Neuroquímica (IUIN-UCM), Plaza Ramón y Cajal s/n, Madrid, 28040, Spain. jrcaso@med.ucm.es.ORCID 0000-0001-8622-749X

Funding

Centro de Investigación Biomédica en Red de Salud Mental CB/07/09/0026Ministerio de Ciencia e Innovación PID2020-113103RB-I00Ministerio de Ciencia e Innovación PID2023-146894NB-I00
6 · The paper itself

Abstract

backgroundMitochondria are very dynamic organelles that maintain cellular homeostasis, crucial in the central nervous system. Mitochondrial abnormalities have been described in neuropsychiatric diseases, namely major depression disorder (MDD) and schizophrenia. Since stress is the predominant non-genetic cause of MDD, and has a direct impact on mitochondrial networks, understanding how psychological stress affects mitochondrial health is vital to improve the current pharmacological therapies.

methodsThe effect of 21 days of unpredictable stress was evaluated in frontal cortex of Wistar male rats comparing protein and gene markers of mitophagy (PINK1, PARKIN, BNIP3, NIX, FUNDC1), mitochondrial biosynthesis (PGC1α, NRF1, TFAM) and dynamics (MFN1, MFN2, OPA1, DRP1), and mitochondrial presence within microglia with the MitoTracker Green FM™ probe.

resultsChronic mild stress (CMS) caused the upregulation of mitochondrial mass, mitochondria depolarization, dysregulation in mitochondrial dynamics towards fusion, the increase of mitophagy markers and the induction of genes that activate mitochondrial biogenesis in frontal cortex. CMS also promoted microglia recruitment and mitochondrial number boosting within them.

conclusionsThere is a dysregulation of mitochondrial dynamics towards fusion, an upregulation of mitophagy markers, and the induction of genes associated with mitochondrial biogenesis in response to CMS in the frontal cortex of adult rats. This study highlights the impact of psychological stress on brain mitochondrial networks.

Indexed as

Frontal LobeMitochondriaMitophagyStress, PsychologicalAnimalsChronic DiseaseMaleMicrogliaMitochondrial DynamicsRatsRats, WistarChronic mild stress (CMS)MicrogliaMitochondriaMitophagyNeuroinflammation

Identifiers

PMID40410878
PMCPMC12102876

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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.