Evidence map›Paper›PMID 25580634›Full record

ArticleImmunology2015

Immune mechanisms linked to depression via oxidative stress and neuroprogression.

Nataliia Bakunina, Carmine M Pariante, Patricia A Zunszain

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 197 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
197citing papers in PubMed, 6 pooled it
10.0field-weighted citation impact, top 1% 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

197 citing papers in PubMed, 6 syntheses or guidelines pooled it, 432 citations in OpenAlex.

  1. Pooled it
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  7. Trial
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  10. Article
  11. Oxidative and Nitrosative Stress in Atopic Dermatitis and Depression: Similarities in Biomarkers and Pathophysiological Mechanisms.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
  12. Article
  13. Article
  14. JZ-1201 modulates depressive-like behaviors in rats through targeting catalase.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

137 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Nataliia BakuninaStress, Psychiatry and Immunology Laboratory, Institute of Psychiatry, Psychology & Neuroscience, King's College London, UK.
Carmine M Pariante
Patricia A Zunszain
King's College London · GB

Funding

Medical Research Council G108/603Medical Research Council MR/J002739/1
6 · The paper itself

Abstract

Emerging evidence suggests the significant role of inflammation and oxidative stress as main contributors to the neuroprogression that is observed in major depressive disorder (MDD), where patients show increased inflammatory and oxidative stress biomarkers. The process of neuroprogression includes stage-related neurodegeneration, cell death, reduced neurogenesis, reduced neuronal plasticity and increased autoimmune responses. Oxidative stress is a consequence of the biological imbalance between Reactive Oxygen Species (ROS) and antioxidants, leading to the alteration of biomolecules and the loss of control of the intracellular redox-related signaling pathways. ROS serve as crucial secondary messengers in signal transduction and significantly affect inflammatory pathways by activating NF-κB and MAPK family stress kinases. When present in excess, ROS inflict damage, affecting cellular constituents with the formation of pro-inflammatory molecules, such as malondialdehyde, 4-Hydroxynonenal, neoepitopes and damage-associated molecular patterns promoting immune response, and ultimately leading to cell death. The failure of cells to adapt to the changes in redox homeostasis and the subsequent cell death, together with the damage caused by inflammatory mediators, have been considered as major causes of neuroprogression and hence MDD. Both an activated immune-inflammatory system and increased oxidative stress act synergistically, complicating our understanding of the pathogenesis of depression. The cascade of antioxidative and inflammatory events is orchestrated by several transcription factors, with Nrf2 and NF-κB having particular relevance to MDD. This review focuses on potential molecular mechanisms through which impaired redox homeostasis and neuroinflammation can affect the neuronal environment and contribute to depression This article is protected by copyright. All rights reserved.

Indexed as

NeuroinflammationNeuroprogressionReactive Oxygen SpeciesSignal TransductionTranscription Factors

Identifiers

PMID25580634
PMCPMC4557673
OpenAlexW2082245790

What OpenQuestion holds

Textmetadata
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.