Evidence map›Paper›PMID 33419006›Full record

ReviewAntioxidants (Basel, Switzerland)2021

Inflaming the Brain with Iron.

Pamela J Urrutia, Daniel A Bórquez, Marco Tulio Núñez

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
11.0field-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

82 citing papers in PubMed, 101 citations in OpenAlex.

  1. Review
  2. A frontotemporal dementia-like phenotype in schizophrenia: links to striatal dopamine and iron accumulation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Observational
  3. Article
  4. Review
  5. Review
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  8. Article
  9. Acidosis, Iron Dyshomeostasis and Inflammatory Injury.International journal of molecular sciences · 2026
    Review
  10. Review
  11. Review
  12. SS-31 improves post-cardiac arrest brain injury by inhibiting microglial ferroptosis and polarization.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
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  19. Article
  20. 5-HTCNS neuroscience & therapeutics · 2025
    Article

22 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 2 institutions in 1 country.

Pamela J UrrutiaDepartment of Biology, Faculty of Sciences, Universidad de Chile, 7800024 Santiago, Chile.
Daniel A BórquezCenter for Biomedical Research, Faculty of Medicine, Universidad Diego Portales, 8370007 Santiago, Chile.ORCID 0000-0002-8747-2048
Marco Tulio NúñezDepartment of Biology, Faculty of Sciences, Universidad de Chile, 7800024 Santiago, Chile.ORCID 0000-0002-1967-8570
University of Chile · CLUniversidad Diego Portales · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Iron accumulation and neuroinflammation are pathological conditions found in several neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD). Iron and inflammation are intertwined in a bidirectional relationship, where iron modifies the inflammatory phenotype of microglia and infiltrating macrophages, and in turn, these cells secrete diffusible mediators that reshape neuronal iron homeostasis and regulate iron entry into the brain. Secreted inflammatory mediators include cytokines and reactive oxygen/nitrogen species (ROS/RNS), notably hepcidin and nitric oxide (·NO). Hepcidin is a small cationic peptide with a central role in regulating systemic iron homeostasis. Also present in the cerebrospinal fluid (CSF), hepcidin can reduce iron export from neurons and decreases iron entry through the blood-brain barrier (BBB) by binding to the iron exporter ferroportin 1 (Fpn1). Likewise, ·NO selectively converts cytosolic aconitase (c-aconitase) into the iron regulatory protein 1 (IRP1), which regulates cellular iron homeostasis through its binding to iron response elements (IRE) located in the mRNAs of iron-related proteins. Nitric oxide-activated IRP1 can impair cellular iron homeostasis during neuroinflammation, triggering iron accumulation, especially in the mitochondria, leading to neuronal death. In this review, we will summarize findings that connect neuroinflammation and iron accumulation, which support their causal association in the neurodegenerative processes observed in AD and PD.

Indexed as

Alzheimer’s diseasehepcidinironiron regulatory protein 1neuroinflammationnitric oxideoxidative stressParkinson’s disease

Identifiers

PMID33419006
PMCPMC7825317
OpenAlexW3118616583

What OpenQuestion holds

Textmetadata
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.