Evidence map›Paper›PMID 27293957›Full record

ReviewParkinson's disease2016

Parkinson's Disease: The Mitochondria-Iron Link.

Yorka Muñoz, Carlos M Carrasco, Joaquín D Campos, Pabla Aguirre, Marco T Núñez

Open access · goldAbstract readReview
In one paragraph

Review in Parkinson's disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Mitochondrial Dysfunction in Genetic and Non-Genetic Parkinson's Disease.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Genetic Markers of Postmortem Brain Iron.Journal of neurochemistry · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Yorka MuñozIron and Biology of Aging Laboratory, Department of Biology, Faculty of Sciences, Universidad de Chile, Santiago, Chile.ORCID 0000-0002-0433-0109
Carlos M CarrascoIron and Biology of Aging Laboratory, Department of Biology, Faculty of Sciences, Universidad de Chile, Santiago, Chile.
Joaquín D CamposIron and Biology of Aging Laboratory, Department of Biology, Faculty of Sciences, Universidad de Chile, Santiago, Chile.ORCID 0000-0001-5613-3142
Pabla AguirreIron and Biology of Aging Laboratory, Department of Biology, Faculty of Sciences, Universidad de Chile, Santiago, Chile.ORCID 0000-0003-3352-0574
Marco T NúñezIron and Biology of Aging Laboratory, Department of Biology, Faculty of Sciences, Universidad de Chile, Santiago, Chile.
University of Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction, iron accumulation, and oxidative damage are conditions often found in damaged brain areas of Parkinson's disease. We propose that a causal link exists between these three events. Mitochondrial dysfunction results not only in increased reactive oxygen species production but also in decreased iron-sulfur cluster synthesis and unorthodox activation of Iron Regulatory Protein 1 (IRP1), a key regulator of cell iron homeostasis. In turn, IRP1 activation results in iron accumulation and hydroxyl radical-mediated damage. These three occurrences-mitochondrial dysfunction, iron accumulation, and oxidative damage-generate a positive feedback loop of increased iron accumulation and oxidative stress. Here, we review the evidence that points to a link between mitochondrial dysfunction and iron accumulation as early events in the development of sporadic and genetic cases of Parkinson's disease. Finally, an attempt is done to contextualize the possible relationship between mitochondria dysfunction and iron dyshomeostasis. Based on published evidence, we propose that iron chelation-by decreasing iron-associated oxidative damage and by inducing cell survival and cell-rescue pathways-is a viable therapy for retarding this cycle.

Identifiers

PMID27293957
PMCPMC4886095
OpenAlexW2408015440

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.