Evidence map›Paper›PMID 24624085›Full record

ReviewFrontiers in pharmacology2014

Mitochondrial iron-sulfur cluster dysfunction in neurodegenerative disease.

Grazia Isaya

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.8field-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

49 citing papers in PubMed, 107 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Biallelic Loss-of-Function Variant inInternational journal of molecular sciences · 2025
    Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Adenylosuccinic Acid: An Orphan Drug with Untapped Potential.Pharmaceuticals (Basel, Switzerland) · 2023
    Article
  16. Article
  17. Article
  18. Steroidogenic electron-transfer factors and their diseases.Annals of pediatric endocrinology & metabolism · 2021
    Article
  19. Mitochondrial Metal Ion Transport in Cell Metabolism and Disease.International journal of molecular sciences · 2021
    Review
  20. Review
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

1 author at 1 institution in 1 country.

Grazia IsayaDepartment of Pediatric & Adolescent Medicine and Mayo Clinic Children's Center Mayo Clinic, Rochester, MN, USA.
Mayo Clinic · US

Funding

NEW DETERMINANTS OF MTDNA INTEGRITY IN YEAST AND HEARTR01AG015709 · NIA · YALE UNIVERSITY · PI ISAYA, GRAZIA · 1997 to 2015
$4.0M
NIA NIH HHS R01 AG015709
6 · The paper itself

Abstract

Growing evidence supports a role for mitochondrial iron metabolism in the pathophysiology of neurodegenerative disorders such as Friedreich ataxia (FRDA) and Parkinson disease (PD) as well as in the motor and cognitive decline associated with the aging process. Iron-sulfur enzyme deficits and regional iron accumulation have been observed in each of these conditions. In spite of significant etiological, clinical and pathological differences that exist between FRDA and PD, it is possible that defects in mitochondrial iron-sulfur clusters (ISCs) biogenesis represent a common underlying mechanism leading to abnormal intracellular iron distribution with mitochondrial iron accumulation, oxidative phosphorylation deficits and oxidative stress in susceptible cells and specific regions of the nervous system. Moreover, a similar mechanism may contribute to the age-dependent iron accumulation that occurs in certain brain regions such as the globus pallidus and the substantia nigra. Targeting chelatable iron and reactive oxygen species appear as possible therapeutic options for FRDA and PD, and possibly other age-related neurodegenerative conditions. However, new technology to interrogate ISC synthesis in humans is needed to (i) assess how defects in this pathway contribute to the natural history of neurodegenerative disorders and (ii) develop treatments to correct those defects early in the disease process, before they cause irreversible neuronal cell damage.

Indexed as

aginganti-oxidantsFriedreich ataxiairon-chelatorsiron–sulfur clustersmitochondriaoxidative damageParkinson disease

Identifiers

PMID24624085
PMCPMC3939683
OpenAlexW2103860452

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.