Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Friedreich ataxia: the oxidative stress paradox

22 Dec 2004

Abstract excerpt

Friedreich ataxia (FRDA) results from a generalized deficiency of mitochondrial and cytosolic iron-sulfur protein activity initially ascribed to mitochondrial iron overload. Recent in vitro data suggest that frataxin is necessary for iron incorporation in Fe-S cluster (ISC) and heme biosynthesis. In addition, several reports suggest that continuous oxidative damage resulting from hampered superoxide dismutases...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Amyotrophic Lateral Sclerosis Research
Share to Genetic Neurodegenerative Diseases
Share to Mitochondrial Function and Pathology

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Source

Identifiers

PMID: 15615771
DOI: 10.1093/hmg/ddi042

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Friedreich ataxia: the oxidative stress paradoxPMID 15615771Read ↗

Neurodegeneration in Friedreich’s Ataxia: From Defective Frataxin to Oxidative StressSemantic proximity Read ↗

Pathophysiogical and therapeutic progress in Friedreich ataxia.Semantic proximity Read ↗

Recent advances in the molecular pathogenesis of Friedreich ataxia.Semantic proximity Read ↗

Recent Advances in the Elucidation of Frataxin Biochemical Function Open Novel Perspectives for the Treatment of Friedreich’s AtaxiaSemantic proximity Read ↗

Friedreich's ataxia: from disease mechanisms to therapeutic interventions.Semantic proximity Read ↗

Frataxin deficiency and the pathology of Friedreich’s Ataxia across tissuesSemantic proximity Read ↗

The ins and outs of mitochondrial iron-loading: the metabolic defect in Friedreich's ataxia.Semantic proximity Read ↗

'Mitochondrial energy imbalance and lipid peroxidation cause cell death in Friedreich's ataxia'.Semantic proximity Read ↗

Aconitase and mitochondrial iron-sulphur protein deficiency in Friedreich ataxia.Semantic proximity Read ↗

Friedreich's ataxia and frataxin: molecular genetics, evolution and pathogenesis (Review).Semantic proximity Read ↗

The Friedreich's ataxia mutation confers cellular sensitivity to oxidant stress which is rescued by chelators of iron and calcium and inhibitors of apoptosis.Semantic proximity Read ↗

Beyond loss of frataxin: the complex molecular pathology of Friedreich ataxia.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.