ReviewJournal of neural transmission (Vienna, Austria : 1996)2011
Iron-dependent functions of mitochondria--relation to neurodegeneration.
Review in Journal of neural transmission (Vienna, Austria : 1996), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 77 citations in OpenAlex.
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- Comparison of inflammatory biomarker levels in neurodegenerative proteinopathies: a case-control study.Journal of neural transmission (Vienna, Austria : 1996) · 2025Article
- Nigrostriatal iron accumulation in the progression of Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Silica Nanoparticles from Melon Seed Husk Abrogated Binary Metal(loid) Mediated Cerebellar Dysfunction by Attenuation of Oxido-inflammatory Response and Upregulation of Neurotrophic Factors in Male Albino Rats.Cerebellum (London, England) · 2024Article
- Mitochondrial Aconitase and Its Contribution to the Pathogenesis of Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Transcriptome analyses reveal molecular mechanisms of novel compound heterozygousFrontiers in cellular neuroscience · 2024Article
- Recent Advances in the Synthesis of Antioxidant Derivatives: Pharmacological Insights for Neurological Disorders.Current topics in medicinal chemistry · 2024Review
- Attenuation of ferroptosis as a potential therapeutic target for neuropsychiatric manifestations of post-COVID syndrome.Frontiers in neuroscience · 2023Review
- Discovery of Therapeutics Targeting Oxidative Stress in Autosomal Recessive Cerebellar Ataxia: A Systematic Review.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Therapeutic targeting of microglia mediated oxidative stress after neurotrauma.Frontiers in medicine · 2022Review
- Mitochondrial iron metabolism and neurodegenerative diseases.Neurotoxicology · 2022Review
- Effects of tocotrienol supplementation in Friedreich's ataxia: A model of oxidative stress pathology.Experimental biology and medicine (Maywood, N.J.) · 2020Article
- Role of mitochondrial calcium uniporter-mediated CaJournal of cellular and molecular medicine · 2019Article
- Brain mitochondrial iron accumulates in Huntington's disease, mediates mitochondrial dysfunction, and can be removed pharmacologically.Free radical biology & medicine · 2018Article
- Astrocyte hepcidin is a key factor in LPS-induced neuronal apoptosis.Cell death & disease · 2017Article
- Role of iron in neurodegenerative diseases.Journal of neural transmission (Vienna, Austria : 1996) · 2016Review
- Reduction in mitochondrial iron alleviates cardiac damage during injury.EMBO molecular medicine · 2016Article
- Region-specific disturbed iron distribution in early idiopathic Parkinson's disease measured by quantitative susceptibility mapping.Human brain mapping · 2015Article
- Assessment of Protective Role of Multifunctional Dopamine Agonist D-512 Against Oxidative Stress Produced by Depletion of Glutathione in PC12 Cells: Implication in Neuroprotective Therapy for Parkinson's Disease.Neurotoxicity research · 2015Article
- Iron in multiple sclerosis: roles in neurodegeneration and repair.Nature reviews. Neurology · 2014Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A number of neurodegenerative diseases are associated with iron dyshomeostasis and mitochondrial dysfunction. However, the pathomechanistic interplay between iron and mitochondria varies. This review summarises the physiological role of iron in mitochondria and subsequently exemplifies two neurodegenerative diseases with disturbed iron function in mitochondria: inherited Friedreich ataxia (FRDA) and idiopathic Parkinson disease (PD). In eukaryotes, mitochondria are main consumers of iron. The respiratory chain relies on iron-containing redox systems in the form of complexes I-III with iron-sulphur clusters and cytochromes with haem as prosthetic groups. The bifunctional enzyme aconitase is not only important in the citric acid cycle, but also functions as a key regulator of cell iron metabolism. Haem biosynthesis occurs partially in mitochondria as well as the biogenesis of iron-sulphur clusters that are co-factors in numerous iron-sulphur proteins. FRDA is characterised by a mutation of the frataxin gene, the protein of which serves as an iron chaperone in iron-sulphur cluster assembly. The lack of frataxin expression leads to defective iron-sulphur cluster biogenesis with decreased respiratory and aconitase activity. The resulting mitochondrial iron overload might fuel reactive oxygen species formation and contribute to clinical signs of oxidative stress. PD is typically associated with an increased iron content of the substantia nigra, the causes of which are largely unknown. Recent research demonstrated raised iron levels in individual dopaminergic neurons of the substantia nigra. Moreover, transferrin/transferrin receptor 2 mediated transport of iron into the mitochondria of these neurons was identified together with increased transferrin immunoreactivity. Resulting accumulation of iron into mitochondria might lead to oxidative stress damaging iron-sulphur cluster-containing proteins.
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