ReviewRedox report : communications in free radical research2014
Aconitase post-translational modification as a key in linkage between Krebs cycle, iron homeostasis, redox signaling, and metabolism of reactive oxygen species.
Review in Redox report : communications in free radical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.
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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.
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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.
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Who cites it
115 citing papers in PubMed, 197 citations in OpenAlex.
- Iron-Sulfur Cluster Targeting: A Novel Perspective for Treating Alcohol-Related Lipid Metabolic Diseases.Journal of biochemical and molecular toxicology · 2026Review
- Spatiotemporal coordination of virulence, metabolism, and stress responses shapes infection dynamics ofApplied and environmental microbiology · 2026Article
- GFER Represents a Target for Dual Disruption of Redox Homeostasis and Reactivation of the Immune Response in Pancreatic Adenocarcinoma.Cancer research · 2026Article
- Mitochondrial Iron Handling and Lipid Peroxidation as Drivers of Ferroptosis.International journal of molecular sciences · 2026Review
- Metabolic plasticity enables Clostridioides difficile growth in coculture with neutrophils and other mammalian cells.Anaerobe · 2025Article
- The immunoproteasome regulates ILC2 responses by modulating mitochondrial capacity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Zinc solubilizing rhizobacteria as bioinoculant for turmeric: transcriptomic insights into acid stress adaptation, zinc mobilization and growth promotion.World journal of microbiology & biotechnology · 2025Article
- NDUFA8 promotes cell viability and inhibits ferroptosis and cisplatin sensitivity by stabilizing Fe-S clusters in cervical cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Molecular Mechanisms of Iron Metabolism and Overload.Biomedicines · 2025Review
- The iron metalloproteome of Pseudomonas aeruginosa under oxic and anoxic conditions.Metallomics : integrated biometal science · 2025Article
- Omaveloxolone, But Not Dimethyl Fumarate, Improves Cardiac Function in Friedreich's Ataxia Mice With Severe Cardiomyopathy.Journal of the American Heart Association · 2025Article
- Iron-Sulfur Clusters and Iron Responsive Element Binding Proteins Mediate Iron Accumulation in Corneal Endothelial Cells in Fuchs Dystrophy.Investigative ophthalmology & visual science · 2025Article
- Early detection of feline chronic kidney disease via 3-hydroxykynurenine and machine learning.Scientific reports · 2025Article
- Ferroptosis: iron release mechanisms in the bioenergetic process.Cancer metastasis reviews · 2025Review
- In vitro effect of hCG on cryptorchid patients' gubernacular cells: a predictive model for adjuvant personalized therapy.Cell communication and signaling : CCS · 2025Article
- Iron-Mediated Regulation in Adipose Tissue: A Comprehensive Review of Metabolism and Physiological Effects.Current obesity reports · 2025Review
- Eye on the horizon: The metabolic landscape of the RPE in aging and disease.Progress in retinal and eye research · 2025Review
- Mitochondrial Aconitase and Its Contribution to the Pathogenesis of Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Article
- Non-Mitochondrial Aconitase-2 Mediates the Transcription of Nuclear-Encoded Electron Transport Chain Genes in Fission Yeast.Journal of microbiology (Seoul, Korea) · 2024Article
55 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aconitase, an enzyme possessing an iron-sulfur cluster that is sensitive to oxidation, is involved in the regulation of cellular metabolism. There are two isoenzymes of aconitase (Aco)--mitochondrial (mAco) and cytosolic (cAco) ones. The primary role of mAdco is believed to be to control cellular ATP production via regulation of intermediate flux in the Krebs cycle. The cytosolic Aco in its reduced form operates as an enzyme, whereas in the oxidized form it is involved in the control of iron homeostasis as iron regulatory protein 1 (IRP1). Reactive oxygen species (ROS) play a central role in regulation of Aco functions. Catalytic Aco activity is regulated by reversible oxidation of [4Fe-4S]²⁺ cluster and cysteine residues, so redox-dependent posttranslational modifications (PTMs) have gained increasing consideration as regards possible regulatory effects. These include modifications of cysteine residues by oxidation, nitrosylation and thiolation, as well as Tyr nitration and oxidation of Lys residues to carbonyls. Redox-independent PTMs such as phosphorylation and transamination also have been described. In the presence of a sustained ROS flux, redox-dependent PTMs may lead to enzyme damage and cell stress by impaired energy and iron metabolism. Aconitase has been identified as a protein that undergoes oxidative modification and inactivation in aging and certain oxidative stress-related disorders. Here we describe possible mechanisms of involvement of the two aconitase isoforms, cAco and mAco, in the control of cell metabolism and iron homeostasis, balancing the regulatory, and damaging effects of ROS.
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Registered trials
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.