ReviewCurrent opinion in genetics & development2016
Mitochondrial iron overload: causes and consequences.
Review in Current opinion in genetics & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Review of ferroptosis in colorectal cancer: Friends or foes?World journal of gastroenterology · 2023Pooled it
- Therapeutic Potential of Deferiprone-Resveratrol Hybrid (DFP-RVT) Against Hepatic Iron Overload in β-Thalassemia Mice: A Proteomic Analysis.Biomolecules · 2026Article
- Phase-dependent iron dysmetabolism in myocardial ischemia-reperfusion injury: From mechanisms to therapies.American heart journal plus : cardiology research and practice · 2025Review
- Review
- Proteomic Research of the Stress Response ofMicroorganisms · 2025Article
- The Protective Effects of Taurine, a Non-essential Amino Acid, Against Metals Toxicities: A Review Article.Biological trace element research · 2025Review
- Enhanced CRC Growth in Iron-Rich Environment, Facts and Speculations.International journal of molecular sciences · 2024Review
- Don´t give up on mitochondria as a target for the treatment of diabetes and its complications.World journal of diabetes · 2024Article
- Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects.Signal transduction and targeted therapy · 2024Review
- The hepcidin-ferroportin axis influences mitochondrial function, proliferation, and migration in pulmonary artery endothelial and smooth muscle cells.Pulmonary circulation · 2024Article
- Subzero project: comparing trace element profiles of enriched mitochondria fractions from frozen and fresh liver tissue.Analytical and bioanalytical chemistry · 2024Article
- N-Myristoytransferase Inhibition Causes Mitochondrial Iron Overload and Parthanatos in TIM17A-Dependent Aggressive Lung Carcinoma.Cancer research communications · 2024Article
- CIAO1 loss of function causes a neuromuscular disorder with compromise of nucleocytoplasmic Fe-S enzymes.The Journal of clinical investigation · 2024Article
- Nanodrug Delivery Systems for Myasthenia Gravis: Advances and Perspectives.Pharmaceutics · 2024Review
- The cell fate regulator DACH1 modulates ferroptosis through affecting P53/SLC25A37 signaling in fibrotic disease.Hepatology communications · 2024Article
- Optical Imaging Opportunities to Inspect the Nature of Cytosolic Iron Pools.Molecules (Basel, Switzerland) · 2023Review
- The synthesis and properties of mitochondrial targeted iron chelators.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2023Article
- Early adaptive responses in the skeletal muscle of young mice with hereditary hemochromatosis.Molecular biology reports · 2023Article
- The beneficial role of Hepcidin peptide inhibitor in improved the symptoms of COVID-19 in diabetics: anti-inflammatory and potential therapeutic effects.Journal of diabetes and metabolic disorders · 2022Review
- Mammalian iron sulfur cluster biogenesis and human diseases.IUBMB life · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Pathological overload of iron in the mitochondrial matrix has been observed in numerous diseases, including sideroblastic anemias, which have many causes, and in genetic diseases that affect iron-sulfur cluster biogenesis, heme synthesis, and mitochondrial protein translation and its products. Although high expression of the mitochondrial iron importer, mitoferrin, appears to be an underlying common feature, it is unclear what drives high mitoferrin expression and what other proteins are involved in trapping excess toxic iron in the mitochondrial matrix. Numerous examples of human diseases and model systems suggest that mitochondrial iron homeostasis is coordinated through transcriptional remodeling. A cytosolic/nuclear molecule may affect a transcriptional factor to coordinate the events that lead to iron accumulation, but no candidates for this role have yet been identified.
Indexed as
Identifiers
What OpenQuestion holds
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.