ReviewBiomedicines2025
Molecular Mechanisms of Iron Metabolism and Overload.
Review in Biomedicines, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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
8 citing papers in PubMed.
- Selective Detection of Fe(III) and Al(III) Using an Azo-Functionalized Rhodamine B Chemosensor: Expansion to F- Ion Detection by Al(III)-Probe Complex.Chemistry, an Asian journal · 2026Article
- The Iron Lung: Ferroptosis and Iron Regulation in Aging and Lung Diseases.Physiology (Bethesda, Md.) · 2026Review
- Review
- Ferroptosis and Nrf-2 signaling: a redox tug of war in leishmaniasis pathogenesis and host directed therapy.Redox biology · 2026Review
- The Potential Role of Iron Homeostasis and Ferroptosis in Exercise Nutrition and Health.Nutrients · 2026Review
- Ferroptosis in diabetes-associated cognitive dysfunction: mechanisms and therapeutic potential.Frontiers in pharmacology · 2026Review
- Doxorubicin-induced cardiotoxicity: Is ferroptosis the primary driver or a downstream amplifier?EXCLI journal · 2026Review
- Improved Iron Uptake and Metabolism Through Combined Heme and Non-Heme Iron Supplementation: An In Vitro Study.Biomedicines · 2025Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Iron represents an essential element required for normal physiologic processes throughout organ systems. A vast network of transporters is involved not only in uptake of this element but in processing, oxidation, and recycling to maintain it in a tight balance to avoid excess storage. This complex network of transporters, including heme and ferroportin, among many others, are responsible for facilitating inter-organ tissue iron exchange and availability, contributing to overall heme homeostasis. However, exposure to high levels of iron can overwhelm compensatory mechanisms that result in its accumulation and toxicity. This is the case of patients with genetic diseases such as hemoglobinopathies who suffer from chronic anemia and require, in most instances, a lifetime of red blood cell transfusions to overcome disease crises. Thus, in light of the extensive role of iron in the body, the aim of this review is to present important metabolic pathways involved in iron homeostasis across the cardiovascular, reproductive, hematopoietic, urinary, respiratory, endocrine, and central nervous systems while contrasting these against negative effects caused by iron excess.
Indexed as
Identifiers
What Socratic 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 Socratic graph.