ReviewMolecular medicine (Cambridge, Mass.)2026
Regulation of mitochondrial iron homeostasis in tumor cells.
Review in Molecular medicine (Cambridge, Mass.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Context-Dependent Modulation of Ferroptosis by Metformin: Mechanisms, Therapeutic Implications and Open Questions.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Nutrient stress-induced FTH1 safeguards redox balance and fuels pancreatic ductal adenocarcinoma growth while serving as a therapeutic target and diagnostic biomarker.Cellular oncology (Dordrecht, Netherlands) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Iron is an indispensable trace element for all living organisms, existing in the form of free iron (Fe2+/Fe3+) and bound iron, and it plays a crucial role in a variety of cellular processes, including biomolecule synthesis, epigenetic regulation, immune modulation, cellular senescence, and mitochondrial respiration. Iron homeostasis is meticulously regulated within biological systems to avert the detrimental effects of both iron overload and deficiency, with imbalances leading to a multitude of diseases. Numerous studies have underscored the importance of rebalancing iron homeostasis in cancers, emphasizing its crucial role in tumorigenesis. Within the cell, mitochondria serve as the central hub for iron metabolism, primarily accountable for the synthesis of heme and iron-sulfur (Fe-S) clusters, the storage of excess iron via mitochondrial ferritin, and the regulation of iron-dependent cell death pathways such as ferroptosis and cuproptosis. Despite decades of in-depth research into the biological functions of iron and its homeostatic regulation, numerous scientific questions remain unresolved. This review offers a comprehensive and integrated analysis of the detailed regulatory mechanisms of mitochondrial iron metabolism and its profound influence on cancer metabolism. Based on the current research progress, we have summarized the challenges and limitations in this field and proposed new conceptual frameworks and research directions to enhance our understanding of mitochondrial iron biology in cancer.
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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.