ReviewCell biology and toxicology2026
Lipocalin 2: a double-edged sword in cellular ferroptosis.
Review in Cell biology and toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Targeting the Fra2/LCN2 axis attenuates PMRedox biology · 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
5 authors.
Funding
Abstract
Ferroptosis is a novel form of programmed cell death that is distinct from apoptosis, necrosis, and autophagy (macroautophagy). It is characterized by alterations in intracellular iron levels and lipid peroxidation. Considering its close association with numerous diseases, the molecular mechanisms underlying cellular ferroptosis have recently emerged as a prominent research focus. Lipocalin 2 (LCN2) is a circulating protein involved in the regulation of diverse cellular processes in eukaryotes and is closely associated with ferroptosis. However, the modulation of ferroptosis by LCN2 exhibits significant tissue and disease specificity. This is not only attributed to the ability of LCN2 to mediate iron metabolism reprogramming, but also to its capacity to bidirectionally regulate oxidative stress and interact with multiple signaling pathways. Therefore, this review summarizes the mechanisms through which LCN2 contributes to ferroptosis and its tissue- and disease-specific regulatory functions. Additionally, the current status of the clinical translation of LCN2 as a biomarker and therapeutic target is explored.
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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 Socratic graph.