ArticleACS omega2025
Perfluorooctanoic Acid Induces Ferroptosis in Hepatocytes via Oxidative Stress and AKT/GSK3β/β-Catenin Pathway Disruption.
Article in ACS omega, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Unveiling the toxic effects of perfluorooctanoic acid on osteoblast function and extracellular matrix deposition using 2D and 3D models.Cell death discovery · 2026Article
- PFOA/PFOS induce ferroptosis in bladder epithelial cells through inhibition of ACSL4 ubiquitination.Frontiers in toxicology · 2026Article
- Synergistic toxicity in alcohol-associated liver disease and PFAS exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Perfluorooctanoic acid (PFOA), a typical environmental contaminant, has been observed in tissue samples of various diseases, including liver cancer. PFOA can lead to hepatotoxicity, but the underlying molecular mechanism remains unclear. Our results showed that PFOA significantly inhibited HL-7702 (L02) and MIHA cell viability in a time- and dose-dependent manner. Furthermore, PFOA could cause oxidative stress, mitochondrial injury, and ferroptosis. In addition, PFOA upregulated the levels of malondialdehyde and glutathione/oxidized glutathione and downregulated the expressions of SLC7A11 and GPX4, which refer to typical phenotypes of ferroptosis. PFOA suppressed phosphorylation of signaling cascades AKT/GSK3β/β-catenin, indicating the signal pathway might be related to ferroptosis. In order to prove the above hypothesis, the Wnt signaling pathway activator chir99021 was used and the result revealed that PFOA-induced inhibition of p-AKT and its downstream effectors p-GSK3β, SLC7A11, and GPX4 was counteracted. On the other hand, the inhibitor of p-AKT, Ly294002, strengthened PFOA's regulatory actions on these factors. Overall, our results suggest that PFOA can lead to liver cell injury by inducing oxidative stress and ferroptosis. The effects are conferred through the regulation of the AKT/GSK3β/β-catenin signaling cascades.
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.