ArticleClinical rheumatology2026
Platelet ferroptosis promotes oxidized DNA release and SLE progression.
Article in Clinical rheumatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
objectivesFerroptosis is a recently identified type of regulated necrosis, and glutathione peroxidase 4 (GPX4) has been recognized as a key enzyme that protects against ferroptosis. However, the role of platelet ferroptosis in systemic lupus erythematosus (SLE) has not been explored. This study aimed to investigate the role of GPX4-mediated platelet ferroptosis in SLE.
methodsGPX4 protein expression in platelets was detected by Western blot and immunofluorescence analysis. The correlation of platelet GPX4 expression with SLE clinical characteristics was evaluated. The ability of platelet activation and ferroptosis was detected, and the release of oxidized DNA by platelets was tested. In addition, GPX4 inhibitor and activator were used to evaluate the effect of GPX4 on platelet ferroptosis and oxidized DNA release. Finally, MRL/lpr mice were treated with GPX4 activator 1 or vehicle and the severity of lupus disease was assessed.
resultsPlatelets of SLE patients showed lower expression of GPX4, which was negatively correlated with disease activity and plasma oxidized DNA levels. These platelets were more activated, prone to ferroptosis, and released higher levels of oxidized DNA. In vitro, GPX4 inhibitor induced ferroptosis and oxidized DNA release in healthy control platelets, whereas the GPX4 activator 1 protected SLE platelets. In MRL/lpr mice, treatment with GPX4 activator 1 alleviated lupus severity, reduced platelet ferroptosis, and decreased oxidized DNA release.
conclusionSLE platelets exhibit low GPX4 expression and are more susceptible to ferroptosis, highlighting the critical role of GPX4 downregulation-mediated platelet ferroptosis in the development of SLE. Therefore, activation of GPX4 may represent a therapeutic strategy for SLE. Key Points • SLE platelets exhibit low GPX4 expression and are more susceptible to ferroptosis and the release of oxidized DNA. • Pharmacological activation of GPX4 inhibits platelet ferroptosis and oxidized DNA release in vitro and in vivo. • Targeting platelet ferroptosis via GPX4 activation alleviates disease severity in MRL/lpr mice.
Indexed as
Identifiers
42461566What 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.