ReviewJournal of inflammation research2025
Ferroptosis: New Strategies for Clinical Treatment of Rheumatoid Arthritis.
Review in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 2 of them syntheses that pooled it.
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
4 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Global research trends in programmed cell death in rheumatoid arthritis from 2001 to 2025: a bibliometric analysis.Frontiers in immunology · 2026Pooled it
- Ferroptosis in gouty arthritis: a potential therapeutic strategy.Frontiers in immunology · 2026Pooled it
- Ferroptosis inhibition and mitochondrial rescue: a novel mechanism of emodin in rheumatoid arthritis.Redox report : communications in free radical research · 2026Article
- Targeting ferroptosis in osteoporosis: mechanisms and natural products therapies.Frontiers in pharmacology · 2026Review
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
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease that can lead to joint deformities, functional loss, and a significant reduction in patients' quality of life. It also imposes a considerable medical and socio-economic burden. Iron-induced cell death, or ferroptosis, is a unique form of programmed cell death characterized by dysregulated iron metabolism and the accumulation of lipid peroxides resulting from increased reactive oxygen species (ROS) and reduced activity of glutathione peroxidase 4 (GPX4). The accumulation of lipid peroxides can cause cellular damage, promotes inflammatory responses and joint destruction. This process not only plays a crucial role in the pathogenesis of RA, but also provides new therapeutic targets for its treatment. In this review, we summarize the regulatory mechanisms of ferroptosis in the pathogenesis of RA. These include its roles in regulating oxidative stress and lipid peroxidation, inhibiting the abnormal proliferation of synovial fibroblasts (FLSs), preventing cartilage erosion, restoring immune homeostasis and inflammatory responses, and other aspects. Finally, we also discuss the potential clinical applications, and future prospects of ferroptosis-based therapies for RA treatment.
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.