SynthesisInflammation2021
ROS-Dependent Lipid Peroxidation and Reliant Antioxidant Ferroptosis-Suppressor-Protein 1 in Rheumatoid Arthritis: a Covert Clue for Potential Therapy.
Synthesis in Inflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 3 of them syntheses that pooled it.
What it found
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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
58 citing papers in PubMed, 3 syntheses or guidelines pooled it, 81 citations in OpenAlex.
- Global research trends in programmed cell death in rheumatoid arthritis from 2001 to 2025: a bibliometric analysis.Frontiers in immunology · 2026Pooled it
- Anti-arthritic and immunomodulatory effects of geniposide: a systematic review and meta-analysis of preclinical studies.Inflammopharmacology · 2025Pooled it
- Experimental Evidence on Acupuncture Targeting Ferroptosis for Neurological Function Improvement in Cerebral Stroke: A Systematic Review and Meta-Analysis.Brain and behavior · 2025Pooled it
- Identification of ferroptosis hub gene cDKN1A relating to immune microenvironment in rheumatoid arthritis via bioinformatic analysis and experimental verification.Clinical rheumatology · 2026Article
- 1,8-Cineole Alleviates PA-Induced Lipid Accumulation, Oxidative Stress, and Inflammation via the TLR4/MyD88/NF-κB Signaling Pathway.Molecules (Basel, Switzerland) · 2026Article
- Nanozyme-based therapies for inflammatory immune disorders: opportunities and challenges.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Programmed cell death in osteoarthritis.Apoptosis : an international journal on programmed cell death · 2026Review
- The Application Prospects and Future Outlook ofDrug design, development and therapy · 2026Review
- Therapeutic effects of Bushen Chushi formula on knee osteoarthritis via modulation of MAPK/SLC7A11/GPX4 signaling in rats.Hereditas · 2025Article
- Ferroptosis in Autoimmune Diseases: Research Advances and Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Integrated analysis of single-cell RNA-seq and bulk RNA-seq reveal macrophage subpopulation characteristics and the role of STAT1 in rheumatoid arthritis.Journal of translational medicine · 2025Article
- Dysregulation of Different Modes of Programmed Cell Death in Rheumatoid Arthritis Fibroblast-Like Synoviocyte.International journal of rheumatic diseases · 2025Review
- GZMK Facilitates Experimental Rheumatoid Arthritis Progression by Interacting with CCL5 and Activating the ERK Signaling.Inflammation · 2025Article
- Crosstalk between ferroptosis and NLRP3, a possible therapeutic target in experimentally-induced rheumatoid arthritis: role of P2Y12R inhibition in modulating P53/SLC7A11/ALOX15 signaling.Inflammopharmacology · 2025Article
- Nanodrug delivery systems targeting ferroptosis as an innovative therapeutic approach for Rheumatoid Arthritis.Materials today. Bio · 2025Review
- Iron metabolism in rheumatic diseases.Journal of translational autoimmunity · 2025Review
- Gypenoside XLIX Activates the Sirt1/Nrf2 Signaling Pathway to Inhibit NLRP3 Inflammasome Activation to Alleviate Septic Acute Lung Injury.Inflammation · 2025Article
- TNFα-reliant FSP1 up-regulation promotes intervertebral disc degeneration via caspase 3-dependent apoptosis.Genes & diseases · 2025Article
- Natural products protect against spinal cord injury by inhibiting ferroptosis: a literature review.Frontiers in pharmacology · 2025Review
- RND1 Induces Ferroptosis to Alleviate Inflammatory Response, Proliferation, Invasion, and Migration of Rheumatoid Synoviocytes.Journal of inflammation research · 2025Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is a common systemic autoimmune disease with a prevalence of about 1% in which genetic and environmental risk factors both participate in performance of disease. Though several studies contributed in identifying its etiology and pathogenesis, the underlying mechanisms are still unknown. To date, so as palliative for RA, cure strategies are still popular. Hypoxia and oxidative stress are implicated to RA development and subsequent ROS-mediated cell death which is a critical feature for RA progression. As for cell death and lipid peroxidation, ferroptosis is a newly discovered, iron-dependent, and non-apoptotic cell death which draws various attention due to its potential strategies for cancer therapy. Meanwhile, ferroptosis-suppressor-protein 1 (FSP1) is recently identified as a seminal breakthrough owing to its property of versus ferroptosis. By virtue of the complicated research progress on FSP1 with ferroptosis, in this review, we summarize the whole region of relevance between ROS and RA. Taken together, we hypothesize that ROS accompanied with ferroptosis may function as a reciprocal with cell death that interplays with RA; besides, FSP1 might become a potential therapeutic target for RA because of its potential interaction with TNF-α/ROS-positive feedback loop. This review systematically concludes the previous understandings about identification of ROS and FSP1 and, in turn, aims to provide references for further achievements of them and hints on elucidation of its thorough underlying mechanisms.
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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 OpenQuestion graph.