ReviewInternational journal of rheumatic diseases2025
Dysregulation of Different Modes of Programmed Cell Death in Rheumatoid Arthritis Fibroblast-Like Synoviocyte.
Review in International journal of rheumatic diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis 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
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Global research trends in programmed cell death in rheumatoid arthritis from 2001 to 2025: a bibliometric analysis.Frontiers in immunology · 2026Pooled it
- Bioelectronic Medicine: A New Horizon for Difficult-To-Treat Rheumatoid Arthritis.International journal of rheumatic diseases · 2026Article
- The PANoptotic mosaic of rheumatoid arthritis: epitranscriptomic regulation, systemic relays, and precision death-mode editing.Frontiers in immunology · 2026Review
- Article
- Dysregulation of Different Modes of Programmed Cell Death in Rheumatoid Arthritis Fibroblast-Like Synoviocyte.International journal of rheumatic diseases · 2025Review
- Stimuli-Responsive Nanoplatforms for Precision Intervention in Rheumatoid Arthritis.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnologyReview
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
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by chronic synovitis and skeletal joint deformities, often accompanied by systemic symptoms. Over the past few decades, various susceptibility factors for RA have been revealed, and numerous therapeutic drugs have been developed, including analgesics, glucocorticoids, non-steroidal anti-inflammatory drugs (NSAIDs), disease-modifying antirheumatic drugs (DMARDs), and biological agents (bDMARDs). Despite the availability of multiple treatment options, the therapeutic outcomes for some patients remain suboptimal due to the complex pathogenesis of RA. As a key pathological mechanism, programmed cell death (PCD) in RA has received extensive attention. Dysregulation of PCD in RA impacts the progression of the disease. This article systematically reviews the roles of various cell death modalities, including apoptosis, necroptosis, ferroptosis, pyroptosis, and autophagy in the pathophysiology of RA, aiming to provide a theoretical basis and direction for the discovery of new therapeutic targets and drug development.
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.