ReviewCurrent rheumatology reports2001
Apoptosis and rheumatoid arthritis: past, present, and future directions.
Review in Current rheumatology reports, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- RA-map: building a state-of-the-art interactive knowledge base for rheumatoid arthritis.Database : the journal of biological databases and curation · 2020Article
- Bcl-x(L) expression in vivo in rheumatoid synovium.Clinical rheumatology · 2006Article
- CII-DC-AdTRAIL cell gene therapy inhibits infiltration of CII-reactive T cells and CII-induced arthritis.The Journal of clinical investigation · 2003Article
- Higher susceptibility to Fas ligand induced apoptosis and altered modulation of cell death by tumor necrosis factor-alpha in periarticular tenocytes from patients with knee joint osteoarthritis.Arthritis research & therapy · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The current studies of apoptosis in rheumatoid arthritis (RA) suggest that molecules (Fas-related or TNF-related), pathways (activation of pro-apoptosis or anti-apoptosis pathway), cell types (lymphocytes or synovial fibroblast), and the mechanism that triggers apoptosis (tolerance induction-related, down-modulation of inflammation-related, or DNA damage-related) all play a fundamental role to determine the induction or prevention of RA. These series of defects at different levels and in different cells lead to hyperproliferation, defective apoptosis, or hyperapoptosis. This review summarizes the available knowledge of apoptosis and RA to help identify candidate target cells and target molecules for delivery of gene constructs or modified biological or chemical reagents to the target site for effective modification of these cells.
Indexed as
Identifiers
11177773What 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.