ReviewOncogene2008
BH3-only proteins in rheumatoid arthritis: potential targets for therapeutic intervention.
Review in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- Targeting the BCL2 Family: Advances and Challenges in BH3 Mimetic-Based Therapies.International journal of molecular sciences · 2025Review
- Bim Expression Promotes the Clearance of Mononuclear Phagocytes during Choroidal Neovascularization, Mitigating Scar Formation in Mice.Life (Basel, Switzerland) · 2022Article
- Silencing of Long Non-Coding RNA (lncRNA) Nuclear Paraspeckle Assembly Transcript 1 (NEAT1) Protects PC-12 Cells from LPS-Induced Injury via Targeting miR-29a.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Review
- Intracellular apoptotic pathways: a potential target for reducing joint damage in rheumatoid arthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Review
- Bim suppresses the development of SLE by limiting myeloid inflammatory responses.The Journal of experimental medicine · 2017Article
- The contribution of the programmed cell death machinery in innate immune cells to lupus nephritis.Clinical immunology (Orlando, Fla.) · 2017Review
- The caspase-8/RIPK3 signaling axis in antigen presenting cells controls the inflammatory arthritic response.Arthritis research & therapy · 2017Article
- Monocyte-derived alveolar macrophages drive lung fibrosis and persist in the lung over the life span.The Journal of experimental medicine · 2017Article
- The inflammatory role of phagocyte apoptotic pathways in rheumatic diseases.Nature reviews. Rheumatology · 2016Review
- Chondrocyte Apoptosis in Rheumatoid Arthritis: Is Preventive Therapy Possible?Immunotherapy (Los Angeles, Calif.) · 2015Article
- Conditional deletion of caspase-8 in macrophages alters macrophage activation in a RIPK-dependent manner.Arthritis research & therapy · 2015Article
- Noxa in rheumatic diseases: present understanding and future impact.Rheumatology (Oxford, England) · 2014Review
- Caspase-8 acts as a molecular rheostat to limit RIPK1- and MyD88-mediated dendritic cell activation.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Induction of apoptosis by fucoidan in human leukemia U937 cells through activation of p38 MAPK and modulation of Bcl-2 family.Marine drugs · 2013Article
- Regulation of antiviral CD8 T-cell responses.Critical reviews in immunology · 2013Review
- Cyclin-dependent kinase inhibitor p21, via its C-terminal domain, is essential for resolution of murine inflammatory arthritis.Arthritis and rheumatism · 2012Article
- The discovery of novel experimental therapies for inflammatory arthritis.Mediators of inflammation · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Rheumatoid arthritis (RA) is a debilitating disease, resulting in the destruction of bone and cartilage, and in the permanent disfigurement of joints. Although the precise cause of RA is currently unresolved, it has become clear that the damaging effects are a result of the toxic milieu caused by an influx of inflammatory cells and the resulting heightened proinflammatory state within the joint. As the amount of literature suggesting that this preponderance of cells is a result of decreased local apoptosis in the joint continues to increase, in this review, we describe how Bcl-2 family pro-apoptotic BH3-only proteins, particularly Bim and Bid, could act to protect against the development of the disease. We also suggest a role for BH3-mimetic drugs as potential therapeutics in the treatment of RA.
Indexed as
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What 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.