ArticleArthritis research & therapy2007
Pro-apoptotic Bid is required for the resolution of the effector phase of inflammatory arthritis.
Article in Arthritis research & therapy, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Prognostic signature and therapeutic drug identification for dilated cardiomyopathy based on necroptosis via bioinformatics and experimental validation.Scientific reports · 2025Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Apoptosis Triggering, an Important Way for Natural Products From Herbal Medicines to Treat Pancreatic Cancers.Frontiers in pharmacology · 2021Review
- BAD inactivation exacerbates rheumatoid arthritis pathology by promoting survival of sublining macrophages.eLife · 2020Article
- Review
- ZAP-70 Regulates Autoimmune Arthritis via Alterations in T Cell Activation and Apoptosis.Cells · 2019Article
- The Role of Macrophages in the Response to TNF Inhibition in Experimental Arthritis.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Genetic deficiency of Wnt5a diminishes disease severity in a murine model of rheumatoid arthritis.Arthritis research & therapy · 2017Article
- Deletion of calponin 2 in macrophages attenuates the severity of inflammatory arthritis in mice.American journal of physiology. Cell physiology · 2016Article
- The inflammatory role of phagocyte apoptotic pathways in rheumatic diseases.Nature reviews. Rheumatology · 2016Review
- BID Mediates Oxygen-Glucose Deprivation-Induced Neuronal Injury in Organotypic Hippocampal Slice Cultures and Modulates Tissue Inflammation in a Transient Focal Cerebral Ischemia Model without Changing Lesion Volume.Frontiers in cellular neuroscience · 2016Article
- Fas signaling in macrophages promotes chronicity in K/BxN serum-induced arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- High-resolution magnetic resonance imaging of ankle joints in murine arthritis discriminates inflammation and bone destruction in a quantifiable manner.Arthritis and rheumatism · 2013Article
- TLR2 deletion promotes arthritis through reduction of IL-10.Journal of leukocyte biology · 2013Article
- Glycoprotein 96 perpetuates the persistent inflammation of rheumatoid arthritis.Arthritis and rheumatism · 2012Article
- Development of a new humanized mouse model to study acute inflammatory arthritis.Journal of translational medicine · 2012Article
- Cyclin-dependent kinase inhibitor p21, via its C-terminal domain, is essential for resolution of murine inflammatory arthritis.Arthritis and rheumatism · 2012Article
- Type I interferon drives dendritic cell apoptosis via multiple BH3-only proteins following activation by PolyIC in vivo.PloS one · 2011Article
- Deficiency of Bid protein reduces sepsis-induced apoptosis and inflammation, while improving septic survival.Shock (Augusta, Ga.) · 2010Article
- Bim-Bcl-2 homology 3 mimetic therapy is effective at suppressing inflammatory arthritis through the activation of myeloid cell apoptosis.Arthritis and rheumatism · 2010Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Rheumatoid arthritis is an autoimmune disease characterized by hyperplasia of the synovial lining and destruction of cartilage and bone. Recent studies have suggested that a lack of apoptosis contributes to the hyperplasia of the synovial lining and to the failure in eliminating autoreactive cells. Mice lacking Fas or Bim, two pro-apoptotic proteins that mediate the extrinsic and intrinsic death cascades, respectively, develop enhanced K/BxN serum transfer-induced arthritis. Since the pro-apoptotic protein Bid functions as an intermediate between the extrinsic and intrinsic apoptotic pathways, we examined the role that it plays in inflammatory arthritis. Mice deficient in Bid (Bid-/-) show a delay in the resolution of K/BxN serum transfer-induced arthritis. Bid-/- mice display increased inflammation, bone destruction, and pannus formation compared to wild-type mice. Furthermore, Bid-/- mice have elevated levels of CXC chemokine and IL-1beta in serum, which are associated with more inflammatory cells throughout the arthritic joint. In addition, there are fewer apoptotic cells in the synovium of Bid-/- compared to Wt mice. These data suggest that extrinsic and intrinsic apoptotic pathways cooperate through Bid to limit development of inflammatory arthritis.
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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.