Hutcheson J, Perlman H
Rheumatic Diseases Division, Department of Internal Medicine, University of Texas - Southwestern Medical Center, Simmons Arthritis Research Center, Dallas, TX, USA.
Oncogene. 2008 Dec;27 Suppl 1(Suppl 1):S168-75. doi: 10.1038/onc.2009.54.
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.
类风湿性关节炎（RA）是一种使人衰弱的疾病，会导致骨骼和软骨破坏以及关节永久性畸形。尽管RA的确切病因目前尚未明确，但已清楚的是，其破坏作用是由炎症细胞涌入所导致的毒性环境以及关节内由此加剧的促炎状态引起的。随着表明关节内局部细胞凋亡减少导致这种细胞优势的文献数量不断增加，在本综述中，我们描述了Bcl-2家族仅含BH3结构域的促凋亡蛋白，特别是Bim和Bid，如何发挥作用来预防该疾病的发展。我们还提出BH3模拟药物作为RA治疗潜在疗法的作用。
