Leahy K M, Koki A T, Masferrer J L
Discovery Pharmacology, G. D. Searle/Monsanto (T3G), 800 North Lindbergh Boulevard, St. Louis, Missouri 63167, USA.
Curr Med Chem. 2000 Nov;7(11):1163-70. doi: 10.2174/0929867003374336.
Angiogenesis is the process by which new blood vessels are formed. This process supports normal physiology as well as contributes to progression of disease. Progressive rheumatoid arthritis and growth of tumors are two pathologies to which angiogenesis contributes. In arthritis, we know that prostaglandins (PGs) and the enzyme cyclooxygenase-2, which catalyses prostaglandin production, are inflammatory mediators. These mediators are involved in rheumatoid arthritis and cancer-induced angiogenic processes. We discuss, herein, recent findings on the expression of cyclooxygenases in both rheumatoid arthritis and human cancer, and the links between COX-2, PGs, and angiogenesis. We also propose a model for the possible mechanistic interaction of the various cell types involved in angiogenesis.
血管生成是新血管形成的过程。这一过程既支持正常生理功能，也会促进疾病进展。进行性类风湿性关节炎和肿瘤生长是血管生成所导致的两种病理情况。在关节炎中，我们知道前列腺素（PGs）以及催化前列腺素生成的环氧化酶-2是炎症介质。这些介质参与类风湿性关节炎和癌症诱导的血管生成过程。在此，我们讨论类风湿性关节炎和人类癌症中环氧化酶表达的最新研究结果，以及COX-2、PGs和血管生成之间的联系。我们还提出了一个关于血管生成过程中各种细胞类型可能的机制相互作用的模型。
