Cipollone Francesco, Fazia Maria Luigia
Centro Regionale per la Prevenzione dell'Aterosclerosi, Via Colle dell'Ara, 66013 Chieti, Italy.
Curr Atheroscler Rep. 2006 May;8(3):245-51. doi: 10.1007/s11883-006-0080-2.
The inducible isoform of cyclooxygenase-2 (COX-2) plays a role in pathophysiologic processes like inflammation and pain but is also constitutively expressed in tissues such as the kidney or vascular endothelium, where it exerts important physiologic functions. Although much evidence exists that implicates COX-2 in atherosclerosis, its role in this setting remains substantially uncertain. This observation is also confirmed by the results of clinical trials of selective COX-2 inhibitors. Treatment with these drugs, developed with the assumption that they would be as effective as nonselective COX inhibitors but without their gastrointestinal side effects, has been reported to be associated with an increased cardiovascular risk. In this article, we review the pattern of expression of COX-2 in the cellular players of atherothrombosis, its role as a determinant of plaque vulnerability, and the vascular effects on prostanoid inhibition by COX-2 inhibitors.
环氧化酶-2(COX-2)的诱导型同工型在炎症和疼痛等病理生理过程中发挥作用,但在肾脏或血管内皮等组织中也有组成性表达,在这些组织中它发挥着重要的生理功能。尽管有大量证据表明COX-2与动脉粥样硬化有关,但其在这种情况下的作用仍存在很大不确定性。选择性COX-2抑制剂的临床试验结果也证实了这一观察结果。据报道,使用这些药物进行治疗(研发这些药物时假设它们与非选择性COX抑制剂一样有效,但没有其胃肠道副作用)与心血管风险增加有关。在本文中,我们综述了COX-2在动脉粥样硬化血栓形成的细胞参与者中的表达模式、其作为斑块易损性决定因素的作用以及COX-2抑制剂对前列腺素抑制的血管效应。