Ghorpade A, Baxter B T
Department of Surgery, University of Nebraska Medical Center, Omaha 68132-3200, USA.
Ann N Y Acad Sci. 1996 Nov 18;800:138-50. doi: 10.1111/j.1749-6632.1996.tb33305.x.
Past concepts of aneurysmal dilatation as a passive process of attenuation are oversimplified and inaccurate. Aneurysm formation is a complex remodeling process that involves both synthesis and degradation of matrix proteins. Interstitial procollagen gene expression is increased in AAA compared to AOD or normal aorta, whereas tropoelastin gene expression is decreased in both AOD and AAA. The medial elastin network is disrupted and discontinuous in small AAA. Thus, the growth rate of an established AAA may well relate to the balance between collagen synthesis and degradation. Although the increased procollagen expression found in AAA may represent a compensatory response, understanding the factors that modulate matrix metabolism in AAA may allow for development of pharmacologic strategies which effectively inhibit the growth of small aneurysms.
过去将动脉瘤扩张视为一种被动的衰减过程的概念过于简单化且不准确。动脉瘤形成是一个复杂的重塑过程，涉及基质蛋白的合成和降解。与主动脉粥样硬化（AOD）或正常主动脉相比，腹主动脉瘤（AAA）中I型前胶原基因表达增加，而原弹性蛋白基因在AOD和AAA中均减少。在小的AAA中，中膜弹性蛋白网络被破坏且不连续。因此，已形成的AAA的生长速率很可能与胶原蛋白合成和降解之间的平衡有关。尽管在AAA中发现的前胶原表达增加可能代表一种代偿反应，但了解调节AAA中基质代谢的因素可能有助于开发有效抑制小动脉瘤生长的药物策略。
