Pathogenesis of aneurysms.
Pathogenesis of aneurysms.
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DOI：
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发表时间：
1995
影响因子：
2.5
通讯作者：
B. Halloran;B. Baxter
中科院分区：
文献类型：
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作者：
B. Halloran;B. Baxter
我们现在知道我们过去对AAA发病机制的概念过于简单和不准确。事实上，与正常主动脉相比，动脉瘤壁的代谢活性显著增加。已经清楚的是，AAA不是被动扩张的结果，而是一个复杂的重塑过程，涉及基质蛋白的合成和降解。通过应用分子生物学技术，我们对这一过程的理解有所提高。尽管弹性蛋白碎裂和中层衰减仍然是AAA组织最显著的组织学特征，但实验和临床证据表明，在没有内侧弹性蛋白网络的情况下，以胶原为主的外膜能够维持主动脉的尺寸稳定性。因此，尽管导致弹性蛋白断裂和减弱的因素在AAA的病因中可能很重要，但调节胶原合成和降解平衡的因素可能决定AAA的进展速度。腹主动脉内滞留的炎性细胞无疑在主动脉扩张中起着重要的病理作用。因此，了解主动脉间充质细胞(平滑肌细胞和成纤维细胞)和炎性细胞(淋巴细胞和巨噬细胞)之间的相互作用应该有助于识别易患AAA的遗传因素。除了早期识别有AAA风险的患者外，对AAA发病机制的新见解可能允许开发抑制小AAA扩张的药理学策略。
We now know our past concepts of AAA pathogenesis to be oversimplified and inaccurate. In fact, the metabolic activity of the aneurysm wall is markedly increased in comparison with normal aorta. It has become clear that AAAs result not from passive dilatation, but from a complex remodeling process involving both the synthesis and degradation of matrix proteins. Our understanding of this process has been advanced by applying molecular biology techniques. Although elastin fragmentation and medial attenuation remain the most striking histological features of AAA tissue, experimental and clinical evidence suggests that the adventitia, which is predominantly collagen, is capable of maintaining the dimensional stability of the aorta in the absence of the medial elastin network. Thus, although factors that result in fragmentation and attenuation of elastin may be important in the etiology of AAA, factors regulating the balance of collagen synthesis and degradation likely determine the rate of AAA progression. The resident inflammatory cells in AAA undoubtedly play an important pathological role in aortic dilatation. Thus, understanding the interaction between aortic mesenchymal cells (smooth muscle cells and fibroblasts) and inflammatory cells (lymphocytes and macrophages) should allow for the identification of genetic factors that predispose to AAA. In addition to the possibility of early identification of patients at risk for AAA, new insights into AAA pathogenesis might allow for development of pharmacological strategies for inhibiting expansion of small AAA.