抄録
Cerebral aneurysm (CA) is a main cause of a lethal subarachnoid hemorrhage. Given the high incidence of CA in general population, the mechanisms of CA formation should be unlabelled and novel medical therapy for CA before rupture should be developed. The typical pathological feature of CA walls is the decrease of extracellular matrix (ECM). Decreased ECM results in the weakness of CA walls leading the enlargement and rupture of CA. In this article, we have reviewed the recent findings about the mechanisms of decreased ECM in CA walls mainly revealed by experiments using rodent CA models. ECM is the dynamic structure with the continuous synthesis and degeneration of matrix protein. In CA walls, the induced expressions of proteinases by chronic inflammation in arterial bifurcation are present and actively participated in the pathogenesis of CA. Further the synthesis of collagen is suppressed in CA wall through inflammatory stimulus in arterial walls. These results combined together indicate that both decreased synthesis and increased degeneration of ECM by chronic inflammation in CA walls contributes to CA formation. Further these results demonstrate the therapeutic potential of anti-inflammatory drugs for CA.
