CNRS EAC 7054, Centre de Recherches Chirurgicales Dominique Chopin, University Paris, 12 Val de Marne, 8 Rue du Général Sarrail, 94010 Créteil Cedex, France.
Eur J Vasc Endovasc Surg. 2010 Oct;40(4):468-74. doi: 10.1016/j.ejvs.2010.05.001. Epub 2010 Jun 15.
Determinants of extracellular matrix (ECM) destruction/reconstruction balance influencing abdominal aortic aneurysm (AAA) diameter may impact length.
Document aortic lengthening, its correlation to diameter, and determine how treatments that impact diameter also affect length.
Three hundred and fifty-five diameter and length measurements were performed in 308 rats during AAA formation, expansion and stabilisation in guinea pig aortas xenografted in rats. Impact of modulation of ECM destructive/reconstructive balance by endovascular Vascular Smooth Muscle Cell (VSMCs) seeding, TIMP-1, PAI-1 and TGF-beta1 overexpression on length has been assessed.
Length increased in correlation with diameter during formation (correlation coefficient (cc): 0.584, P<0.0001) and expansion (cc: 0.352, P=0.0055) of AAAs. Overexpression of TIMP-1 and PAI-1 decreased lengthening (P=0.02 and 0.014, respectively) demonstrating that elongation is driven by matrix metalloproteinases and their activation by the plasmin pathway. Overexpression of TGF-beta1 controlled length in formed AAAs (17.3 ± 9.6 vs. 5.9 ± 7.4mm, P=0.022), but not VSMC seeding, although both therapies efficiently prevented further diameter increase. Length and diameter correlation was lost after biotherapies.
Length increases in correlation with diameter during AAA formation and expansion, as a consequence of ECM injury driven by MMPs activated by the plasmin pathway. Correlation between length and diameter increases is not universally preserved.
影响腹主动脉瘤（AAA）直径的细胞外基质（ECM）破坏/重建平衡的决定因素可能会影响长度。
记录主动脉的伸长及其与直径的相关性，并确定影响直径的治疗方法如何也影响长度。
在豚鼠胸主动脉异种移植于大鼠的模型中，对 308 只大鼠的 355 个直径和长度测量值进行了分析，以研究 ECM 破坏/重建平衡的调节对 AAA 形成、扩张和稳定过程中的直径和长度的影响。
在 AAA 的形成（相关系数（cc）：0.584，P<0.0001）和扩张（cc：0.352，P=0.0055）过程中，长度与直径呈正相关。TIMP-1 和 PAI-1 的过表达减少了伸长（P=0.02 和 0.014），表明伸长是由基质金属蛋白酶及其通过纤溶途径的激活所驱动。TGF-β1 的过表达控制了形成的 AAA 中的长度（17.3±9.6 与 5.9±7.4mm，P=0.022），但不影响血管平滑肌细胞的种植，尽管这两种治疗方法都能有效地防止直径进一步增加。生物治疗后，长度和直径之间的相关性丢失。
在 AAA 的形成和扩张过程中，长度与直径呈正相关，这是由于 MMPs 激活所导致的 ECM 损伤所致，而 MMPs 的激活是由纤溶途径驱动的。长度和直径之间的相关性并非普遍存在。
