Saha Cardiovascular Research Center, University of Kentucky.
Department of Physiology, University of Kentucky.
Circ J. 2020 Apr 24;84(5):825-829. doi: 10.1253/circj.CJ-19-0955. Epub 2020 Mar 31.
Angiotensin (Ang)I is cleaved by angiotensin-converting enzyme (ACE) to generate AngII. The purpose of this study was to determine the roles of ACE in endothelial and smooth muscle cells in aortic aneurysms.
AngI infusion led to thoracic and abdominal aortic aneurysms in low-density lipoprotein receptor-deficient mice, which were ablated by ACE inhibition. Endothelial or smooth muscle cell-specific ACE deletion resulted in reduction of AngI-induced thoracic, but not abdominal, aortic dilatation.
AngI infusion causes thoracic and abdominal aortic aneurysms in mice. ACE in aortic resident cells has differential effects on AngI-induced thoracic and abdominal aortic aneurysms.
血管紧张素(Ang)I 可被血管紧张素转换酶(ACE)切割生成血管紧张素 II。本研究旨在确定 ACE 在胸主动脉和腹主动脉瘤中的内皮细胞和平滑肌细胞中的作用。
AngI 输注可导致载脂蛋白 E 基因敲除小鼠的胸主动脉和腹主动脉瘤,而 ACE 抑制可使其消融。内皮细胞或平滑肌细胞特异性 ACE 缺失可减少 AngI 诱导的胸主动脉扩张,但不减少腹主动脉扩张。
AngI 输注可导致小鼠胸主动脉和腹主动脉瘤。主动脉固有细胞中的 ACE 对 AngI 诱导的胸主动脉和腹主动脉瘤有不同的作用。