Wang Susanna S, Martin Lisa J, Schadt Eric E, Meng Haijin, Wang Xuping, Zhao Wei, Ingram-Drake Leslie, Nebohacova Martina, Mehrabian Margarete, Drake Thomas A, Lusis Aldons J
Department of Human Genetics, UCLA David Geffen School of Medicine, Los Angeles, CA, USA.
Circ Cardiovasc Genet. 2009 Dec;2(6):573-82. doi: 10.1161/CIRCGENETICS.109.860270. Epub 2009 Oct 19.
Disruption of the elastic lamina, as an early indicator of aneurysm formation, and vascular calcification frequently occur together in atherosclerotic lesions of humans.
We now report evidence of shared genetic basis for disruption of the elastic lamina (medial disruption) and medial calcification in an F(2) mouse intercross between C57BL/6J and C3H/HeJ on a hyperlipidemic apolipoprotein E (ApoE(-/-)) null
gene, known to mediate myocardial calcification. Using transgenic complementation, we show that Abcc6 also contributes to aortic medial calcification.
Our data indicate that calcification, though possibly contributory, does not always lead to medial disruption and that in addition to aneurysm formation, medial disruption may be the precursor to calcification.
弹性层破裂作为动脉瘤形成的早期指标,与血管钙化在人类动脉粥样硬化病变中经常同时出现。
我们现在报告在高脂血症载脂蛋白E(ApoE(-/-))基因敲除的C57BL/6J和C3H/HeJ的F(2)小鼠杂交中,弹性层破裂(中膜破裂)和中膜钙化存在共同遗传基础的证据,已知该基因介导心肌钙化。通过转基因互补,我们表明Abcc6也促成主动脉中膜钙化。
我们的数据表明,钙化虽然可能有促成作用,但并不总是导致中膜破裂,并且除了动脉瘤形成外,中膜破裂可能是钙化的先兆。