NIH Undiagnosed Diseases Program, Office of Rare Disease Research and National Human Genome Research Institute and NIH Clinical Center, National Institutes of Health, Bethesda, MD 20892, USA.
Mol Genet Metab. 2011 May;103(1):44-50. doi: 10.1016/j.ymgme.2011.01.018. Epub 2011 Feb 3.
Arterial Calcification due to Deficiency of CD73 (ACDC) results from mutations in the NT5E gene encoding the 5' exonucleotidase, CD73. We now describe the third familial case of ACDC, including radiological and histopathological details of the arterial calcifications. The medial lesions involve the entire circumference of the elastic lamina, in contrast to the intimal plaque-like disease of atherosclerosis. The demonstration of broken and fragmented elastic fibers leading to generalized vascular calcification suggests an analogy to pseudoxanthoma elasticum (PXE), which exhibits similar histopathology. Classical PXE is caused by deficiency of ABCC6, a C type ABC transporter whose ligand is unknown. Other C type ABC proteins transport nucleotides, so the newly described role of adenosine in inhibiting vascular calcification, along with the similarity of ACDC and PXE with respect to vascular pathology, suggests that adenosine may be the ligand for ABCC6.
由于 CD73(ACDC)缺乏引起的动脉钙化是由于编码 5'核苷酸外切酶 CD73 的 NT5E 基因突变所致。我们现在描述了 ACDC 的第三个家族病例,包括动脉钙化的放射学和组织病理学细节。中膜病变累及弹性膜的整个圆周,与动脉粥样硬化的内膜斑块样疾病相反。断裂和碎片化的弹性纤维导致广泛的血管钙化的证明表明与假性黄色瘤弹性组织营养不良(PXE)具有类似性,其表现出相似的组织病理学。经典的 PXE 是由 ABCC6 缺乏引起的,ABCC6 是一种 C 型 ABC 转运蛋白,其配体尚不清楚。其他 C 型 ABC 蛋白转运核苷酸,因此,新描述的腺苷在抑制血管钙化中的作用,以及 ACDC 和 PXE 在血管病理学方面的相似性,表明腺苷可能是 ABCC6 的配体。