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1 Cardiovascular risk factors were related to arterial calcification.
2 eritable risk for CAD/MI is mediated through arterial calcification.
3 tients present a more severe, often prenatal arterial calcification.
4 stal deposition underlies the development of arterial calcification.
5 t an additional protective mechanism against arterial calcification.
6 f the osteoclastic V-H+-ATPase, will inhibit arterial calcification.
7 e decoy receptor also crucial for preventing arterial calcification.
8 that estrogen may play a regulatory role in arterial calcification.
9 potential role of osteoregulatory factors in arterial calcification.
10 c studies in three families with symptomatic arterial calcifications.
13 Lower fetuin-A levels are associated with arterial calcification and death in end-stage renal dise
14 mutation as causing SMS and leading to early arterial calcification and dental inflammation and resor
15 is review we address potential mechanisms of arterial calcification and, in particular, ways in which
17 rotegerin (OPG) is a marker and regulator of arterial calcification, and it is related to cardiovascu
19 icient in both MGP and OPN had twice as much arterial calcification as MGP(-/-) OPN(+/+) at 2 wk, and
21 In a murine model, Sort1-deficiency reduced arterial calcification but did not affect bone mineraliz
23 a marker of atherosclerotic inflammation, to arterial calcification detected by contemporaneous CT.
30 tery stiffness, which is caused, in part, by arterial calcification in patients with chronic kidney d
31 ) that share the ability to potently inhibit arterial calcification in the rat, the V-H+-ATPase inhib
32 play a prominent role in the pathogenesis of arterial calcification, including duration of dialysis a
33 fferences of two distinct pathomechanisms of arterial calcifications: intimal associated with atheros
37 e process, there is increasing evidence that arterial calcification is actually an active, regulated
39 ried out to further test the hypothesis that arterial calcification is linked to bone resorption by d
42 gility after estrogen loss (osteocalcin) and arterial calcification linked to cardiovascular disease
44 ropathy (CN); however, the links with medial arterial calcification (MAC) seen in people with CN are
46 development in individuals with generalized arterial calcification of infancy (GACI) due to loss-of-
48 m lethal orphan diseases such as generalized arterial calcification of infancy (GACI), to common dise
50 rs, with phenotypic overlap with generalized arterial calcification of infancy and arterial calcifica
51 apping clinical features include generalized arterial calcification of infancy and arterial calcifica
52 decreased bone mineralization in generalized arterial calcification of infancy caused by ENPP1 mutati
54 nosis, pseudoxanthoma elasticum, generalized arterial calcification of infancy, and arterial calcific
55 (asj) mutant mouse as a model of generalized arterial calcification of infancy, and we have now explo
59 , recent developments in the pathogenesis of arterial calcification provide valuable information pert
60 ude hemostasis, apoptosis, bone development, arterial calcification, signal transduction, and growth
61 alvulopathies, calciphylaxis, and idiopathic arterial calcification, vascular calcification is now re
64 erm but die within two months as a result of arterial calcification which leads to blood-vessel ruptu
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