Novel mechanisms in accelerated atherosclerosis in kidney disease
Küçük Resim Yok
Tarih
2008
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
W B Saunders Co-Elsevier Inc
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
Objective: Urea undergoes a spontaneous, nonenzymatic transformation to cyanate, the active part of which is isocyanic acid, which can cause modifications of a variety of proteins in a process called carbamylation. We postulated that, in patients with renal disease, the carbamylation of low-density lipoprotein (LDL) is a nontraditional risk factor for cardiovascular disease, and that elevated urea leads to carbamylated LDL (cLDL), which causes vascular injury and leads to atherosclerosis. Results: We showed that carbamylated LDL manifests all of the biological effects relevant to atherosclerosis, including endothelial-cell injury, the expression of adhesion molecules, and vascular smooth muscle cell proliferation. We also developed an enzyme-linked immunosorbent assay to measure carbamylated LDL in patients, and showed that cLDL is markedly elevated in dialysis patients. Conclusions: Our data indicate that cLDL may be an important nontraditional risk factor for atherosclerosis in patients with kidney disease. (c) 2008 by the National Kidney Foundation, Inc.
Açıklama
Anahtar Kelimeler
Kaynak
Journal of Renal Nutrition
WoS Q Değeri
Q3
Scopus Q Değeri
N/A
Cilt
18
Sayı
1
