A Novel player in atherosclerotic diseases in renal patients: tumor necrosis factor-like weak ınducer of apoptosis (tweak)

Böbrek hastalarında ateroskleroz gelişiminde yeni bir oyuncu: tumor necrosis factor-like weak ınducer of apoptosis (tweak)

Özet

Kronik böbrek yetmezliği hastalarında kardiyovasküler olaylar sık görülür. Ateroskleroz, kardiyovasküler olayların patogenezinde önemli bir yere sahiptir. Tumor Necrosis factor- Like Weak Inducer of Apoptosis (TWEAK) TNF süper familyasına ait bir glikoproteindir. TWEAK organizmada hücresel büyüme, proliferasyon, migrasyon, osteoklastogenezis, anjiogenezis ve apoptoziste rol oynar. Son zamanlarda TWEAKin ateroskleroz gelişiminde de rol oynayabileceği ileri sürülmüştür. Böbrek yetmezliği durumlarında TWEAK düzeylerinin azaldığı bilinirken renal hasta popülasyonunda TWEAK-ateroskleroz ilişkisi netlik kazanmamıştır. Bu derlemede böbrek hastalarında TWEAK- ateroskleroz ilişkisi gözden geçirilmiştir.

Abstract

Cardiovascular disease is common in patients with chronic kidney disease. Atherosclerosis has a very mportant role in pathogenesis of cardiovascular diseases. Tumor Necrosis factor- Like Weak Inducer of Apoptosis (TWEAK) is a glycoprotein that belongs to the TNF superfamily. TWEAK plays important oles in cellular proliferation, growth, migration, osteoclastogenesis, angiogenesis and apoptosis. In he recent years, TWEAK has been suggested to have a role in atherosclerosis. While it is known that TWEAK levels are decreased in patient with renal failure, its association with atherosclerosis is not well-defined. This review focuses on the association of TWEAK with atherosclerosis in patients with enal patients.