Cytokines, atherogenesis, and hypercatabolism in chronic kidney disease: a dreadful triad.
The term cytokine clusters denotes a copious family of molecules and correspondent receptors implicated in numerous processes mediating health and disease. In the context of chronic kidney disease (CKD), generation and metabolism of most of these cytokines are disturbed. Available evidence suggests that cytokine imbalances contribute to the progression of common CKD complications, such as atherosclerosis, mineral-bone disease, and protein-energy wasting via pleiotropic effects. The belief that cytokine CKD research is solely represented by interleukins (IL) and tumor-necrosis factors (TNF) (mainly IL-6 and TNF-alpha) is a common misconception among nephrologists. We here explore recent findings concerning the pathophysiological role of various cytokines in uremic complications, and discuss how cytokines could be used as novel potential therapeutic targets in CKD. At the same time, we provide a brief overview of current discoveries in the main transforming growth factors and chemokines.
Carrero
Juan Jesus
JJ
Division of Renal Medicine and Baxter Novum, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.
Park
Sun-Hee
SH
Axelsson
Jonas
J
Lindholm
Bengt
B
Stenvinkel
Peter
P
D050197:Atherosclerosis / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D016207:Cytokines / Q000502:physiology*; D006801:Humans; D007674:Kidney Diseases / Q000209:etiology* / Q000378:metabolism* / Q000628:therapy
D016207:Cytokines