Cytokines, Atherogenesis, and Hypercatabolism in Chronic Kidney Disease: A Dreadful Triad

摘要: The term cytokine clusters denotes a copious family of molecules and correspondent receptors implicated in numerous processes mediating health disease. In the context chronic kidney disease (CKD), generation metabolism most these cytokines are disturbed. Available evidence suggests that imbalances contribute to progression common CKD complications, such as atherosclerosis, mineral-bone disease, protein-energy wasting via pleiotropic effects. belief research is solely represented by interleukins (IL) tumor-necrosis factors (TNF) (mainly IL-6 TNF-a) misconception among nephrologists. We here explore recent findings concerning pathophysiological role various uremic discuss how could be used novel potential therapeutic targets CKD. At same time, we provide brief overview current discoveries main transforming growth chemokines. Cytokines soluble messenger proteins produced whole range different cell types which exert their actions within local environment or systemic manner modify regulate immunological inflammatory reactions part response (1). mediate modulate responses, hematopoietic development, cell-to-cell communication participate well host responses infectious agents stimuli. interact with each other complex ways may additive, synergistic, antagonistic, involve induction subsequent cascades substances. For instance, whereas proinflammatory promote inflammation, anti-inflammatory suppress activity reduce inflammation; therefore, balance between opposing more important than absolute amounts single cytokine. binding specific cellsurface at membrane initiates cascade immune-related events leads induction, enhancement inhibition cytokine-regulated gene transcription, ultimately, altered behavior.