https://doi.org/10.4081/jbr.2011.4498

The human kidney as a regulator of body cytokine homeostasis

Vol. 84 No. 1 (2011)
Submitted: July 4, 2014
Accepted: July 4, 2014
Published: January 30, 2011
inflammation, adipokines, Leptin, IL-6, chronic kidney disease
Abstract Views: 755
PDF: 495
Publisher's note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

Authors

A. Bonanni
A. Sofia
S. Saffioti
I. Mannucci
D. Verzola
P. Gramegna
L. Cappuccino
G. Garibotto
gari@unige.it
Evidence is accumulating that the human kidney is a major site for the removal of several cytokines and growth factors, which can accumulate in body pools in patients with acute and chronic kidney disease (CKD). In addition, progressive renal failure and the increase in circulating proinflammatory cytokines are associated with mortality, suggesting that altered cytokines handling by the kidney is associated with worse outcome. Also, the kidney itself may be damaged by signals arising by endothelia and peripheral tissues during the course of the metabolic syndrome, type 2 diabetes and obesity. In this paper we provide a review of kidney handling of several adipokines and myokines, with special emphasis to interleukin-6 (IL-6), leptin, resistin and transforming growth factor-beta (TGF-beta).

Dimensions

Altmetric

PlumX Metrics

Downloads

Download data is not yet available.

Citations

Crossref
Scopus
Google Scholar
Europe PMC

How to Cite

Bonanni, A., Sofia, A., Saffioti, S., Mannucci, I., Verzola, D., Gramegna, P., Cappuccino, L., & Garibotto, G. (2011). The human kidney as a regulator of body cytokine homeostasis. Journal of Biological Research - Bollettino Della Società Italiana Di Biologia Sperimentale, 84(1). https://doi.org/10.4081/jbr.2011.4498

PAGEPress has chosen to apply the Creative Commons Attribution NonCommercial 4.0 International License (CC BY-NC 4.0) to all manuscripts to be published.