Helmke A, von Vietinghoff S. Extracellular vesicles as mediators of vascular inflammation in kidney disease. World J Nephrol 2016; 5(2): 125-138 [PMID: 26981436 DOI: 10.5527/wjn.v5.i2.125]
Corresponding Author of This Article
Dr. med. Sibylle von Vietinghoff, Division of Nephrology and Hypertension, Hannover Medical School, Carl-Neuberg-Strasse 1, D-30625 Hannover, Germany. vonvietinghoff.sibylle@mh-hannover.de
Research Domain of This Article
Immunology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Nephrol. Mar 6, 2016; 5(2): 125-138 Published online Mar 6, 2016. doi: 10.5527/wjn.v5.i2.125
Extracellular vesicles as mediators of vascular inflammation in kidney disease
Alexandra Helmke, Sibylle von Vietinghoff
Alexandra Helmke, Sibylle von Vietinghoff, Division of Nephrology and Hypertension, Hannover Medical School, D-30625 Hannover, Germany
Author contributions: Both authors contributed to all aspects of manuscript preparation.
Conflict-of-interest statement: We have no conflicts of interest regarding this work.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. med. Sibylle von Vietinghoff, Division of Nephrology and Hypertension, Hannover Medical School, Carl-Neuberg-Strasse 1, D-30625 Hannover, Germany. vonvietinghoff.sibylle@mh-hannover.de
Received: August 28, 2015 Peer-review started: September 2, 2015 First decision: November 27, 2015 Revised: December 18, 2015 Accepted: January 8, 2016 Article in press: January 11, 2016 Published online: March 6, 2016
Core Tip
Core tip: This review addresses the role of extracellular vesicles (EVs) in vascular inflammation that can cause renal damage and is also shaped by uremic mediators. Vasculitides are common causes of renal damage. Functionally, neutrophil EVs induced by anti-neutrophil cytoplasmic antibody contribute to endothelial damage. EVs are main distributors of shiga toxin in the circulation and into tissues in typical hemolytic uremic syndrome. In atherosclerosis in patients with and without kidney disease, endothelial EVs are elevated. Uremic EVs are deficient in mediating vascular relaxation. EVs modulate mononuclear phagocyte differentiation, cytokine production, lipid phagocytosis and antigen presentation, atherosclerotic inflammatory processes significantly altered in uremia.
