Mechanisms of Disease: advanced glycation end-products and their receptor in inflammation and diabetes complications
Shi Fang Yan, Ravichandran Ramasamy and Ann Marie Schmidt*
Correspondence *Division of Surgical Science, Department of Surgery, Columbia University Medical Center, 630 West 168th Street, P&S 17-401, New York, NY 10032, USA
Email ams11@columbia.edu
Injury to the vasculature is an important adverse outcome in diabetes. In this Review, Yan et al. explore how advanced glycation end-products and their main receptor, RAGE, might have roles in the development of diabetes and some of its complications–nephropathy, atherosclerosis and inflammatory response–through activation of inflammatory signaling cascades.
Full text of this article is available with one of the following:
- Personal subscription Purchase your own personal subscription to this journal. Already a subscriber? Please log in for immediate access.
- 7 day single article pass for US$32 In order to purchase this article you must be a registered user. Please register or log in.
- Site licence Learn more about institutional site licences
Current Subscribers
Please log in to access the full text article using the login box at the top of the page.
MORE ARTICLES LIKE THIS
These links to content published by NPG are automatically generated.
NEWS AND VIEWS
The dark side of glucoseNature Medicine News and Views (01 Oct 1995)
Amyloids: Tombstones or triggers?Nature Medicine News and Views (01 Jun 2000)
RESEARCH
Suppression of accelerated diabetic atherosclerosis by the soluble receptor for advanced glycation endproductsNature Medicine Article (01 Sep 1998)
Advanced glycation endproducts induce podocyte apoptosis by activation of the FOXO4 transcription factorKidney International Original Article
See all 16 matches for Research