424
Views
19
CrossRef citations to date
0
Altmetric
Review Article

Cell signaling and receptors in toxicity of advanced glycation end products (AGEs): α-dicarbonyls, radicals, oxidative stress and antioxidants

&
Pages 332-339 | Received 17 Jun 2011, Accepted 19 Jul 2011, Published online: 19 Sep 2011
 

Abstract

Considerable attention has been paid to the toxicity of advanced glycation end products (AGEs), including relation to various illnesses. AGEs, generated nonenzymatically from carbohydrates and proteins, comprises large numbers of simple and more complicated compounds. Many reports deal with a role for receptors (RAGE) and cell signaling, including illnesses and aging. Reactive oxygen species appear to participate in signaling. RAGE include angiotensin II type 1 receptors. Many signaling pathways are involved, such as kinases, p38, p21, TGF-β, NF-κβ, TNF-α, JNK and STAT. A recent review puts focus on α-dicarbonyl metabolites, formed by carbohydrate oxidation, and imine derivatives from protein condensation, as a source via electron transfer (ET) of ROS and oxidative stress (OS). The toxic species have been related to illnesses and aging. Antioxidants alleviate the adverse effects.

Acknowledgements

Editorial assistance by Thelma Chavez is acknowledged.

Declaration of interest

Authors declare no conflict of interest.

Log in via your institution

Log in to Taylor & Francis Online

PDF download + Online access

  • 48 hours access to article PDF & online version
  • Article PDF can be downloaded
  • Article PDF can be printed
USD 65.00 Add to cart

Issue Purchase

  • 30 days online access to complete issue
  • Article PDFs can be downloaded
  • Article PDFs can be printed
USD 1,339.00 Add to cart

* Local tax will be added as applicable

Related Research

People also read lists articles that other readers of this article have read.

Recommended articles lists articles that we recommend and is powered by our AI driven recommendation engine.

Cited by lists all citing articles based on Crossref citations.
Articles with the Crossref icon will open in a new tab.