Role of advanced glycation end products in cellular signaling.

Ott C, Jacobs K, Haucke E, Navarrete Santos A, Grune T, Simm A

Redox biology 2014

Improvements in health care and lifestyle have led to an elevated lifespan and increased focus on age-associated diseases, such as neurodegeneration, cardiovascular disease, frailty and arteriosclerosis. In all these chronic diseases protein, lipid or nucleic acid modifications are involved, including cross-linked and non-degradable aggregates, such as advanced glycation end products (AGEs). Formation of endogenous or uptake of dietary AGEs can lead to further protein modifications and activation of several inflammatory signaling pathways. This review will give an overview of the most prominent AGE-mediated signaling cascades, AGE receptor interactions, prevention of AGE formation and the impact of AGEs during pathophysiological processes.

6 Figures Extracted

Fig. 1 PMC

Formation of advanced glycation end products in vivo. Endogenous formation of advanced glycation end products has been described by three different ...

Fig. 2 PMC

Formation of AGEs via Wolff'-, Namiki- and Hodge-pathway. Autoxidation of monosaccharides or carbonyl compounds (Wolff' pathway), aldimins...

Fig. 3 PMC

Structure of AGE receptors. Scavenger receptor family and AGE receptors. The scavenger receptor family is divided into class A, class B, class C and o...

Fig. 4 PMC

AGE-mediated signaling and detoxification of AGEs via lysosomal system. AGE–RAGE interaction stimulates a various number of signaling cascades, incl...

Fig. 5 PMC

Physiological role of RAGE. AGE–RAGE mediated changes in physiology of lung homeostasis, bone metabolism, immune system and neuronal system.

Fig. 6 PMC

Expression of RAGE in the early rabbit embryo. Transcripts of RAGE were detected in day 3, 4, and 6 p.c. embryos and blastocysts in gastrulation stage...