Received 19 December 2013; Accepted 19 December 2013; Available online 9 January 2014 | Christiane Ott, Kathleen Jacobs, Elisa Haucke, Anne Navarrete Santos, Tilman Grune, Andreas Simm
This review article focuses on the role of advanced glycation end products (AGEs) in cellular signaling and their impact on various chronic diseases. The formation of AGEs, both endogenous and dietary, can lead to protein modifications and activation of inflammatory signaling pathways. The article discusses the most prominent AGE-mediated signaling cascades, including the involvement of receptors such as RAGE, AGE-R1/OST-48, AGE-R2/80K-H, and galectin-3. These receptors play crucial roles in the internalization and degradation of AGEs, as well as in the activation of signaling pathways that contribute to disease progression. The review also explores the cross-talk between AGEs and reactive oxygen and nitrogen species (ROS and RNS), which can lead to a vicious cycle of oxidative and nitrosative stress. Additionally, the article examines the impact of AGEs on vascular calcification, bone metabolism, and the regulation of transcription factors through the Jak/Stat pathway. The overall aim is to provide an overview of the complex mechanisms involving AGEs and their significance in age-associated diseases.This review article focuses on the role of advanced glycation end products (AGEs) in cellular signaling and their impact on various chronic diseases. The formation of AGEs, both endogenous and dietary, can lead to protein modifications and activation of inflammatory signaling pathways. The article discusses the most prominent AGE-mediated signaling cascades, including the involvement of receptors such as RAGE, AGE-R1/OST-48, AGE-R2/80K-H, and galectin-3. These receptors play crucial roles in the internalization and degradation of AGEs, as well as in the activation of signaling pathways that contribute to disease progression. The review also explores the cross-talk between AGEs and reactive oxygen and nitrogen species (ROS and RNS), which can lead to a vicious cycle of oxidative and nitrosative stress. Additionally, the article examines the impact of AGEs on vascular calcification, bone metabolism, and the regulation of transcription factors through the Jak/Stat pathway. The overall aim is to provide an overview of the complex mechanisms involving AGEs and their significance in age-associated diseases.