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<p>Chronic inflammation serves as a prevalent precursor for the onset of several non-communicable illnesses, namely atherosclerosis, stroke, and coronary artery disease among others. The clinical progression of numerous illnesses is impacted by the stimulation of the axis, which includes advanced glycation end products (AGEs) and its receptor RAGE. This is a major contributor to chronic inflammation. Increased oxidative stress and glycation reactions are the causes of the body’s accumulation of AGEs. By interacting with RAGE, AGEs initiate signaling pathways including NF-κB, which facilitates inflammatory mediator release, intensifying cellular damage and inflammation, hence accelerating atherosclerotic plaque formation and other diseases related to the vascular system. The molecular processes via which the AGE-RAGE pathway causes long-term inflammation in the disorders listed will be reviewed, as well as methods for blocking this axis to slow or stop the development of long-term inflammation and associated disorders. This includes developing RAGE antagonists and AGE inhibitors as well as tactics to alter signaling channels, both upstream and downstream. Furthermore, RAGE expression and AGE level early detection as biomarkers offer novel opportunities for the prevention and management of diabetes, atherosclerosis, stroke, and coronary artery disease among others.</p>

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Targeting the AGE-RAGE system as a therapeutic approach for endotheliopathy

  • 期刊论文

  • 发表日期：

    2026年4月2日

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  • C. F. Emereonye,
  • S. E. Areloegbe,
  • C. A. Oladele,
  • O. A. Akpor,
  • L. A. Olatunji,
  • O. O. Alese,
  • K. S. Olaniyi

摘要

Chronic inflammation serves as a prevalent precursor for the onset of several non-communicable illnesses, namely atherosclerosis, stroke, and coronary artery disease among others. The clinical progression of numerous illnesses is impacted by the stimulation of the axis, which includes advanced glycation end products (AGEs) and its receptor RAGE. This is a major contributor to chronic inflammation. Increased oxidative stress and glycation reactions are the causes of the body’s accumulation of AGEs. By interacting with RAGE, AGEs initiate signaling pathways including NF-κB, which facilitates inflammatory mediator release, intensifying cellular damage and inflammation, hence accelerating atherosclerotic plaque formation and other diseases related to the vascular system. The molecular processes via which the AGE-RAGE pathway causes long-term inflammation in the disorders listed will be reviewed, as well as methods for blocking this axis to slow or stop the development of long-term inflammation and associated disorders. This includes developing RAGE antagonists and AGE inhibitors as well as tactics to alter signaling channels, both upstream and downstream. Furthermore, RAGE expression and AGE level early detection as biomarkers offer novel opportunities for the prevention and management of diabetes, atherosclerosis, stroke, and coronary artery disease among others.