Targeting advanced glycation endproducts and mitochondrial dysfunction in cardiovascular disease

Micheal S Ward, Amelia K Fotheringham, Mark E. Cooper, Josephine M. Forbes

Research output: Contribution to journalArticleOtherpeer-review

41 Citations (Scopus)

Abstract

Cardiovascular disease (CVD) is a leading cause of mortality in the Western World. The development and onset of disease can be attributed to many risk factors including genetic susceptibility, diabetes, obesity and atherosclerosis. Numerous studies highlight the production of advanced glycation endproducts (AGEs) and interaction with their receptor (RAGE) as playing a key pathogenic role. The AGEs- RAGE axis is thought to contribute to a proinflammatory environment inducing cellular dysfunction which cascades towards pathology. Mitochondrial dysfunction concurrently plays a role in these proinflammatory responses presenting excess reactive oxygen species (ROS) production under pathological conditions. This ROS release can exacerbate the production of AGEs fuelling the fire somewhat. However, the AGEs-RAGE axis may influence mitochondrial function independently of inflammation. Therefore instigation of the AGEs-RAGE axis may facilitate spiralling towards pathology on many fronts including CVD development. 

Original languageEnglish
Pages (from-to)654-661
Number of pages8
JournalCurrent Opinion in Pharmacology
Volume13
Issue number4
DOIs
Publication statusPublished - 2013
Externally publishedYes

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