Targeting advanced glycation endproducts and mitochondrial dysfunction in cardiovascular disease

Ward, Micheal S., Fortheringham, Amelia K., Cooper, Mark E . and Forbes, Josephine M. (2013) Targeting advanced glycation endproducts and mitochondrial dysfunction in cardiovascular disease. Current Opinion in Pharmacology, 13 4: 654-661. doi:10.1016/j.coph.2013.06.009

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Author Ward, Micheal S.
Fortheringham, Amelia K.
Cooper, Mark E .
Forbes, Josephine M.
Title Targeting advanced glycation endproducts and mitochondrial dysfunction in cardiovascular disease
Journal name Current Opinion in Pharmacology   Check publisher's open access policy
ISSN 1471-4892
Publication date 2013-01-01
Year available 2013
Sub-type Article (original research)
DOI 10.1016/j.coph.2013.06.009
Open Access Status Not yet assessed
Volume 13
Issue 4
Start page 654
End page 661
Total pages 8
Place of publication Kidlington, Oxford, United Kingdom
Publisher Elsevier
Language eng
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.
Keyword Pharmacology & Pharmacy
Pharmacology & Pharmacy
Q-Index Code C1
Q-Index Status Confirmed Code
Grant ID 3-2013-217
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Mater Research Institute-UQ (MRI-UQ)
Official 2014 Collection
School of Medicine Publications
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Citation counts: TR Web of Science Citation Count  Cited 21 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 27 times in Scopus Article | Citations
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Created: Mon, 28 Apr 2014, 23:26:01 EST by Dominique Rossouw on behalf of Mater Research Institute-UQ