Title:Tapping into Mitochondria to Find Novel Targets for Diabetes Complications
Volume: 17
Issue: 12
Author(s): Nicole B. Flemming, Linda A. Gallo, Micheal S. Ward and Josephine M. Forbes
Affiliation:
Keywords:
Diabetic complications, mitochondria, nephropathy, networking, oxidative phosphorylation, retinopathy, ROS,
superoxide.
Abstract: Mitochondria produce the majority of cellular energy via the “slow burn”
of substrates such as glucose, free fatty acids and ketones. In diabetes, altered mitochondrial
energetics and substrate utilisation may explain, in part, an organ’s susceptibility
to complications. This is particularly evident at sites such as the kidney, heart,
neurons and retina, which have high energy demands and oxygen consumption rates
to meet functional requirements. Within this review we highlight the recent research
implicating mitochondrial dysfunction, with particular focus on the contribution of
mitochondrial reactive oxygen species, on the development and progression of diabetes
complications. Finally, we discuss the current strategies which are being assessed
to combat mitochondrial dysfunction in diabetes complications.