The involvement of diabetes induced damage to mitochondrial DNA in diabetic complications: A novel hypothesis

Activity: Talk or presentationInvited talk


Diabetes results in increased risk of diabetic complications which affect major organs, including eyes (retinopathy), heart (diabetic cardiomyopathy), blood vessels (peripheral vascular disease) and brain (dementia). As diabetes reaches epidemic levels, the associated multi-morbidities have become a growing drain on the health system, predicted to cost >$2trillionpa by 2030 and are the leading cause of adult blindness, kidney disease, amputations and many other serious outcomes in the western world. Numerous complex and overlapping biochemical pathways, including oxidative stress and chronic inflammation, are implicated in diabetic complications, however strategies to target pathways, correct the redox balance and/or inflammation have been largely unsuccessful, suggesting there may be other factors contributing to progression. To date genetic studies have identified numerous loci with small and additive effects, but generally there has been little advancement in identifying genetic risk of diabetic complications. The multi-organ nature of diabetic complications resembles mitochondrial genetic disease. Mitochondria, cellular organelles in the cytosol of eukaryotic cells, harbour their own circular DNA genome (mtDNA). In patients with mitochondrial genetic disease, specific mtDNA mutations can lead to diabetes, as well as symptoms involving the kidney, heart, eyes, muscle, nerves and brain. These rare genetic mtDNA mutations that cause acute disease analogous to chronic diabetic complications could provide insight into the mechanisms of organ damage. This view is strengthened by our findings of mtDNA damage in experimental models and in patients. The body of evidence linking diabetes and mitochondrial dysfunction is growing, however the specific mechanisms of damage to mitochondria, and the implications of this for the risk of complications, have not been elucidated. In this talk I will review data from my own group and from others to examine the hypothesis that diabetes-induced damage to mtDNA contributes to diabetic complications.
Period23 May 2019
Event title Annual Scientific Meeting of the European Society for Clinical Invesitgation : 53rd ESCI 2019.
Event typeConference
LocationCoimbra , PortugalShow on map
Degree of RecognitionInternational


  • mitochondrial workshop. ESCI 53rd Meeting. Coimbra, Portugal