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19th World Congress on Heart Disease



Qiangrong Liang, M.D., Ph.D., New York Institute of Technology, Old Westbury, NY, USA


Most diabetic patients die from heart disease or stroke, highlighting the importance of understanding and treating cardiovascular complications of diabetes. A large body of evidence indicates that mitochondrial dysfunction and increased generation of reactive oxygen species (ROS) are critical to diabetic heart damage. However, several clinical trials have failed to confirm the ability of antioxidant therapies to reduce heart failure in diabetic patients. This may reflect the fact that antioxidants can only scavenge existing ROS, but cannot curb continuous ROS generation from injured mitochondria, which are a major source and a target of intracellular ROS in diabetes. A healthy mitochondrial network is maintained through a number of quality control mechanisms including mitochondrial autophagy, also known as mitophagy, which degrades dysfunctional mitochondria that are segregated from the network by mitochondrial fission. Using distinct fluorescent reporters, we found that the general autophagy is inhibited while the selective mitophagy is enhanced in cardiomyocytes treated with high glucose, an independent risk factor for heart failure in diabetic patients. This result is associated with increased mitochondrial fragmentation, suggesting that autophagy, mitophagy and mitochondrial fission are coordinately but differentially regulated by high glucose. Intriguingly, using genetic gain- and loss-of-function approaches, we showed that autophagy inhibition, mitophagy activation or mitochondrial fragmentation each is an adaptive response that limits high glucose cardiotoxicity as measured by the levels of oxidative injury, mitochondrial damage, ROS generation and cardiomyocyte death. Consistently, autophagy is inhibited in type 1 diabetic mouse heart, which protects against diabetic cardiac injury. Using a novel mitophagy reporter mouse, we are assessing mitophagy and mitochondrial fragmentation in the diabetic heart and determining the functional significance of these two events in the pathogenesis of diabetic cardiomyopathy. This study will provide a basis for designing drugs that may reduce diabetic cardiac injury by enhancing mitochondria quality control mechanisms.



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