Mitochondria are highly dynamic and communicative organelles that regulate a variety of cellular processes including energy homeostasis, redox status, thermogenesis and cell death via apoptosis. Mitochondria collaborate with a host of intracellular organelles including endoplasmic reticulum, peroxisomes, lysosomes and nuclei to maintain metabolic homeostasis. Mitochondrial dysfunction disrupts metabolism and is thought to underlie cellular aging as well as the development of chronic diseases such as type 2 diabetes, cardiovascular disease, heart failure and aging-associated sarcopenia. Since mitochondria are enriched in cardiac and striated skeletal muscle, and since these tissues are critical in regulating whole body metabolism, insulin action and locomotion, the objective of this conference is to identify novel mechanisms controlling mitochondrial function and connect mitochondrial phenotypes with improved health and disease pathobiology. New insight into the biology and pathobiology of mitochondria will allow for the advance of therapeutic approaches that can be utilized to combat metabolic-related diseases associated with mitochondrial dysfunction. Our understanding of the precise molecular signaling that links mitochondrial function (biogenesis, fission-fusion-mitophagy dynamics, and mitochondrial genome integrity) with integrative metabolism and muscle action remains inadequate. This deficiency in our fundamental knowledge of mitochondrial biology and the implications of this knowledge gap for the treatment and clinical care of common and rare mitochondrial diseases underpin the importance of this Keystone Symposia conference. 

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