MITOCHONDRIAL FUNCTION AND INTESTINAL INFLAMMATION

Society: AGA

Reactive oxygen species (ROS) are by-products of normal cellular metabolism with low to moderate amounts being beneficial in several physiological processes in the intestine. Chemotherapy and radiotherapies are largely based upon ROS generation to destroy malignant cells by inducing apoptosis. Nonetheless, disproportionate generation of ROS causes oxidative tissue damage and development of a range of gut disorders including inflammatory bowel diseases. Considering the role of oxidative stress in IBD, implementation of antioxidant therapy such as 5-aminosalicylic acid has been commonly used in patients. However, given the challenges in antioxidant therapies in IBD including effectiveness and interference with normal redox signaling, there is a dire need to develop efficient and targeted therapies. Thus, there has been a growing interest in understanding the metabolic precursors of ROS, their effects on host intestinal epithelium as well as implications in diseases including intestinal inflammation. This basic and translational symposium aims to bring together various aspects of redox signaling ranging from role of ROS in modulating intestinal barrier function, role of mitochondria and ER in epithelial cell lineages and discussing the role of microbiota in intestinal oxidative stress. In addition, the experts in the field will be discussing the mechanisms pertinent to protect intestinal epithelium from oxidative insult and illuminate the current landscape and prospectives on redox targeted therapeutics for GI diseases.