MITOCHONDRIAL TURNOVER IS ELEVATED IN RESPONSE TO INTESTINAL INFLAMMATION AND IS AMENABLE TO THERAPUTIC TARGETING VIA UROLITHIN A

Inflammatory bowel disease (IBD) is a complex, multifactorial set of diseases defined by chronic and relapsing inflammation of the gut. Changes in oxidative stress, inflammation, and metabolism are central to the disease process, linking mitochondrial health to IBD pathogenesis. Mitophagy is a quality-control mechanism that selectively removes dysfunctional mitochondria. Multiple mitophagy pathways co-exist in the intestine, including the canonical PINK1/PARKIN pathway and NIX. We have previously shown that NIX is increased in IBD, removing damaged mitochondria in the epithelium.