Abstract
Hypoxia has been associated with multiple sclerosis (MS) and is an important area of research. Hypoxia can exacerbate inflammation via the prolylhydroxylase pathway. Inflammation can also trigger hypoxia by damaging mitochondria and endothelial cells to impair blood flow regulation. We hypothesize that there is a "hypoxia-inflammation cycle" in MS which plays an important role in MS disease progression. Therapies that break this cycle may be an interesting area of exploration for treatment of MS.