Researchers investigated the mechanism by which intestinal epithelial cell death induced arthritis. Effects of hypoxia-inducible factor 1α (HIF1α) stabilization by inhibition of prolyl hydroxylase domain-containing enzymes and treatment with the inhibitor of receptor-interacting protein kinase-3 (RIPK3) were tested in intestinal organoids and in collagen-induced arthritis.
[Annals Of The Rheumatic Diseases]