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The Regulation of Intestinal Smooth Muscle Cell Proliferation in Crohn’s Disease – Is NR4A1 a Novel Target to Treat Fibrostenosis?

Intestinal fibrosis and stricture formation are common complications of Crohn’s disease (CD). Recently, the stricturing phenotype has been recognized to be primarily attributable to hypertrophy/hyperplasia of smooth muscle, rather than an increase in fibrosis alone. Despite advances in treatment of CD, current therapies do little to prevent or reverse strictures. NR4A1 is an orphan nuclear receptor that has been reported as anti‐fibrotic in non‐intestinal systems and exhibits anti‐proliferative effects in smooth muscle cells (SMCs). NR4A1 gene variants have been associated with increased risk of inflammatory bowel disease, however, the mechanisms regulating NR4A1 expression and its role in intestinal SMC function have not been investigated.