The gastrointestinal (GI) tract is a vital organ that digests food, absorbs nutrients,
and excretes waste. Normal GI motility is the basis for these functions. The interstitial
cells of Cajal (ICC) in the GI muscularis layer promote GI motility together with the
enteric nervous system and smooth muscle cells. Since GI motility results from complex
coordination of these heterogeneous cells, failure of any one of them can lead to GI
dysmotility. Knowledge about ICC in physiological conditions has accumulated in recent
decades, while the pathophysiology of ICC in GI inflammatory diseases, such as
inflammatory bowel disease, is not well understood. In this review, we summarize the
previous studies about the pathophysiological changes of ICC in inflammatory diseases and
discuss the inflammatory mediators that induce ICC dysfunction.