Published online May 26, 2021. doi: 10.12998/wjcc.v9.i15.3498
Peer-review started: October 16, 2020
First decision: December 28, 2020
Revised: January 8, 2021
Accepted: March 17, 2021
Article in press: March 17, 2021
Published online: May 26, 2021
Processing time: 207 Days and 7.5 Hours
Cholesterol gallstone (CG) is a common, frequent biliary system disease in China, with a complex and multifactorial etiology. Declined gallbladder motility reportedly contributes to CG pathogenesis. Furthermore, interstitial Cajal-like cells (ICLCs) are reportedly present in human and guinea pig gallbladder tissue. ICLCs potentially contribute to the regulation of gallbladder motility, and aberrant conditions involving the loss of ICLCs and/or a reduction in its pacing potential and reactivity to cholecystokinin may promote CG pathogenesis. This review discusses the association between ICLCs and CG pathogenesis and provides a basis for further studies on the functions of ICLCs and the etiologies of CG.
Core Tip: Interstitial Cajal-like cells (ICLCs) in the gallbladder have been reported to play an important role in the regulation of gallbladder motility. Loss and/or dysfunction of ICLCs may contribute to motion abnormality of the gallbladder and promote cholesterol gallstone (CG) formation. However, the underlying mechanism is still unclear. This mini-review highlights recent findings on the association between gallbladder ICLCs and CG formation.
