Regulation of bile secretion by calcium signaling in health and disease

Biochim Biophys Acta Mol Cell Res. 2018 Nov;1865(11 Pt B):1761-1770. doi: 10.1016/j.bbamcr.2018.05.010. Epub 2018 May 19.

Abstract

Calcium (Ca2+) signaling controls secretion in many types of cells and tissues. In the liver, Ca2+ regulates secretion in both hepatocytes, which are responsible for primary formation of bile, and cholangiocytes, which line the biliary tree and further condition the bile before it is secreted. Cholestatic liver diseases, which are characterized by impaired bile secretion, may result from impaired Ca2+ signaling mechanisms in either hepatocytes or cholangiocytes. This review will discuss the Ca2+ signaling machinery and mechanisms responsible for regulation of secretion in both hepatocytes and cholangiocytes, and the pathophysiological changes in Ca2+ signaling that can occur in each of these cell types to result in cholestasis.

Keywords: Bile secretion; Calcium; Cholangiocyte; Cholestasis; Hepatocyte; Inositol 1,4,5-trisphosphate receptor.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Bile / metabolism*
  • Calcium / metabolism*
  • Calcium Signaling* / drug effects
  • Cholestasis / drug therapy
  • Cholestasis / etiology
  • Cholestasis / metabolism
  • Disease Susceptibility*
  • Gap Junctions / metabolism
  • Hepatocytes / metabolism
  • Homeostasis*
  • Humans
  • Inositol 1,4,5-Trisphosphate Receptors / genetics
  • Inositol 1,4,5-Trisphosphate Receptors / metabolism
  • Intracellular Space / metabolism
  • Liver / metabolism
  • Molecular Targeted Therapy

Substances

  • Inositol 1,4,5-Trisphosphate Receptors
  • Calcium