Inositol 1,4,5-trisphosphate receptor in the liver: Expression and function.
Fernanda de Oliveira Lemos1, Rodrigo M Florentino1, Antônio Carlos Melo Lima Filho1
1Department of Physiology and Biophysics, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais 31270-901, Brazil.
World Journal of Gastroenterology
|December 6, 2019
Summary
Inositol 1,4,5-trisphosphate (InsP3) receptors in liver cells are crucial for calcium signaling and maintaining homeostasis. Their altered expression links to liver diseases, highlighting their pathological significance.
Area of Science:
- Hepatology
- Cellular Biology
- Molecular Physiology
Background:
- The liver maintains homeostasis through complex functions modulated by calcium signaling.
- Inositol 1,4,5-trisphosphate (InsP3) receptors (ITPR) are the sole intracellular calcium release channels in liver epithelial cells (hepatocytes and cholangiocytes).
- Three ITPR isoforms (types 1, 2, and 3) exist and are differentially expressed in liver cells.
Purpose of the Study:
- To review the role of ITPR isoforms in hepatic homeostasis.
- To highlight the involvement of ITPR expression, modulation, and localization in liver pathology.
- To connect ITPR function to liver diseases and hepatic dysfunctions.
Main Methods:
- Literature review of studies on ITPR in liver cells.
- Analysis of ITPR isoform expression patterns in hepatocytes and cholangiocytes.
- Examination of the link between ITPR alterations and liver disease states.
Main Results:
- ITPR isoforms are differentially expressed in liver cells, regulating distinct physiological functions.
- Altered expression levels of ITPR isoforms correlate with various liver diseases.
- The localization and modulation of ITPR isoforms are critical for liver cell function.
Conclusions:
- ITPRs play a vital role in maintaining hepatic homeostasis through calcium signaling.
- Dysregulation of ITPR isoforms contributes to the pathogenesis of liver diseases.
- Targeting ITPR function may offer therapeutic strategies for liver conditions.
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