Hepatoprotective impact of the bile acid receptor TGR5

Farnesoid X receptor Primary Biliary Cirrhosis
DOI: 10.1111/liv.14427 Publication Date: 2020-03-08T00:54:37Z
ABSTRACT
Abstract During liver repair after injury, bile secretion has to be tightly modulated in order preserve parenchyma from acid (BA)‐induced injury. The mechanisms allowing the maintain biliary homeostasis during injury are not completely understood. Besides their historical role lipid digestion, acids (BA) and receptors constitute a signalling network with multiple impacts on repair, both stimulating regeneration protecting BA overload. signal through nuclear (mainly Farnesoid X Receptor, FXR) membrane G Protein‐coupled Receptor 1, GPBAR‐1 or TGR5) elicit wide array of biological responses. While great number studies have been dedicated hepato‐protective impact FXR signalling, TGR5 is by far less explored this context. Because face massive potentially harmful overload partial ablation destruction, BA‐induced protective responses crucially contribute spare capacities. Based available literature, receptor protects remnant maintains homeostasis, mainly control inflammation, epithelial barrier permeability, pool hydrophobicity sinusoidal blood flow. Mouse experimental models reveal that lack TGR5, excessive leaky epithelium hydrophobic result parenchymal insult compromise optimal restoration functional mass. Translational perspectives thus opened target aim context
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