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. 2022 Oct 2;10(10):2464. doi: 10.3390/biomedicines10102464

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Molecular mechanism of hepatic OCA pharmacodynamics. OCA activates FXR, thereby triggering cellular pathways leading to a reduction in the synthesis and hepatic uptake of BAs, and an increase in their efflux from the liver. Furthermore, OCA acts on LSEC and KC, exerting anti-inflammatory and antifibrotic effects by reducing the production of proinflammatory cytokines and HSC activation, respectively. Abbreviations: farnesoid X receptor (FXR), retinoid X receptor (RXR), bile acid (BA), Kupffer cell (KC), liver sinusoidal endothelial cell (LSEC), hepatic stellate cell (HSC), small heterodimer partner (SHP), liver receptor homolog 1 (LRH-1), fibroblast growth factor-19 (FGF-19), sodium taurocholate co-transporting polypeptide (NTCP), bile salt export pump (BSEP), multidrug resistance protein-3 (MDR3), organic solute transporters (OST), transforming growth-factor β (TGFβ), connective tissue growth factor (CTGF), platelet-derived growth factor β-receptor (PDGFR-β), monocyte chemo-attractant protein-1 (MCP1), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), inhibitor of kB (IκB).