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Mechanisms for the protection of cholangiocytes against bile acid cytotoxicity include negative feedback loops via farnesoid X nuclear receptor (<jats:styled-content style=\"fixed-case\">FXR<\/jats:styled-content>) activation, the bicarbonate umbrella, cholehepatic shunting and anti\u2010inflammatory signalling, among others. By altering or overwhelming these defence mechanisms, cholestatic diseases such as primary biliary cholangitis (<jats:styled-content style=\"fixed-case\">PBC<\/jats:styled-content>) and primary sclerosing cholangitis (<jats:styled-content style=\"fixed-case\">PSC<\/jats:styled-content>) can further progress to biliary cirrhosis, end\u2010stage liver disease and death or liver transplantation. While <jats:styled-content style=\"fixed-case\">PBC<\/jats:styled-content> is currently treated with ursodeoxycholic acid (<jats:styled-content style=\"fixed-case\">UDCA<\/jats:styled-content>) and obeticholic acid (<jats:styled-content style=\"fixed-case\">OCA<\/jats:styled-content>), many fail treatment, and we have yet to find an effective therapy for <jats:styled-content style=\"fixed-case\">PSC<\/jats:styled-content>. Novel therapies under evaluation target nuclear and surface receptors including <jats:styled-content style=\"fixed-case\">FXR<\/jats:styled-content>, transmembrane G\u2010protein\u2013coupled receptor 5 (<jats:styled-content style=\"fixed-case\">TGR<\/jats:styled-content>5), peroxisome proliferator\u2010activated receptor (<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>) and pregnane X receptor (<jats:styled-content style=\"fixed-case\">PXR<\/jats:styled-content>). Modulation of these receptors leads to altered bile composition, decreased cytotoxicity, decreased inflammation and improved metabolism. 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