Cholestasis is a common feature of human liver diseases. Potentially toxic bile salts accumulate in the cholestatic liver and promote hepatocyte damage by apoptosis and necrosis, thereby contributing to disease progression. The glycine and taurine conjugates of chenodeoxycholate (GCDC, TCDC) are the predominant dihydroxy bile salts in cholestatic patients and have been held responsible for cholestasis-associated liver injury (1). Other potentially toxic bile salts like deoxycholate (DC) are quantitatively less relevant in cholestatic liver disease (2). In the past decade, potential mechanisms by which bile salts induce cell injury and apoptosis in hepatocytes, have been investigated extensively. A better understanding of these mechanisms might offer new therapeutic options to ameliorate the detrimental effects of longstanding cholestasis, as seen in patients with chronic cholestatic disorders such as primary biliary cirrhosis (PBC) or primary sclerosing cholangitis (PSC).
展开▼
