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The main sinusoidal transport system for bile-salt uptake is the Na+-taurocholate cotransporting polypeptide, which has been cloned from both rat (Ntcp, Slc10a1)50 and human liver (NTCP, SLC10A1).51 Ntcp/NTCP is driven by a transmembrane Na+ gradient maintained by the Na+/K+-ATPase pump, which is also strategically localized in the sinusoidal membrane.52 Ntcp/NTCP accounts for the transport of more than 80% of amidated bile salts (the major circulating bile salts), and only 40% of their unconjugated, parent compounds.53 The remaining fraction of circulating bile salts is taken up by a non-electrogenic, Na+-independent transport system, formed by a family of transporters collectively named organic aniontransporting polypeptides (Oatps/OATPs for rat and human, respectively).54 Humans possess four OATPs: OATP1A2 (SLCO1A2/SLC21A3), OATP1B1 (SLC21A6), OATP1B3 (SLC21A8) and OATP2B1 (SLC21A9)

Future research should focus on delving deeper into the pathological mechanism of HAPH, developing more effective diagnosis and treatment methods, and ultimately providing more hope and well-being for patients

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Current therapeutic strategies mainly focus on reducing Cu bioavailability (chelators, Zn) or mitigating its downstream effects (nanoparticles)