Abstract

This study identified for the first time that sodium taurocholate cotransporting polypeptide (NTCP) can mediate HBV direct infection and damage to human podocytes, and the NTCP157-165 locus is the main HBV entry site. The findings provide theoretical support for the pathogenesis of direct infection of HBV with kidney tissue. The findings provide a new target and theoretical basis for the treatment of HBV-related glomerulonephritis (HBV-GN). Blocking NTCP is a new target for the treatment of HBV-GN. We found that tacrolimus, a calcineurin inhibitor that blocks NTCP, can effectively treat HBV-GN. This study also provides a theoretical basis for the effective and safe treatment of immunosuppressant tacrolimus for HBV-GN.

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