Does nephrotic syndrome cause upregulation of HDL endocytic receptor and PDZK-1-dependent downregulation of HDL docking receptor?
NS results in elevation of hepatic HDL endocytic receptor and deficiency of HDL docking receptor. The latter is associated with and, in part, mediated by downregulation of PDZK1. Together, these abnormalities can increase catabolism and diminish recycling of HDL and contribute to the defective reverse cholesterol/lipid transport in NS.
The current study is the first to reveal that dioscin can promote osteoblasts proliferation and differentiation via Lrp5 and ER pathway.