Does association of common variants in NPPA and NPPB with blood pressure translate into kidney damage in a general population study?
This was consistent with a lack of effect on clinical renal outcomes found in previous studies and showed that even replicated and biologically plausible genetic association studies based on surrogate markers do not easily translate into clinically meaningful prognosis.
These results suggest that decreased expression of TGF-betaIIR in the HT diabetic mice can inhibit the progression of diabetic renal injury by inhibiting the downstream Smad signaling pathway and subsequent ECM gene expression. Thus, TGF-betaIIR appears to play an important role in the progression of diabetic nephropathy by mediating intracellular Smad signaling.