RhoA protects the podocytes against high glucose-induced apoptosis through YAP and plays critical role in diabetic nephropathy

Highlights: • RhoA expression and its activity were decreased in HG-injured podocytes in vitro and in vivo. • Loss of RhoA by siRNA resulted in podocyte apoptosis and proteinuria. • RhoA deficiency could reduce the nuclear protein expression of YAP in vitro and in vivo. • Podocyte apoptosis induced by RhoA knockdown was significantly abolished by over expressing active YAP. • RhoA played a critical role in DN probably by mediating the podocyte apoptosis through YAP. RhoA may be a novel target for the treatment of DN. Podocyte apoptosis is important mechanism that leading to proteinuria in Diabetic nephropathy (DN), but the underling mechanisms that cause podocyte apoptosis in DN are not very clear. We have recently demonstrated that RhoA, a small GTPase protein, effectively protected podocyte apoptosis induced by LPS and ADR in vitro. However, the potential role of RhoA in DN is unknown.