TLR4 and liver dysplastic nodule: Replication of these findings for podocytes in vitro, activation of the TLR4 pathway in podocytes in response to high glucose, and attenuation of albuminuria, glomerular injury, podocyte depletion and expression of inflammatory cytokines and chemokines in TLR4−/− mice with diabetes strongly implicates TLR4 in the mediation of podocytopathy in DN.