Diabetic nephropathy (DN) presents with a gradual breakdown of the glomerular filtration barrier to protein, culminating in widespread glomerular damage and renal failure. The podocyte is the central cell of the glomerular filtration barrier, and possesses unique architectural and signaling properties guided by the expression of key podocyte specific proteins. How these cellular features are damaged by the diabetic milieu is unclear, but what is becoming increasingly clear is that damage to the podocyte is a central event in DN. Here we present accumulating evidence that insulin action itself is important in podocyte biology, and may be deranged in the pathomechanism of early DN. This introduces a rationale for therapeutic intervention to improve podocyte insulin sensitivity early in the presentation of DN.
Keywords: Podocytes, Diabetic nephropathy, Insulin, Glomerular filtration barrier, Diabetic nephropathy (DN), albuminuria, renin-angiotensin cascade, polyols, hexosamines, AGEs, PKC, transforming growth factor-beta, Macrophage Migration Inhibitory Factor, CD74, GBM, ECM, carnosinase, fibronectin, collagen, Reactive oxygen species (ROS), C (APC), Advanced glycation endproducts (AGE), RAGE, proteinuria, neph-ropathy, retinopathy, glycosylated hemo-globin, VEGF, lipodystrophies, adipokines, hypertriglyceridemic, MPGN, FSGS, Grave's disease, systemic lupus erythematosus, acanthosis nigricans, hyperandrogenism, lupus nephritis, lipodystrophy, PPAR agonists, thiazolidinediones, urine albumin-to-creatinine, Pioglitazone, Glomerular endothelial cell, PI3 kinase, MAP kinase pathways, endothelin-1, NF kappa, E selectin, monocyte chemoattractant, GEnC, GLUT1, GLUT4
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