Transforming growth factor β1 (TGFβ1) is established to be involved in the pathogenesis of diabetic nephropathy. The diabetic milieu enhances oxidative stress and induces the expression of TGFβ1. TGFβ1 promotes cell hypertrophy and extracellular matrix accumulation in the mesangium, which decreases glomerular filtration rate and leads to chronic renal failure. Recently, TGFβ1 has been demonstrated to regulate urinary albumin excretion by both increasing glomerular permeability and decreasing reabsorption in the proximal tubules. TGFβ1 also increases urinary excretion of water, electrolytes and glucose by suppressing tubular reabsorption in both normal and diabetic conditions. Although TGFβ1 exerts hypertrophic and fibrogenic effects in diabetic nephropathy, whether suppression of the function of TGFβ1 can be an option to prevent or treat the complication is still controversial. This is partly because adrenal production of mineralocorticoids could be augmented by the suppression of TGFβ1. However, differentiating the molecular mechanisms for glomerulosclerosis from those for the suppression of the effects of mineralocorticoids by TGFβ1 may assist to develop novel therapeutic strategies for diabetic nephropathy. In this review we discuss recent findings on the role of TGFβ1 in diabetic nephropathy.
- Proximal tubule
- Sodium-glucose cotransporter
- Copyright © 2015, American Journal of Physiology - Renal Physiology