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10.1152/ajprenal.00502.2015

http://scihub22266oqcxt.onion/10.1152/ajprenal.00502.2015
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C4835922!4835922!26719364
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suck abstract from ncbi


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pmid26719364      Am+J+Physiol+Renal+Physiol 2016 ; 310 (8): F689-96
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  • Transforming growth factor-?1 and diabetic nephropathy #MMPMID26719364
  • Chang AS; Hathaway CK; Smithies O; Kakoki M
  • Am J Physiol Renal Physiol 2016[Apr]; 310 (8): F689-96 PMID26719364show ga
  • Transforming growth factor-?1 (TGF-?1) is established to be involved in the pathogenesis of diabetic nephropathy. The diabetic milieu enhances oxidative stress and induces the expression of TGF-?1. TGF-?1 promotes cell hypertrophy and extracellular matrix accumulation in the mesangium, which decreases glomerular filtration rate and leads to chronic renal failure. Recently, TGF-?1 has been demonstrated to regulate urinary albumin excretion by both increasing glomerular permeability and decreasing reabsorption in the proximal tubules. TGF-?1 also increases urinary excretion of water, electrolytes and glucose by suppressing tubular reabsorption in both normal and diabetic conditions. Although TGF-?1 exerts hypertrophic and fibrogenic effects in diabetic nephropathy, whether suppression of the function of TGF-?1 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 TGF-?1. However, differentiating the molecular mechanisms for glomerulosclerosis from those for the suppression of the effects of mineralocorticoids by TGF-?1 may assist in developing novel therapeutic strategies for diabetic nephropathy. In this review, we discuss recent findings on the role of TGF-?1 in diabetic nephropathy.
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