Halofuginone prevents extracellular matrix deposition in diabetic nephropathy,10.1016/j.bbrc.2008.12.088,Biochemical and Biophysical Research Communic

Halofuginone prevents extracellular matrix deposition in diabetic nephropathy (Citations: 2)


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Transforming growth factor-β (TGF-β) is known to promote the accumulation of extracellular matrix (ECM) and the development of diabetic nephropathy. Halofuginone, an analog of febrifugine, has been shown to block TGF-β1 signaling and subsequent type I collagen production. Here, the inhibitory effect of halofuginone on diabetic nephropathy was examined. Halofuginone suppressed Smad2 phosphorylation induced by TGF-β1 in cultured mesangial cells. In addition, the expression of TGF-β type 2 receptor decreased by halofuginone. Halofuginone showed an inhibitory effect on type I collagen and fibronectin expression promoted by TGF-β1. An in vivo experiment using db/db mice confirmed the ability of halofuginone to suppress mesangial expansion and fibronectin overexpression in the kidneys. Moreover, an analysis of urinary 8-OHdG level and dihydroethidium fluorescence revealed that halofuginone reduced oxidative stress in the glomerulus of db/db mice. These data indicate that halofuginone prevents ECM deposition and decreases oxidative stress, thereby suppressing the progression of diabetic nephropathy.

Journal: Biochemical and Biophysical Research Communications - BIOCHEM BIOPHYS RES COMMUN , vol. 379, no. 2, pp. 411-416, 2009

DOI: 10.1016/j.bbrc.2008.12.088

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Halofuginone prevents extracellular matrix deposition in diabetic nephropathy,10.1016/j.bbrc.2008.12.088,Biochemical and Biophysical Research Communic

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Citations (2)

Desnutrin/ATGL Is Regulated by AMPK and Is Required for a Brown Adipose Phenotype (Citations: 2)

Recent advances in pharmacotherapy for diabetic nephropathy: Current perspectives and future directions (Citations: 8)


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