Abstract
Recent studies indicate that immune activation may play a role in pathogenesis of diabetic nephropathy (DN). We have previously described a mouse model exhibiting characteristics of human DN including high-grade albuminuria and glomerulosclerosis. In this model, glomerular immune and inflammatory pathways, including networks associated with tumor necrosis factor (TNF)-α signaling are upregulated. In this study, we examine the functional impact of the TNF-α pathway in DN.
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