From the Large Scale Expression Analysis of Lupus Nephritis to Targeted Molecular Medicine.
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Cross-species transcriptional network analysis defines shared inflammatory responses in murine and human lupus nephritis.
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Recent advances in animal models of diabetic nephropathy.
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Gα12 activation in podocytes leads to cumulative changes in glomerular collagen expression, proteinuria and glomerulosclerosis.
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Next-generation sequencing identifies TGF-β1-associated gene expression profiles in renal epithelial cells reiterated in human diabetic nephropathy.
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Hyperglycemia and renin-dependent hypertension synergize to model diabetic nephropathy.
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Identification of nephropathy candidate genes by comparing sclerosis-prone and sclerosis-resistant mouse strain kidney transcriptomes.
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Urine podocin:nephrin mRNA ratio (PNR) as a podocyte stress biomarker.
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Angiotensin II-dependent persistent podocyte loss from destabilized glomeruli causes progression of end stage kidney disease.
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Growth-dependent podocyte failure causes glomerulosclerosis.
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