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Neurology (2009) 26;72(21):1850-7

Taken together, GH excess associated with poorly controlled T1DM induces podocyte injury, characterized by podocyte hypertrophy, apoptosis, dedifferentiation of podocytes (epithelialmesenchymal transition) and/or cross-linking of the basement membrane resulting in increased podocyte permeability to albumin and detachment of podocytes from the glomerular basement membrane (Fig

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Histone Deacetylase Inhibitors MS-275 and SAHA Induced Growth Arrest and Suppressed Lipopolysaccharide-Stimulated NF-kappaB P65 Nuclear Accumulation in Human Rheumatoid Arthritis Synovial Fibroblastic E11 Cells