Publication: Role of Smad1 in diabetic nephropathy: Molecular
mechanisms and implications as a diagnostic marker
Authors
Abe, H. ; Matsubara, Takeshi ; Arai, Hidenori ; Doi, Toshio
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Publisher
Murcia: F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Diabetic nephropathy (DN) is the leading
cause of chronic kidney failure. Moreover, DN is
associated with elevated cardiovascular morbidity and
mortality. DN is characterized by progressive expansion
of the mesangial matrix and thickening of the glomerular
basement membrane, resulting in the obliteration of
glomerular capillaries. Advanced glycation endproducts
(AGEs) produced as the result of hyperglycemia are
known to stimulate the production of extracellular
matrix (ECM) proteins, resulting in glomerulosclerosis.
Exposure of cultured mesangial cells to AGEs results in
a receptor-mediated upregulation of mRNA and protein
secretion of type IV collagen (Col4), which is a major
component of ECM. Here we review recent novel
insights into the pathogenesis and diagnosis of DN, with
a special emphasis on the emerging concept that diabetic
glomerulosclerosis can result from activation of the
signaling cascade leading to irreversible ECM
overproduction. Finally, we describe signaling pathways
involved in the initial change of DN and how these
pathways can be manipulated for therapeutic benefit.
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