The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Central role of TGF-beta in the pathogenesis of diabetic nephropathy and macrovascular complications: a hypothesis.

Patients with insulin-dependent diabetes mellitus (IDDM) and albuminuria are at high risk for severe micro- and macrovascular complications. Diabetic vascular complications are characterized by structural alterations of extracellular matrix ( ECM) components in glomeruli and large vessel walls, namely, accumulation of collagen IV, collagen VI and fibronectin and relative decrease of heparan sulphate proteoglycan ( HSPG). We hypothesize that the defect remodelling of ECM contributing to nephropathy and macrovascular disease is induced by overproduction of transforming growth factor-beta (TGF-beta). Recent reports indicate that hyperglycaemia, increased intraglomerular pressure, and glycated proteins potentially induce overproduction of TGF-beta in diabetes. TGF-beta stimulates production of ECM components such as collagen IV, fibronectin, proteoglycans (decorin and biglycan) without increasing HSPG. TGF-beta overproduction leads to glomerulosclerosis and TGF-beta is a causal factor in myointimal hyperplasia after balloon injury of carotid artery. It mediates angiotensin II modulator effect on smooth muscle cell growth. These findings may indicate TGF-beta overproduction to be a common pathogenetic step explaining the well-known association between micro- and macrovascular complications in diabetic patients. TGF-beta antagonists, such as decorin, betaglycan, and possibly also heparin, might be potential candidates for future therapy to prevent diabetic vascular disease.[1]

References

 
WikiGenes - Universities