Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2005-5-26
pubmed:abstractText
Although abnormalities in the glomerular epithelial cell, the podocyte, have been appreciated for some time, it is only recently that their significance and the underlying mechanisms for the changes have begun to be explored. There is a decrease in podocyte number early in diabetes, with further decreases as albuminuria increases. The number of podocytes is inversely related to the degree of albuminuria in both cross-sectional and longitudinal studies. Foot process width is increased in proteinuria, the width correlating with albuminuria. Loss of nephrin - both mRNA and protein - occurs some time after the onset of diabetes and is also inversely related to proteinuria. The amount of the alpha3beta1 integrin on the basement-membrane surface of the foot process of the podocyte is also reduced in diabetes. Loss of nephrin and alpha3beta1 integrin is induced by both hyperglycaemia and mechanical stretch. Agents that inhibit the renin-angiotensin system, but not other agents that reduce proteinuria, restore nephrin expression and prevent the structural changes seen in the podocyte in diabetes. Thus, changes in the podocyte contribute to the proteinuria of diabetic nephropathy and can be ameliorated by inhibition of the renin-angiotensin system.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0018-5043
pubmed:author
pubmed:issnType
Print
pubmed:volume
37 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
9-16
pubmed:dateRevised
2009-2-19
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
The podocyte: a major player in the development of diabetic nephropathy?
pubmed:affiliation
Diabetes Research Group, University of Newcastle upon Tyne. s.m.marshall@ncl.ac.uk
pubmed:publicationType
Journal Article, Review