15
Views
0
CrossRef citations to date
0
Altmetric
Review

Alteration of glomerulogenesis- and podocyte structure-related gene expression in early diabetic nephropathy

&
Pages 615-622 | Published online: 10 Jan 2014
 

Abstract

Diabetic nephropathy is a leading cause of end-stage renal disease. Several pathways, including the renin–angiotensin system, have been postulated as potential mechanisms of diabetic nephropathy. In addition, glomerulogenesis-related molecules are involved in the pathogenesis of diabetic nephropathy, especially at the early stage. They can be divided into three groups by function, that is, fibrosis-related, podocyte differentiation-related and angiogenesis-related molecules. Most of the molecules are expressed in the podocyte and upregulated, even during the normoalbuminuric stage. Expression of several podocyte structure-related molecules are also altered at the normoalbuminuric stage. They can contribute to the structural alteration of the podocyte in diabetic nephropathy. Thus, normalization of the expression of glomerulogenesis-related molecules could be a new target for preventing the initiation and progression of diabetic nephropathy.

Financial disclosure

The authors have no relevant financial interests related to this manuscript, including employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.