Transforming growth factor-beta and the glomerular filtration barrier

• Ngā kaituhi matua: Ayesha Ghayur (Author), Peter J. Margetts (Author)
• Hōputu: Pukapuka
• I whakaputaina: The Korean Society of Nephrology, 2013-03-01T00:00:00Z.
• Ngā marau: article
• Urunga tuihono: Connect to this object online.
• Notes: 2211-9132; 10.1016/j.krcp.2013.01.003
• Keywords: Proteinuria; Podocyte; Glomerular endothelial cell; Transforming growth factor beta; Angiopoietin; Internal medicine; RC31-1245; Specialties of internal medicine; RC581-951
• Source: Kidney Research and Clinical Practice, Vol 32, Iss 1, Pp 3-10 (2013)

The increasing burden of chronic kidney disease worldwide and recent advancements in the understanding of pathologic events leading to kidney injury have opened up new potential avenues for therapies to further diminish progression of kidney disease by targeting the glomerular filtration barrier and reducing proteinuria. The glomerular filtration barrier is affected by many different metabolic and immune-mediated injuries. Glomerular endothelial cells, the glomerular basement membrane, and podocytes-the three components of the filtration barrier-work together to prevent the loss of protein and at the same time allow passage of water and smaller molecules. Damage to any of the components of the filtration barrier can initiate proteinuria and renal fibrosis. Transforming growth factor-beta (TGF-β) is a pleiotropic cytokine strongly associated with the fibrogenic response. It has a known role in tubulointerstitial fibrosis. In this review we will highlight what is known about TGF-β and how it interacts with the components of glomerular filtration barrier and causes loss of function and proteinuria.