Jocelyn Wiggins

TL;DR: A transgenic rat strain in which the human diphtheria toxin receptor is specifically expressed in podocytes was developed, providing strong support for the concept that podocyte depletion could be a major mechanism driving glomerulosclerosis and progressive loss of renal function in human glomerular diseases.

TL;DR: This report supports the growing body of data linking glomerulosclerosis directly to a reduction in relative podocyte number [increased glomerular area per podocyte (GAPP)], and raises important questions related to the mechanisms of podocytes loss, strategies for prevention of podocyte depletion, and the prevention of progression of glomersular diseases.

TL;DR: Hypertrophy above a certain threshold was associated with podocyte stress and then failure, culminating in reduced podocyte numbers in sclerotic glomeruli, which could be prevented by calorie restriction.

TL;DR: Podocyte density reduction with age may directly lead to focal global glomerulosclerosis, and all progressive glomerular diseases can be considered superimposed accelerators of this underlying process.

TL;DR: It is expected that this receptor might play a role in maintaining foot process structure and/or function by regulating tyrosine phosphorylation of podocyte proteins by analogy with the CD45 PTPase of T cells.