Roger C. Wiggins

TL;DR: All glomerular diseases are placed within this spectrum of podocytopathies with predictable outcomes based on podocyte biology impacted by temporal, genetic, and environmental cues to rationalize clinical effort toward podocyte preservation and prevention of progression.

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: These findings, together with the zebrafish model of human nephrotic syndrome generated by plce1 knockdown, open new inroads into pathophysiology and treatment mechanisms of nephrotsic syndrome.

TL;DR: It is shown that activity of mTOR complex 1 (mTORC1), a kinase that senses nutrient availability, was enhanced in the podocytes of diabetic animals and suggested that reduction of podocyte mTORC 1 activity is a potential therapeutic strategy to prevent DN.

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.