Current Funding


NIH  1R01 AG046231-01A1       (Shankland)             07/01/2016-06/30/2021           

Reduced Glomerular Progenitors Impair Regeneration in Aged Kidney

The grant will define how the decline in podocyte number with advancing age cannot adequately be replaced by their neighboring parietal epithelial cell progenitors,

which leads to kidney scarring.


DOD PR151965   (Pun)    05/01/2016-10/31/2017           

Development of cell therapies for FSGS

The major goal of this proposal is to develop urine-derived renal progenitor cells as a cell therapy for treatment of FSGS.


DOD  PR151175    (Shankland and Pun)   05/01/2016-04/30/2019        

New podocyte-targeted treatments for focal segmental glomerulosclerosis (FSGS)

We propose the development of two synergistic kidney-targeting technologies: (i) “passive” targeting, kidney-accumulating polymers and (ii) “active” targeting

podocyte-specific peptide


NIH/NIDDK   5 T32 DL07467-31 (Shankland)  7/1/2014-6/30/2019

 Training in Renal Disease

This is a training grant that supports research training for three M.D. post-graduate fellows who undergoperiods of both renal and basic science research training.


NIH R01 5 R01 DK093493-02 Shankland SJ (PI)   9/03/2012-6/30/2017                                                                                    

Pericyte-endothelial cross talk in vascular stability after kidney injury

These studies will investigate the mechanisms by which pericytes nurture kidney blood vessels and the mechanisms by which they detach in response to injury and

thereafter fail to nurture. In understanding  these processes we hope to develop new therapies to treat kidney diseases.


NIH/NIDDK 1 R01 DK097598-01A1 Shankland SJ (PI)     07/01/2014-06/30/2019                                                                            

Juxta-glamerular cells serve as glomerular epithelial cell progenitors in glomerular disease

The purpose of this proposal is to study the existing problem of age-related podocyte depletion in a completely new context. The goal is to prove that with advancing

age, kidney regeneration, and thus repair, is inadequate because progenitors are unable to replace and restore glomerular podocytes. We anticipate that the results will

provide compelling evidence for a new paradigm in aging kidneys in which recently identified progenitors are unable to adequately regenerate to replace podocytes,

which leads to glomerulosclerosis and reduced kidney function.


NIH/NIDDK  1 UH2 DK107343-01 (Shankland and Zheng) 07/01/2015-06/30/2020  

Rebuilding the glomerular filtration barrier by regenerating adult podocytes  (Re)

Podocytes are cells in the kidney’s glomerular filtering units that limit the passage of proteins from the blood in to the urine. As adults, they cannot proliferate to replace

themselves, and therefore they are reliant on other stem cells for their regeneration. In this grant, we will study such stem cells in podocyte repair to rebuild a kidney.