Recent News

What we've been up to

in the

Shankland Lab!



ASN 2017- Kidney Week in New Orleans


Andrea discussing her research
20th Annual Undergraduate
Research Symposium

  Shankland Lab Research featured on cover of  Kidney International

Shankland Lab Research featured on cover of Kidney International

Dr. Mariya Sweetwyne's paper accepted to Kidney International

"Mitochondrial-targeted peptide, SS-31, improves glomerular architecture in mice of advanced age"

link to PubMed


Lineage Tracing Aged Mouse Kidneys Shows Lower Number of Cells of Renin Lineage and Reduced Responsiveness to RAAS Inhibition


Charting the transcriptional landscape of cells of renin lineage following podocyte depletion


Gene-Edited Human Kidney Organoids Reveal Mechanisms of Disease in Podocyte Development


WT1 Is Necessary for the Proliferation and Migration of Cells of Renin Lineage Following Kidney Podocyte Depletion


Retinoic acid improves nephrotoxic serum-induced glomerulonephritis through activation of podocyte retinoic acid receptor α.


Tracking the stochastic fate of cells of the renin lineage after podocyte depletion using multicolor reporters and intravital imaging.


Can podocytes be regenerated in adults?


Compound effects of aging and experimental FSGS on glomerular epithelial cells.


(Re)Building a Kidney.


The mitochondrial-targeted peptide, SS-31, improves glomerular architecture in mice of advanced age.


A bone marrow factor contributes to kidney disease


Activated ERK1/2 increases CD44 in glomerular parietal epithelial cells leading to matrix expansion.


Reducing mTOR augments parietal epithelial cell density in a model of acute podocyte depletion and in aged kidneys


Krüppel-Like Factor 15 Mediates Glucocorticoid-Induced Restoration of Podocyte Differentiation Markers.


Partial Podocyte Replenishment in Experimental FSGS Derives from Non-Podocyte Sources.


Renin-Angiotensin-Aldosterone System Inhibition Increases Podocyte Derivation from Cells of Renin Lineage.


Cells of renin lineage express hypoxia inducible factor 2α following experimental ureteral obstruction.


A Systematic Method for Categorizing GN.

New Funding for FSGS Research
FY 2015 Investigator-Initiated Research Award – Partnering PI Option

Suzie Pun – University of Washington

Stuart Shankland – University of Washington



NIH/NIA  (Shankland) 08/15/2016-03/31/2021

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  PR151175    (Shankland and Pun)   09/30/2016-04/30/2019         

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


DOD  PR151965   (Shankland and Pun)   6/15/2016-12/14/2018

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


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

Rebuilding the glomerular filtration barrier by regenerating adult podocytes


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 , 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.


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

Juxta-glomerular 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



NIH/NIDDK   5 T32 DL07467-31 (Shankland)  7/15/1993-6/30/2019

 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) 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.



Kaverina, Natalya

Abstract: [FR-PO316]

Multi-Clonal Population of Cells of Renin Lineage (CoRL) Transdifferentiate into Podocytes and PECs in Experimental FSGS


Lichtnekert, Julia

Abstract: [FR-PO342]

RAS Inhibition Enhances Proliferation and Migration of Cells of Renin Lineage (CoRL) as Progenitors in Experimental FSGS



Shankland, Stuart

2017 American Society of Nephrology Annual Meeting, New Orleans, LA

“Podocyte Regeneration from Renin Lineage Cells”


2015 American Society of Nephrology Annual Meeting, San Diego, CA

"What is Aging Nephropathy?" 

"Role of Parietal Cells Following Glomerular Injury"


The Lab Gang