Commentary 10.1172/JCI127927

c-Src is in the effector pathway linking uPAR and podocyte injury

Jeffrey B. Kopp and Jurgen Heymann

Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), NIH, Bethesda, Maryland, USA.

Address correspondence to: Jeffrey B. Kopp, 10 Center Dr., 3N116, NIH, Bethesda, Maryland 20892-1268, USA. Phone: 301.594.3403; Email: jbkopp@nih.gov.

Find articles by Kopp, J. in: JCI | PubMed | Google Scholar |

Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), NIH, Bethesda, Maryland, USA.

Address correspondence to: Jeffrey B. Kopp, 10 Center Dr., 3N116, NIH, Bethesda, Maryland 20892-1268, USA. Phone: 301.594.3403; Email: jbkopp@nih.gov.

Find articles by Heymann, J. in: JCI | PubMed | Google Scholar

First published April 2, 2019 - More info

Published in Volume 129, Issue 5 on May 1, 2019
J Clin Invest. 2019;129(5):1827–1829. https://doi.org/10.1172/JCI127927.
© 2019 American Society for Clinical Investigation
First published April 2, 2019 - Version history

The role of urokinase-type plasminogen activator receptor (uPAR) in kidney physiology and pathology has attracted considerable attention. The protein uPAR has dual functions: as a key regulator of plasmin generation and a component of the innate immune system. In the current issue, Wei and colleagues describe a transgenic mouse expressing Plaur RNA in glomerular podocytes. The mice manifested podocyte injury, including c-Src phosphorylation, proteinuria, and focal segmental glomerulosclerosis (FSGS). Plaur-transgenic mice on a β3 integrin–deficient background were protected from podocyte injury. Renal biopsies from subjects with FSGS, but not those with other glomerular diseases, manifested increased c-Src phosphorylation in podocytes. These findings suggest a novel injury mechanism in FSGS, with possible implications for new treatment strategies.

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