Review Article Open Access
Volume 3 | Issue 1 | DOI: https://doi.org/10.33696/Signaling.3.068

c-JUN n-Terminal Kinase (JNK) Signaling in Autosomal Dominant Polycystic Kidney Disease

  • 1Program in Molecular Medicine, University of Massachusetts Medical School, Biotech II, Suite 213, 373 Plantation Street, Worcester,MA, USA 01605
  • 2Department of Microbiology and Physiological Systems, University of Massachusetts Medical School, 55 Lake Avenue North,Worcester, MA, USA 01655
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Corresponding Author

Gregory J. Pazour, gregory.pazour@umassmed.edu

Received Date: January 10, 2022

Accepted Date: February 08, 2022


Polycystic kidney disease is an inherited degenerative disease in which the uriniferous tubules are replaced by expanding fluid-filled cysts that ultimately destroy organ function. Autosomal dominant polycystic kidney disease (ADPKD) is the most common form, afflicting approximately 1 in 1,000 people and is caused by mutations in the transmembrane proteins polycystin-1 (Pkd1) and polycystin-2 (Pkd2). The mechanisms by which polycystin mutations induce cyst formation are not well understood, however pro-proliferative signaling must be involved for tubule epithelial cell number to increase over time. We recently found that the stress-activated mitogen-activated protein kinase (MAPK) pathway c-Jun N-terminal kinase (JNK) pathway is activated in cystic disease and genetically removing JNK reduces cyst growth driven by a loss of Pkd2. This review covers the current state of knowledge of signaling in ADPKD with an emphasis on the JNK pathway.


Polycystic kidney disease, Jun N Terminal kinase, Polycystin-1, Polycystin-2, Cilia, Mus musculus, Mitogen-activated protein kinase signaling

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