STAT signaling in polycystic kidney disease

Sebastian Strubl; Jacob A Torres; Alison K Spindt; Hannah Pellegrini; Max C Liebau; Thomas Weimbs

doi:10.1016/j.cellsig.2020.109639

STAT signaling in polycystic kidney disease

Cell Signal. 2020 Aug:72:109639. doi: 10.1016/j.cellsig.2020.109639. Epub 2020 Apr 20.

Authors

Sebastian Strubl¹, Jacob A Torres², Alison K Spindt², Hannah Pellegrini², Max C Liebau³, Thomas Weimbs⁴

Affiliations

¹ Department of Molecular, Cellular, and Developmental Biology, Neuroscience Research Institute, University of California Santa Barbara, Santa Barbara, CA 93106-9625, USA; Department II of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
² Department of Molecular, Cellular, and Developmental Biology, Neuroscience Research Institute, University of California Santa Barbara, Santa Barbara, CA 93106-9625, USA.
³ Department of Pediatrics and Center for Molecular Medicine Cologne, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany; Department II of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
⁴ Department of Molecular, Cellular, and Developmental Biology, Neuroscience Research Institute, University of California Santa Barbara, Santa Barbara, CA 93106-9625, USA. Electronic address: weimbs@ucsb.edu.

Abstract

The most common form of polycystic kidney disease (PKD) in humans is caused by mutations in the PKD1 gene coding for polycystin1 (PC1). Among the many identified or proposed functions of PC1 is its ability to regulate the activity of transcription factors of the STAT family. Most STAT proteins that have been investigated were found to be aberrantly activated in kidneys in PKD, and some have been shown to be drivers of disease progression. In this review, we focus on the role of signal transducer and activator of transcription (STAT) signaling pathways in various renal cell types in healthy kidneys as compared to polycystic kidneys, on the mechanisms of STAT regulation by PC1 and other factors, and on the possibility to target STAT signaling for PKD therapy.

Publication types

Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review

MeSH terms

Animals
Humans
Janus Kinases / antagonists & inhibitors
Janus Kinases / metabolism
Kidney / pathology
Models, Biological
Polycystic Kidney Diseases / metabolism*
STAT Transcription Factors / metabolism*
Signal Transduction*

Substances

STAT Transcription Factors
Janus Kinases

Grants and funding

R01 DK109563/DK/NIDDK NIH HHS/United States