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J Am Soc Nephrol. 2014 Jun;25(6):1140-7. doi: 10.1681/ASN.2013101037. Epub 2014 Feb 20.

Vasopressin-2 receptor signaling and autosomal dominant polycystic kidney disease: from bench to bedside and back again.

Author information

1
Department II of Internal Medicine and Center for Molecular Medicine Cologne, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, and.
2
Department II of Internal Medicine and Center for Molecular Medicine Cologne, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, and Systems Biology of Aging Cologne, University of Cologne, Cologne, Germany.
3
Department II of Internal Medicine and Center for Molecular Medicine Cologne, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, and Systems Biology of Aging Cologne, University of Cologne, Cologne, Germany thomas.benzing@uk-koeln.de.

Abstract

Blockade of the vasopressin-2 receptor (V2R) in the kidney has recently emerged as a promising therapeutic strategy in autosomal dominant polycystic kidney disease. The pathophysiologic basis of V2R-dependent cyst proliferation and disease progression, however, is not fully understood. Recent evidence suggests that polycystic kidney disease is characterized by defects in urinary concentrating mechanisms and subsequent deregulation of vasopressin excretion by the neurohypophysis. On the cellular level, several recent studies revealed unexpected crosstalk of signaling pathways downstream of V2R activation in the kidney epithelium. This review summarizes some of the unexpected roles of V2R signaling and suggests that vasopressin signaling itself may contribute crucially to loss of polarity and enhanced proliferation in cystic kidney epithelium.

KEYWORDS:

ADPKD; Cell & Transport Physiology; Cell Signaling; collecting ducts; vasopressin

PMID:
24556353
PMCID:
PMC4033383
DOI:
10.1681/ASN.2013101037
[Indexed for MEDLINE]
Free PMC Article

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