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Nephrol Dial Transplant (2001) 16: 1529-1531
© 2001 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Role of thrombin receptors in the kidney: lessons from PAR1 knock-out mice

Eric Rondeau, Cécile Vigneau and Jeannig Berrou

Service de Néphrologie A, Association Claude Bernard, and INSERM U489, Hôpital Tenon, Paris, France

Keywords: kidney; knock-out strategy; PAR1; receptor; thrombin

Introduction

Thrombin is a serine proteinase which cleaves fibrinogen into fibrin and constitutes the key enzyme of blood coagulation. In addition, it is a potent activator of platelet aggregation, and of several cell types including endothelial cells, smooth muscle cells, fibroblasts, neurones, and mononuclear white blood cells. The role of thrombin in renal pathophysiology has been suspected for many years, due to the frequent fibrin deposition observed in the kidney in various vascular or glomerular diseases [1].

During the last 10 years, the cellular receptors mediating the mechanisms of action of thrombin and several other serine proteinases have been discovered, and their roles in vivo have been demonstrated, mainly due to gene knock-out (KO) strategy. It is beyond the scope of this paper to describe all that is known today about these receptors, and excellent recent reviews are available [2,3]. Our objective is to present . . . [Full Text of this Article]

The protease-activated receptor family: a subgroup of the 7-transmembrane domain receptors

The first thrombin receptor: PAR1 is expressed in the kidney

Experimental nephropathies in PAR1-/- mice

Conclusions and perspectives

Notes

References


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