Affiliation:
1. Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee, United States
2. Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, United States
Abstract
The contribution of the thrombin receptor protease-activated receptor 4 (PAR4) to acute kidney injury (AKI) and chronic kidney disease (CKD) is not well understood. Here we report that PAR4 expression is upregulated after kidney injury and PAR4 knockout (KO) mice are protected against fibrosis following kidney injury in two mouse models. First, PAR4 KO mice are protected against unilateral ureter obstruction. Second, PAR4 KO mice are protected against an AKI-CKD model of ischemia-reperfusion followed by contralateral nephrectomy.
Funder
Vanderbilt Center for Kidney Disease
HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases
HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases
HHS | NIH | National Institute on Aging
Veterans Administration Medical Center
Publisher
American Physiological Society