Pharmacological blockade of the EP3 prostaglandin E2 receptor in the setting of type 2 diabetes enhances β-cell proliferation and identity and relieves oxidative damage

• Main Authors: Karin J. Bosma (Author), Spencer R. Andrei (Author), Liora S. Katz (Author), Ashley A. Smith (Author), Jennifer C. Dunn (Author), Valerie F. Ricciardi (Author), Marisol A. Ramirez (Author), Sharon Baumel-Alterzon (Author), William A. Pace (Author), Darian T. Carroll (Author), Emily M. Overway (Author), Elysa M. Wolf (Author), Michelle E. Kimple (Author), Quanhu Sheng (Author), Donald K. Scott (Author), Richard M. Breyer (Author), Maureen Gannon (Author)
• Format: Book
• Published: Elsevier, 2021-12-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Objective: Type 2 diabetes is characterized by hyperglycemia and inflammation. Prostaglandin E2, which signals through four G protein-coupled receptors (EP1-4), is a mediator of inflammation and is upregulated in diabetes. We have shown previously that EP3 receptor blockade promotes β-cell prolifera...