Studies in Zebrafish and Rat Models Support Dual Blockade of EP2 and EP4 (Prostaglandin E Receptors Type 2 and 4) for Renoprotection in Glomerular Hyperfiltration and Albuminuria.

Background: Glomerular hyperfiltration (GH) is an important mechanism in the development of albuminuria in hypertension. Upregulation of COX2 (cyclooxygenase 2) and prostaglandin E (PGE) was linked to podocyte damage in GH. We explored the potential renoprotective effects of either separate or combined pharmacological blockade of EP2 (PGE receptor type 2) and EP4 (PGE receptor type 4) in GH.

15-keto-Prostaglandin E exhibits bioactive role by modulating glomerular cytoarchitecture through EP2/EP4 receptors.

Aims: Prostaglandins are important signaling lipids with prostaglandin E (PGE) known to be the most abundant prostaglandin across tissues. In kidney, PGE plays an important role in the regulation of kidney homeostasis through its EP receptor signaling. Catabolism of PGE yields the metabolic products that are widely considered biologically inactive.

Concerted EP2 and EP4 Receptor Signaling Stimulates Autocrine Prostaglandin E Activation in Human Podocytes.

Glomerular hyperfiltration is an important mechanism in the development of albuminuria. During hyperfiltration, podocytes are exposed to increased fluid flow shear stress (FFSS) in Bowman's space. Elevated Prostaglandin E2 (PGE) synthesis and upregulated cyclooxygenase 2 (Cox2) are associated with podocyte injury by FFSS.