Figure 9.

Schematic representation of the pathways through which FABP5 modulates PGE₂ biosynthesis during inflammation. A, activation of the interleukin 1 receptor (IL-1R) by IL-1β triggers NF-κB phosphorylation and translocation to the nucleus wherein it binds to the mPGES-1 promoter and initiates mPGES-1 transcription. In parallel, FABP5 may transport arachidonic acid to COX-1/2 and mPGES-1, the main biosynthetic enzymes for PGE₂, which reside on the endoplasmic reticulum. B, inhibition of FABP5 blunts NF-κB activation and nuclear translocation, resulting in attenuated induction of mPGES-1. FABP5 inhibition may additionally reduce arachidonic acid delivery to COX-1/2, resulting in suppression of PGE₂ biosynthesis.