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. Author manuscript; available in PMC: 2017 Jul 26.
Published in final edited form as: Circulation. 2016 Jul 26;134(4):328–338. doi: 10.1161/CIRCULATIONAHA.116.022308

Figure 6. Simplified schema for the cardiovascular consequences of COX-2 versus mPGES-1 inhibition.

Figure 6

Inhibition of COX-2 predisposes mice to thrombosis, atherogenesis and hypertension, attributable to suppression of PGI2 and PGE2 biosynthesis. Deletion of mPges-1 results in rediversion of accumulated PGH2 substrate to prostacyclin synthase, augmenting PGI2 while suppressing PGE2 biosynthesis. This shift in substrate to PGI2 restrains thrombosis, hypertension and atherogenesis. X- Inhibition or deletion of enzyme.