April 10, 2008Journal of Internal Medicine
Microsomal prostaglandin E synthase‐1 inhibition in cardiovascular inflammatory disease
Why the study?
Does mPGES-1 inhibition reduce cardiovascular inflammation and atherogenesis without the adverse cardiovascular effects seen with COX-2 inhibitors?
Population
Hyperlipidaemic mice and patients with cardiovascular inflammatory diseases
Comparison
Microsomal prostaglandin E synthase-1 inhibitors vs Cyclooxygenase-2 (COX-2) inhibitors
Design
Review
Authors
Discussion
Loading...
Member takes
Implication
mPGES-1 inhibition merits human trials for atherosclerosis; leaves open whether mouse benefits translate without COX-2 risks.
Structured PICO
Does mPGES-1 inhibition reduce cardiovascular inflammation and atherogenesis without the adverse cardiovascular effects seen with COX-2 inhibitors?
P
Population
Hyperlipidaemic mice and patients with cardiovascular inflammatory diseases (atherosclerosis and aortic aneurysm)
I
Intervention
Microsomal prostaglandin E synthase-1 (mPGES-1) inhibitors
C
Comparator
Cyclooxygenase-2 (COX-2) inhibitors
O
Outcome
Atherogenesis and aortic aneurysm formation
mPGES-1 inhibitors demonstrate therapeutic potential for cardiovascular inflammatory syndromes like atherosclerosis and aortic aneurysm without the thrombotic risks associated with COX-2 inhibitors.
Limitations
- Products of substrate rediversion vary according to cell type, potentially causing contrasting impacts among individuals at varied stages of disease evolution
- Increased PGI2 may attenuate relief of pain
Cite This Study
Wang et al. (2008) studied this question.