Key result
AMPKα2 deletion induced vascular smooth muscle cell phenotypic switching and promoted features of atherosclerotic plaque instability in a nuclear factor-κB-KLF4-dependent manner.
Population
ApoeAMPKα2 mice, VSMC-specific AMPKα2 mice in an Apoe background (ApoeAMPKα2), and isolated vascular smooth…
Comparison
AMPKα2 deletion and pravastatin treatment vs Apoe(-/-) and Apoe(-/-)AMPKα2(sm+/+) control mice
Design
Preclinical
Follow-up
10 weeks
Authors
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Does not inform clinical practice; leaves open AMPK activation for plaque stabilization in humans.
AMPKα2 deletion promotes atherosclerotic plaque instability and VSMC phenotypic switching via an NF-κB-KLF4-dependent pathway, suggesting AMPK activation as a potential therapeutic target for plaque stabilization.
Ye et al. (2016) studied Atherosclerosis. AMPKα2 deletion vs. Apoe(-/-) and Apoe(-/-)AMPKα2(sm+/+) control mice was evaluated on Atherosclerotic plaque stability and VSMC phenotypic switching. AMPKα2 deletion induced vascular smooth muscle cell phenotypic switching and promoted features of atherosclerotic plaque instability in a nuclear factor-κB-KLF4-dependent manner.
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