Journal
CORONARY ARTERY DISEASE
Volume 26, Issue 4, Pages 322-327Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MCA.0000000000000243
Keywords
acute coronary syndrome; AMP-activated protein kinase; atherosclerotic plaques; autophagy; mTOR
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Funding
- National Natural Science Foundation of China [30971216, 30871040]
- Shandong Province Natural Science Foundation [ZR2010HM063]
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Background Coronary atherosclerotic plaque formation is driven by macrophage infiltration. Monocytes and macrophages contribute to the progression of atherosclerosis. However, research on the relationship between AMP-activated protein kinase (AMPK) and vulnerable atherosclerotic plaques is still insufficient. In the present study, we aimed to elucidate the adaptive mechanism between autophagy of peripheral blood monocytes (PBMs) and the rupture of atherosclerotic plaques. We investigated whether AMPK and autophagy of monocytes can enhance the stability of coronary atherosclerotic plaques in the human body. Patients and methods Samples of PBMs were collected and isolated from all patients with stable angina pectoris (SAP), non-ST-segment elevation acute coronary syndrome, ST-segment elevation acute myocardial infarction, and without coronary artery disease (control). Then, western blot was used to detect the expression levels of AMPK and autophagy-related protein. Results The expression levels of beclin-1 and ATG7 were all significantly lower in the acute coronary syndrome groups than those in the SAP and control groups (all P < 0.01). The level of phosphorylated AMPK was significantly decreased in patients with acute coronary syndrome compared with those in the SAP and control groups (P < 0.01). However, there was no statistical difference between the SAP group and the control group. The activation of mTOR was distinctly increased in the STEMI group (P < 0.05). Conclusion Therefore, our work is novel in showing that AMPK of PBMs may decrease plaque vulnerability and subsequent plaque rupture through activation of autophagy. Copyright (C) 2015 Wolters Kluwer Health, Inc. All rights reserved.
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