Autophagy of monocytes attenuates the vulnerability of coronary atherosclerotic plaques

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Kai Zhao1, Xing Sheng Xu, Xiao Meng

  • 1aDepartment of Cardiology, The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Qilu Hospital of Shandong University bThe School of Medicine, Shandong University, Jinan, People's Republic of China.

Coronary Artery Disease
|November 12, 2013
PubMed

Insights

Autophagy in peripheral blood monocytes (PBMs) is reduced in acute coronary syndromes, indicating a role in plaque vulnerability. Enhancing monocyte autophagy may stabilize atherosclerotic plaques.

Area of Science:

  • Cardiovascular Biology
  • Cellular Mechanisms
  • Immunology

Background:

  • Atherosclerotic plaque vulnerability is a major cause of acute coronary syndromes.
  • Monocytes play a critical role in the inflammatory processes underlying atherosclerosis.
  • Autophagy is a cellular process involved in maintaining cellular homeostasis.

Purpose of the Study:

  • To investigate the role of autophagy in monocytes in the context of atherosclerotic plaque vulnerability.
  • To compare autophagy levels in monocytes from patients with different stages of coronary artery disease.

Main Methods:

  • Peripheral blood monocytes (PBMs) were isolated from patients with stable angina pectoris (SAP), unstable angina pectoris (UAP), acute myocardial infarction (AMI), and controls.
  • Expression of autophagy markers beclin-1 and light chain 3 (LC3) in PBMs was analyzed using Western blot and immunofluorescence.
  • Correlation between autophagy markers and C-reactive protein levels was assessed.

Main Results:

  • Beclin-1 and LC3 expression were significantly lower in acute coronary syndrome (ACS) patients (UAP and AMI) compared to SAP and control groups.
  • Monocyte autophagy markers were further decreased in AMI patients compared to UAP patients.
  • Lower beclin-1 levels in UAP and AMI groups correlated negatively with C-reactive protein levels.

Conclusions:

  • Reduced autophagy in PBMs is associated with plaque vulnerability and rupture in ACS.
  • Autophagy of PBMs is implicated in the pathogenesis of atherosclerotic plaque instability.
  • Augmenting monocyte autophagy presents a potential therapeutic strategy for stabilizing atherosclerotic plaques.
Abstract

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