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High Uric Acid Promotes Atherosclerotic Plaque Instability by Apoptosis Targeted Autophagy

Weidong Liu1, Wei Yu1, De Xie1

  • 1Department of Internal Medicine, Xiang'an Hospital of Xiamen University, Xiamen University.

Journal of Atherosclerosis and Thrombosis
|November 27, 2022
PubMed

Insights

High uric acid (HUA) promotes atherosclerosis and plaque instability by increasing foam cell apoptosis through autophagy inhibition. Rapamycin, an autophagy activator, partially reversed these effects in a mouse model.

Area of Science:

  • Cardiovascular Research
  • Atherosclerosis Pathophysiology
  • Metabolic Syndrome

Background:

  • Atherosclerotic cardiovascular disease (ASCVD) poses significant health risks, with plaque rupture being a major cause of myocardial infarction and stroke.
  • High uric acid (HUA) is linked to increased cardiovascular event risk, but its role in atherosclerosis progression and plaque stability remains unclear.

Purpose of the Study:

  • To investigate the mechanism by which HUA influences atherosclerosis and plaque stability.
  • To determine the impact of HUA on plaque vulnerability, cellular apoptosis, and autophagy.

Main Methods:

  • Atherosclerotic Apoe-/- mice were induced with HUA to model the disease.
  • Atherosclerosis progression and plaque characteristics were assessed using Oil Red O, H&E, and Masson staining.
  • Apoptosis and autophagy within plaques were evaluated using TUNEL assay and immunohistochemistry, with in vitro validation in RAW 264.7 macrophages.

Main Results:

  • HUA significantly promoted atherosclerosis and plaque vulnerability, characterized by increased macrophage infiltration, lipid accumulation, necrotic core size, and reduced collagen.
  • HUA treatment led to increased cellular apoptosis and inhibited autophagy in atherosclerotic plaques.
  • In vitro studies confirmed that HUA decreased foam cell viability and increased apoptosis, effects partially reversed by rapamycin, an autophagy activator.

Conclusions:

  • HUA exacerbates atherosclerosis and promotes plaque vulnerability.
  • HUA facilitates foam cell apoptosis by inhibiting autophagy, contributing to the progression of atherosclerotic cardiovascular disease.
Abstract

Keywords:
ApoptosisAtherosclerosisAutophagyHigh uric acidPlaque instability

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