Intermedin_1-53 attenuates atherosclerotic plaque vulnerability by inhibiting CHOP-mediated apoptosis and inflammasome in macrophages.

ABSTRACT: Atherosclerotic plaque vulnerability and rupture increase the risk of acute coronary syndromes. Advanced lesion macrophage apoptosis plays important role in the rupture of atherosclerotic plaque, and endoplasmic reticulum stress (ERS) has been proved to be a key mechanism of macrophage apoptosis. Intermedin (IMD) is a regulator of ERS. Here, we investigated whether IMD enhances atherosclerotic plaque stability by inhibiting ERS-CHOP-mediated apoptosis and subsequent inflammasome in macrophages. We studied the effects of IMD on features of plaque vulnerability in hyperlipemia apolipoprotein E-deficient (ApoE^-/-) mice. Six-week IMD_1-53 infusion significantly reduced atherosclerotic lesion size. Of note, IMD_1-53 lowered lesion macrophage content and necrotic c

SUBMITTER: Ren JL 

PROVIDER: S-EPMC8088440 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature