Interleukin-16 upregulates tissue inhibitor of metalloproteinase 3 to promote atherosclerotic plaque stability.

ABSTRACT:

Background

High levels of circulating interleukin (IL)-16 are associated with a reduced incidence of cardiovascular events. The disruption of atherosclerotic plaques commonly causes myocardial infarction and stroke. In this study, we investigated the effects of IL-16 on phenotypic modification of plaques.

Methods

Mice with deficiencies in IL-16 and apolipoprotein E (IL16^-/-ApoE^-/-) were generated and used for plaque phenotype analysis. RNA sequencing was performed to identify changes in cellular processes and molecular expression in response to IL-16 deficiency.

Results

IL-16 deficiency increased the necrotic core and reduced fibrous cap thickness in the plaques. IL-16 deletion accelerated the degradation of intraplaque collagen and elastin, incr

SUBMITTER: He H 

PROVIDER: S-EPMC12903335 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature