Targeting the ACOD1-itaconate axis stabilizes atherosclerotic plaques.

ABSTRACT: Inflammatory macrophages are key drivers of atherosclerosis that can induce rupture-prone vulnerable plaques. Skewing the plaque macrophage population towards a more protective phenotype and reducing the occurrence of clinical events is thought to be a promising method of treating atherosclerotic patients. In the current study, we investigate the immunomodulatory properties of itaconate, an immunometabolite derived from the TCA cycle intermediate cis-aconitate and synthesised by the enzyme Aconitate Decarboxylase 1 (ACOD1, also known as IRG1), in the context of atherosclerosis. Ldlr^-/- atherogenic mice transplanted with Acod1^-/- bone marrow displayed a more stable plaque phenotype with smaller necrotic cores and showed increased recruitment of monocytes to the vessel

SUBMITTER: Harber KJ 

PROVIDER: S-EPMC10848031 | biostudies-literature | 2024 Apr

REPOSITORIES: biostudies-literature