APM⁺ macrophages associated with plaque vulnerability via MIF-CD74 signaling: a multi-omics study.

ABSTRACT:

Background

Atherosclerosis (AS) is a chronic vascular disease and the principal cause leading to ischemic cardiomyopathy (ICM). It involves complex metabolic dysregulation beyond the resolution of single-omics. Emerging evidence implicates arginine-proline metabolism (APM) in driving inflammation and impairing efferocytosis, yet the cellular basis of plaque instability remains elusive.

Methods

We employed a five-stage analytical framework. First, metabolomic profiling revealed shared pathways between AS and ICM. Second, single-cell RNA sequencing identified APM-enriched macrophage subtypes in both diseases. Pseudotime analysis, Scissor algorithm, and cell-cell communication analyses linked these subtypes to APM signaling, stroke prognosis, and key ligand-receptor interaction

SUBMITTER: Xu X 

PROVIDER: S-EPMC12821923 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature