Myeloid Cells in Abdominal Aortic Aneurysm.

purpose of reviewAbdominal aortic aneurysm (AAA) is a life-threatening vascular disorder with high mortality upon rupture, yet effective pharmacotherapy remains lacking. This review synthesizes the pivotal roles of myeloid cells-key mediators of aortic inflammation and remodeling-in AAA pathogenesis, highlighting their therapeutic targeting potential. RECENT

findingsSingle-cell RNA sequencing has revealed myeloid diversity in AAA. Among these myeloid populations, macrophages (including interferon-responsive monocytes, pro- and anti-inflammatory subsets, and reparative populations) emerge as central regulators of AAA pathogenesis, influencing disease initiation, progression, and tissue repair processes. Neutrophils promote vascular injury via neutrophil extracellular traps, while dendritic cells bridge innate-adaptive immunity. Eosinophils and myeloid-derived suppressor cells exhibited protective effects by immunoregulation. Mechanistic studies identified transcriptional, metabolic, and epigenetic regulators of myeloid plasticity. Clonal hematopoiesis and trained immunity may serve as potential novel mechanisms of myeloid cells involved in AAA. These mechanistic insights have inspired therapeutic innovation, with nanoparticle-targeted myeloid cell therapies showing promising immunomodulatory effects in mitigating AAA progression. Myeloid cells play a pivotal role in AAA pathogenesis by driving inflammatory responses, extracellular matrix degradation, and maladaptive vascular remodeling. Their functional heterogeneity, encompassing both destructive and protective subsets, highlights the need for precisely targeted therapeutic approaches. While single-cell technologies have significantly advanced our understanding of myeloid diversity, clinical translation remains challenged by microenvironmental crosstalk and potential off-target effects. Future research should prioritize: (1) spatial multi-omics characterization of myeloid-vascular interactions, (2) development of precision therapies targeting clonal hematopoiesis-driven subpopulations, and (3) combinatorial strategies to reprogram pathogenic myeloid phenotypes. Addressing these critical gaps may lead to transformative therapies for aneurysm stabilization, ultimately fulfilling the urgent unmet needs in AAA clinical management.