Ihan Alojz
Institute of Microbiology and Immunology, Faculty of Medicine, University of Ljubljana, 1000 Ljubljana, Slovenia.
Cells. 2025 Sep 3;14(17):1374. doi: 10.3390/cells14171374.
Cardiovascular diseases (CVDs) are a group of disorders in which inflammatory processes play a crucial role. Age-related chronic systemic inflammation is characterized by elevated levels of inflammatory mediators in the bloodstream. It can occur even in the absence of overt infection, contributing to endothelial dysfunction, vascular stiffness, and atherosclerosis. The regulation of vascular tissue homeostasis and inflammation is primarily mediated by tissue-resident macrophages (TRMs) and monocyte-derived macrophages. The proportion of monocyte-derived macrophages increases with age, contributing to vascular damage and accelerating CVD progression. In aging tissue, monocyte-derived macrophages exposed to various microenvironmental stimuli are predominantly polarized into the pro-inflammatory M1 phenotype. This polarization, in turn, triggers the release of pro-inflammatory cytokines (IL-1β, IL-6, and IL-18) and promotes the generation of oxidative stress molecules. In this review, we examine the role of macrophages in cardiovascular aging, their secretory phenotypes, and the impact of chronic low-grade inflammation on vascular integrity. We also propose reliable biomarkers of chronic cardiovascular inflammation that may aid in risk prediction, patient stratification, and the development of senotherapeutic interventions for cardiovascular disease.
心血管疾病(CVDs)是一组炎症过程起关键作用的病症。与年龄相关的慢性全身炎症的特征是血液中炎症介质水平升高。即使在没有明显感染的情况下也可能发生,导致内皮功能障碍、血管僵硬和动脉粥样硬化。血管组织稳态和炎症的调节主要由组织驻留巨噬细胞(TRMs)和单核细胞衍生的巨噬细胞介导。单核细胞衍生的巨噬细胞比例随年龄增加,导致血管损伤并加速CVD进展。在衰老组织中,暴露于各种微环境刺激的单核细胞衍生的巨噬细胞主要极化为促炎M1表型。这种极化反过来又触发促炎细胞因子(IL-1β、IL-6和IL-18)的释放,并促进氧化应激分子的产生。在本综述中,我们研究了巨噬细胞在心血管衰老中的作用、它们的分泌表型以及慢性低度炎症对血管完整性的影响。我们还提出了慢性心血管炎症的可靠生物标志物,这可能有助于风险预测、患者分层以及心血管疾病衰老治疗干预措施的开发。