单细胞分辨率下心肌梗死后巨噬细胞异质性在心室重塑中的作用与干预相关进展

The role of macrophage heterogeneity in ventricular remodeling after myocardial infarction at single-cell resolution and related intervention progress

摘要:

心肌梗死(MI)后的心室重塑是心血管疾病中的重要病理过程,巨噬细胞在其中起着关键作用。单细胞与空间转录组学技术揭示了巨噬细胞的异质性、来源及时空动态变化。不同亚群在炎症期、修复期及纤维化期呈现功能转变:Ly6C^hi/CCR2＋促炎巨噬细胞主导早期炎症反应,TREM2^hi修复型促进炎症消退与瘢痕成熟,BHLHE41＋亚群抑制胶原沉积,脾源性CD169＋TIM4＋巨噬细胞维持免疫稳态。文章综述巨噬细胞亚群在心室重塑中的分布、功能及互作网络,探讨其对心肌修复与纤维化的调控作用,并提出精准干预策略,为防治提供新靶点。

Abstract:

Ventricular remodeling after myocardial infarction (MI) is a critical pathological process in cardiovascular diseases, in which macrophages serve as essential regulators. Advances in single-cell and spatial transcriptomic technologies have revealed the heterogeneity, origins, and spatiotemporal dynamics of cardiac macrophages following injury. Distinct macrophage subsets exhibit stage-specific functional switching during inflammation, tissue repair, and fibrosis:Ly6C^hi/CCR2＋ pro-inflammatory macrophages dominate the early inflammatory response; TREM2^hi reparative macrophages facilitate inflammation resolution and scar maturation; BHLHE41＋ macrophages restrict excessive collagen deposition; and spleen-derived CD169＋TIM4＋ macrophages help maintain local cardic immune homeostasis. This review summarizes the distribution, functional roles, and interaction networks of these macrophage populations during ventricular remodeling, elaborates their regulatory effects on myocardial repair and fibrotic progression, and proposes precision intervention strategies that may offer new therapeutic targets for post-MI remodeling.