心肌梗死后的心室重构及其伴随的心肌纤维化是心力衰竭进展的核心病理机制。现有研究证实，免疫细胞的时空动态调控在心肌梗死后心室重构中发挥着至关重要的作用，其贯穿心脏炎症扩散、组织修复与纤维化的全过程。心肌梗死不仅诱发局部炎症反应，还可通过炎症因子释放及交感神经激活等途径远程调控骨髓、脾脏等造血器官，驱动造血干/祖细胞向髓系细胞分化倾斜，形成“髓系上升-淋系下降”的造血失衡现象。这一失衡表现为中性粒细胞、单核/巨噬细胞等促炎性髓系细胞过度增殖与释放，而T细胞、B细胞等淋系细胞则相对减少。该系统性免疫失衡重塑了心脏及外周器官的免疫细胞的构成，加剧心脏持续性炎症反应、氧化应激、细胞凋亡及细胞外基质过度沉积，最终导致心脏纤维化加重、心室扩张与收缩功能恶化，是驱动心肌梗死后不良重构与心力衰竭发生的关键环节。该文旨在系统探讨心肌梗死后造血失衡驱动的免疫亚群在时间与空间维度上的动态变化及其功能特征，并进一步提出通过精准调控造血干细胞分化路径与关键免疫细胞亚群，以改善心脏炎症微环境、延缓纤维化进程、抑制不良心室重构的新型干预策略，为心肌梗死后心力衰竭的防治提供潜在靶点。

Ventricular remodeling following myocardial infarction (MI) and its associated myocardial fibrosis represent a core pathological mechanism in the progression of heart failure. Accumulating evidence confirms that the spatiotemporal dynamics of immune cells play a crucial role in post-MI ventricular remodeling, spanning the entire process of cardiac inflammation, tissue repair, and fibrosis. MI not only triggers a local inflammatory response but also remotely regulates hematopoietic organs such as the bone marrow and spleen via pathways including inflammatory factor release and sympathetic nervous system activation. This drives hematopoietic stem/progenitor cells (HSPCs) to differentiate with a bias toward the myeloid lineage, resulting in a hematopoietic imbalance phenomenon described as "myeloid upsurge-lymphoid decline". This imbalance is characterized by excessive proliferation and release of proinflammatory myeloid cells, such as neutrophils and monocytes/macrophages, alongside a relative reduction in lymphoid cells like T cells and B cells. This systemic immune imbalance reshapes the immune cell composition in the heart and peripheral organs. It exacerbates sustained cardiac inflammation, oxidative stress, cell apoptosis, and excessive extracellular matrix deposition, ultimately leading to aggravated cardiac fibrosis, ventricular dilation, and systolic function deterioration. It is a key driver of adverse post-MI remodeling and the onset of heart failure. This article aims to systematically explore the spatiotemporal dynamics and functional characteristics of immune cell subsets driven by this post-MI hematopoietic imbalance. Furthermore, it proposes novel intervention strategies focused on precisely modulating hematopoietic stem cell differentiation pathway and key immune cell subsets. These strategies aim to improve the cardiac inflammatory microenvironment, delay the fibrotic process, and inhibit adverse ventricular remodeling, thereby offering potential therapeutic targets for preventing and treating post-MI heart failure.