Macrophage proliferation and skewed myelopoiesis-induced monocytosis, as well as neutrophils, enhance the generation of atherogenic inflammatory cells in a lesion area, leading to plaque formation and Cardiovascular Disease (CVD). Among all risk factors, accumulated data have shown that hyperlipidemia activates Hematopoietic Stem/Progenitor Cells (HSPCs) in the Bone Marrow (BM) niche. Recently, proliferation of Granulocyte-Monocyte Progenitors (GMPs) has been demonstrated to drive skewed myelopoiesis, while HSPCs remain quiescent. In this review, we discuss how HSPCs and GMPs participate in atherosclerosis of mice in terms of proliferation and cell mobilization from BM to peripheral blood and the lesion area. We also describe how the spleen, an extramedullary organ, is involved in skewed myelopoiesis and inflammation in atherosclerosis. We further summarize the clinical evidence of the relationship of HSPCs with coronary stenoses in patients with CVD. Ultimately, this review facilitates understanding the pathological roles of HSPCs and GMPs in atherosclerosis for future treatments.

巨噬细胞增殖和偏态骨髓细胞生成诱导的单核细胞增多症以及中性粒细胞增加病变区域致动脉粥样硬化性炎症细胞的产生，导致斑块形成和心血管疾病 (CVD)。在所有风险因素中，积累的数据表明，高脂血症会激活骨髓 (BM) 生态位中的造血干/祖细胞 (HSPC)。最近，粒细胞-单核细胞祖细胞 (GMPs) 的增殖已被证明可以驱动偏斜的骨髓细胞生成，而 HSPCs 保持静止。在这篇综述中，我们讨论了 HSPCs 和 GMPs 如何在增殖和细胞从 BM 到外周血和病变区域的动员方面参与小鼠的动脉粥样硬化。我们还描述了作为髓外器官的脾脏如何参与动脉粥样硬化中的偏态骨髓细胞生成和炎症。我们进一步总结了 HSPCs 与 CVD 患者冠状动脉狭窄关系的临床证据。最终，本综述有助于了解 HSPC 和 GMP 在动脉粥样硬化中的病理作用，以供未来治疗。