Cen Yan, Yu-Ze Li, Xiao-Min Luo, Xiao-Jiang Quan* and Ying-Mei Feng* Pages 589 - 598 ( 10 )
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.
Myelopoiesis, hematopoietic stem cells, atherosclerosis, hyperlipidemia, niche, progenitor cells.
Department of Science and Technology, Beijing You-An Hospital, Capital Medical University, Beijing 100069, Department of Nutrition, Province Hospital, Ha-Er-Bin, Hei Long Jiang 150086, Department of Science and Technology, Beijing You-An Hospital, Capital Medical University, Beijing 100069, Lu-He Central Laboratory, Lu He Hospital, Capital Medical University, Beijing 101149, Department of Science and Technology, Beijing You-An Hospital, Capital Medical University, Beijing 100069