作者: Xiaojuan Ma , Yingmei Feng
DOI: 10.3390/IJMS17071162
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摘要: As the pathological basis of cardiovascular disease (CVD), atherosclerosis is featured as a chronic inflammation. Hypercholesterolemia an independent risk factor for CVD. Accumulated studies have shown that hypercholesterolemia associated with myeloid cell expansion, which stimulates innate and adaptive immune responses, strengthens inflammation, accelerates progression. Hematopoietic stem/progenitor cells (HSPC) in bone marrow (BM) expresses panel lipoprotein receptors to control cholesterol homeostasis. Deficiency these abrogates cellular efflux, resulting HSPC proliferation differentiation hypercholesterolemic mice. Reduction level lipid rafts by infusion reconstituted high-density (HDL) or its major apolipoprotein, apoA-I, reverses hypercholesterolemia-induced expansion. Apart from impaired metabolism, inhibition reactive oxygen species production suppresses activation leukocytosis. These data indicate mechanisms underlying effects on could be multifaceted. Furthermore, dyslipidemia also regulates HSPC-neighboring cells, mobilization. In article, we review how evokes mobilization directly via modification BM microenvironment. We hope this will bring light finding key molecules treatment