Table 2.
Some examples in recent studies using a single-cell model for atherosclerosis mechanism exploration.
| Model | Biological process | Model function | References |
|---|---|---|---|
| Macrophage | Efferocytosis or/and phagocytosis, or pyroptosis | To study the effect of allele G of rS9349379, an intron of PHACTR1 gene, on impairing the efferocytosis in human atherosclerotic lesional macrophages | (81) |
| To explore whether GATA2 overexpression can impair macrophage phagocytosis and efferocytosis | (82) | ||
| To study the mitochondrial outer membrane protein effect on inhibiting macrophage pyroptosis resulting from Ox-LDL | (83) | ||
| Cellular senescence | To explore the mechanism of formation of senescent macrophages during atherosclerosis and whether LPS can induce macrophage senescence | (84) | |
| Lipid uptake or/and foam cell formation | To investigate the direct role of IgE on macrophage-sterol-responsive-network gene expression and foam cell formation | (85) | |
| To study the relationship between the phenotype-specific difference of macrophages and their ability of LDL uptake, cellular cholesterol levels, and cholesterol efflux. | (86) | ||
| To explore whether the inhibition of bromodomain-containing protein 4 could prevent lipid accumulation in senescent macrophages | (84) | ||
| To study the function of the RAC1 gene on regulating inflammatory cytokine secretion and lipid uptake of macrophages | (87) | ||
| To explore the underlying mechanism of vascular inflammation effect on the foam cell formation derived from marchpane, mainly focusing on the role of NOS1 in macrophage lipid up take | (88) | ||
| Inflammation | To investigate whether the role of TREML4 in human macrophages and the pathogenesis of atherosclerosis | (89) | |
| To investigate whether NOS1 could enhance the pro-inflammatory cytokine secretion by macrophages | (88) | ||
| EC | Pyroptosis | To explore the molecular mechanism of FGF21 function against atherosclerosis and the effect of FGF21 on suppressing proteins associated with pyroptosis in HUVECs | (90) |
| Inflammation or/and Apoptosis | To explore whether NLRP3 activation in ECs can promote atherosclerosis development associated with diabetes | (91) | |
| To study how disturbed flow regulating enzymes as well as their roles in the apoptosis and inflammation | (92) | ||
| To explore how exosome lncRNA GAS5 regulates apoptosis of HUVECs in atherosclerosis | (93) | ||
| Cell senescence | To study whether the disturbed flow can induce HUVEC senescence and associated pathway | (94) | |
| SMC | Phenotypic modulation | To study the oxidized lipid effect and SMC phenotype changes | (72) |
| To study whether there are differences between Ox-LDL-loaded SMCs in vitro and in vivo at a genetic level. | (95) |
LPS, Lipopolysaccharide; PHACTR1, Phosphatase and Actin Regulator 1; IgE, Immunoglobulin E; NOS1, Nitric oxide synthase; lncRNA, Long non-coding RNAs; FGF21, Fibroblast growth factor 21; HUVECs, Human umbilical vein endothelial cells; GAS5, Growth Arrest Specific 5; ECs, endothelial cells; Ox-LDL, Oxidized lipoprotein.