Table 2.

Factors involved in dyslipidemia‐induced endothelial progenitor cell (EPC) senescence

Factors	Functions	Mechanisms
Oxidized LDL	Decreased tube formation and adhesion	Downregulated E‐selectin and integrin (Di Santo et al., 2008)
	Impaired telomerase activity and proliferation Impaired telomerase activity; increased ROS	PI3K/AKT/ERK (Ming et al., 2016) AKT/hTERT (Lai & Liu, 2015)
Carbamylated LDL	Increased genomic damage and impaired proliferation	Downregulated γH2AX (Carracedo et al., 2011)
Electronegative LDL	Impaired telomerase activity and differentiation	AKT (Tang et al., 2008)
RLPs	Decreased proliferation, adhesion, migration and telomerase activity	Inhibited AKT and hTERT (Liu et al., 2009a; Yang et al., 2011)
HG and FAs	Impaired angiogenesis	PGC‐1α/ SIRT1/p53/p21 (Song et al., 2017a)
Low HDL	Increased tube formation and anti‐senescence	Activated PI3K/AKT/eNOS (Huang et al., 2012)
High HDL	Decreased tube formation and pro‐senescence	Inhibited PI3K/AKT/eNOS (Huang et al., 2012)

AKT, protein kinase B; eNOS, endothelial nitric oxide synthase; ERK, extracellular regulated protein kinase; FAs, fatty acid; γH2AX, phosphorylated histone protein H2AX; HDL, high‐density lipoprotein; HG, high glucose; hTERT, human telomerase reverse transcriptase; LDL, low‐density lipoprotein; PGC‐1α, peroxisome proliferator‐activated receptor coactivator1‐α; PI3K, phosphatidylinositol 3‐kinase; RLPs, remnant‐like lipoprotein; ROS, reactive oxygen species; SIRT1, silent information regulator 1.