Table 4.

Factors involved in dyslipidemia‐induced macrophage senescence

Factors	Functions	Mechanisms
Oxidized LDL	Reduced cell viability, increased lipid accumulation and upregulated p53 and p21	MST1‐ mediated autophagy (Cao et al., 2019) CKIP‐1/REGγ (Jia et al., 2019; Li et al., 2018)
	Increased ROS Increased ROS Increased ROS and cell death Increased ROS and apoptosis	Caveolin‐1/NOX2 (Wang et al., 2018a) Lysosomal dysfunction (Ahmad & Leake, 2019) MEK1/ERK/NOX4 (Lee et al., 2010) Inhibited autophagy (Liu et al., 2016)
	Increased inflammation	ERK/MAPK/TLR4 (Youk et al., 2021)
Palmitate	Increased inflammation	ERK/MAPK/TLR4 (Youk et al., 2021)

CKIP‐1, casein kinase 2‐interacting protein‐1; ERK, extracellular regulated protein kinase; LDL, low‐density lipoprotein; MAPK, mitogen‐activated protein kinase; MEK1, mitogen‐activated protein kinase 1; MST1, mammalian ste20‐like kinase 1; NOX, NADPH oxidase; REGγ, 11S regulatory particles, 28 kDa proteasome activator, proteasome activator subunit 3; ROS, reactive oxygen species; TLR4, toll‐like receptor 4.