TABLE 1.

The effect of oxLDL on key mechanisms involved in atherogenesis.

Atherogenic process	Involved cells	OxLDL effect	References
Endothelial dysfunction	ECs	OxLDL induces endothelial dysfunction via cytoplasmic adapter protein TRAF3IP2	Valente et al. (2014)
NO production	ECs	OxLDL inhibits eNOS activity and NO production	Blair et al. (1999)
Apoptosis	VSMCs	OxLDL overproduction triggers LOX-1 expression and apoptosis	Wu et al. (2017)
Cell adhesion	ECs, leukocytes	OxLDL can stimulate the activation of endothelial cells and the production of adhesion molecules that mediate the adhesion of blood leukocytes, that adhere to the endothelium and migrate into the intima. As the consequence of the macrophage activation, proinflammatory cytokines are released, ROS are synthesized, and proteolytic enzymes that contribute to the matrix degradation are also produced. This leads to plaque destabilization	Chen and Khismatullin (2015); Obermayer et al. (2018)
Proliferation	ECs	OxLDL induces cell proliferation via Rho/ROCK/Akt/p27kip1 signaling	Zhang et al. (2017)
Cell death	ECs	OxLDL induces cell death via cytoplasmic adapter protein TRAF3IP2	Valente et al. (2014)
NLRP3 inflammasome activation	Macrophages	OxLDL and cholesterol crystal accumulation are important triggers of inflammasome activation. OxLDL can activate NLRP3 inflammasome even without cholesterol crystals. Macrophages uptake oxLDL via CD36, which results in the intracellular nucleation of cholesterol crystals in lysosomes	Grebe et al. (2018); Poznyak et al. (2020b)