Table 2 Molecular pathways involved in atherosclerosis

Expression of vascular cell adhesion molecule-1 (VCAM-1), E-selectin and P-selectin

Inflammatory response induced by LDL oxidation

[7, 8]

Nuclear factor-kappa B (NF-κB) activation

Chemotaxis via regulation of chemokines, such as CCL2, CCL5, CCL8, and CXCL9

[166, 169]

Release of platelet derived growth factor

Fibrous cap formation

[12, 13]

CHOP activation

Macrophage apoptosis via endoplasmic reticulum stress

[107, 108]

Pattern recognition receptor activation

Macrophage apoptosis via activation of CD36-TLR2 pathway

[111, 112]

Activation of mitochondrial, Ca²⁺-dependent pathways

Vascular smooth muscle cell apoptosis via calpain/mPTP/cytochrome C/caspase-3 and apoptosis-inducing factor

[140]

cytochrome c release and activation of caspase-9 and the effector caspases

Macrophage apoptosis induced by cholesterol loading

[141]

Toll-like receptor activation

Immune activation through recognition of mitochondrial DNA, which can act as damage-associated molecular patterns (DAMPs)

[148]

Upregulation of transient receptor potential cation (TRPC) channels

VSMC, migration, proliferation and apoptosis; neointimal proliferation

[158, 160–162]