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Table 2 Molecular pathways involved in atherosclerosis

From: Mouse models of atherosclerosis: a historical perspective and recent advances

Molecular mechanisms

Role 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


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

Macrophage apoptosis induced by cholesterol loading


Toll-like receptor activation

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


Upregulation of transient receptor potential cation (TRPC) channels

VSMC, migration, proliferation and apoptosis; neointimal proliferation

[158, 160162]