Table 2.
Molecular pathways involved in atherosclerosis
| Molecular mechanisms | Role in Atherosclerosis | References |
|---|---|---|
| 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] |