Table 2 Potential drugs for joint pharmacologic prevention of cardiovascular disease and cancer (Masoudkabir et al. [181])
Drug | Direct target | Indirect targets | Action on CVD | Action on cancer |
|---|---|---|---|---|
Statins | HMG-CoAreductase inhibition | • AMPK activation • Inhibition of Cyclines & cycline-dependent kinases • Up-regulation of tumor-suppressors (p53, p27, p21) • Inhibition of PI3K, serineethreonine kinases, NF-κB, and MAPKs signaling pathways | Improving endothelial function Plaque stabilization ↓ Atherosclerosis progression ↓ Myocardial infarction and stroke ↓ Cardiovascular mortality | Tumor-suppressor and anti-cancer role through: ↑ Apoptosis ↓ Proliferation ↓ Invasion ↑ Radiosensitization ↓ DNA damage |
ASA | Inhibition of COX1 | • AMPK activation? | ↓ Myocardial infarction and stroke ↓ Cardiovascular mortality | ↓ Cancer incidence ↓ Cancer death |
ACEIs/ARBs | ACE inhibition/angiotensin II receptor antagonism | • ↓ VEGF expression • PPAR-γ activation | Improving endothelial function Plaque stabilization ↓ Atherosclerosis progression ↓ Myocardial infarction and stroke ↓ Cardiovascular mortality | ↓ Cancer incidence Tumor-suppressor and anti-cancer role through: ↓ DNA damage ↑ Apoptosis ↑ Differentiation ↓ Angiogenesis ↓ Cell growth |
Metformin | Unknown | • AMPK activation |  | ↓ Cancer incidence Tumor suppression by regulating cellular proliferation, cell cycle progression and cellular survival |
TZDs | PPAR-γ agonism | • AMPK activation • Wnt/β-catenin signaling pathway inhibition • IGF-1 inhibition • Inhibition of leptin gene expression | ↓ Coronary and carotid atherosclerosis ↓ Thrombus formation and acute myocardial infarction and stroke ↓ Blood pressure | Tumor suppression through: ↓ Angiogenesis ↑ Apoptosis ↓ Self-renewal of cancer cells ↑ Differentiation |