Anti-atherosclerotic agent

An anti-atherosclerotic agent is not a specific biological target molecule or receptor, but rather a broad therapeutic category that includes drugs and compounds designed to prevent, halt, or reverse the progression of atherosclerosis [2, 4, 9]. These agents exert their effects by targeting various distinct molecular pathways involved in the pathogenesis of the disease, such as lipid metabolism, chronic vascular inflammation, and endothelial dysfunction [2, 7]. Prominent specific targets for these agents include enzymes like 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and proprotein convertase subtilisin/kexin type 9 (PCSK9), as well as inflammatory modulators like interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) [2, 8, 9]. By reducing the accumulation of oxidized low-density lipoproteins (ox-LDL) and preventing the formation of macrophage-derived foam cells within the arterial wall, these therapies aim to stabilize vulnerable plaques and reduce the risk of major adverse cardiovascular events (MACE) such as myocardial infarction and stroke [3, 9, 10]. Modern research also explores targeting novel pathways, including the mammalian target of rapamycin (mTOR) and transient receptor potential (TRP) channels, to enhance atheroprotection [6, 10].

Other names

Anti-atherogenic agentAtheroprotective agentAnti-atherosclerotic drugAtherosclerosis-modifying agent

Anti-atherosclerotic agents operate through diverse mechanisms depending on their specific subclass, including the inhibition of HMG-CoA reductase to decrease cholesterol synthesis, inhibition of PCSK9 to enhance LDL receptor recycling, antagonism of pro-inflammatory cytokines like IL-1β to reduce vascular inflammation, and activation of nuclear receptors such as PPARs or LXRs to promote cholesterol efflux from macrophages.