Endothelial Dysfunction and Oxidative Stress in Atherosclerosis: Modern Therapeutic Targets.

Atherosclerosis has two crucial causes: endothelial dysfunction and oxidative stress, which cause blood vessels to become inflamed, stop producing adequate levels of nitric oxide, produce oxidized lipids, and form plaques. The continued presence of oxidants causes an increase in activated endothelial cells and the accumulation of immune cells, proliferation of smooth muscle cells, and degradation of extracellular matrix material, leading to the accelerated formation of atherosclerotic plaques and subsequent adverse cardiovascular events. Several recent studies have identified many molecular mechanisms mediating the effects of oxidative stress and endothelial dysfunction. These mechanisms include the generation of reactive oxygen radicals, mitochondrial damage, signalling by inflammatory cytokines, and failure of antioxidant defences. Using these mechanisms as biological markers will increase the accuracy of assessing a person’s risk of developing cardiovascular disease and monitoring the progression of their disease. Current treatment approaches are aimed at addressing vascular inflammation, oxidative stress, lipid metabolism, and endothelial regeneration using such means as lipid-lowering agents, inflammatory blocking agents, antioxidants, modulating the renin-angiotensin system, and making lifestyle changes. The emerging therapeutic approaches that specifically seek to improve endothelial function and lessen oxidative stress have the potential to enhance a person's cardiovascular outcomes. https://doi.org/10.52783/jchr.v16.i4.15486