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Review
. 2018 May;1864(5 Pt A):1562-1572.
doi: 10.1016/j.bbadis.2018.02.006. Epub 2018 Feb 14.

Nutraceuticals as therapeutic agents for atherosclerosis

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Review

Nutraceuticals as therapeutic agents for atherosclerosis

Joe W E Moss et al. Biochim Biophys Acta Mol Basis Dis. 2018 May.

Abstract

Atherosclerosis, a chronic inflammatory disorder of medium and large arteries and an underlying cause of cardiovascular disease (CVD), is responsible for a third of all global deaths. Current treatments for CVD, such as optimized statin therapy, are associated with considerable residual risk and several side effects in some patients. The outcome of research on the identification of alternative pharmaceutical agents for the treatment of CVD has been relatively disappointing with many promising leads failing at the clinical level. Nutraceuticals, products from food sources with health benefits beyond their nutritional value, represent promising agents in the prevention of CVD or as an add-on therapy with current treatments. This review will highlight the potential of several nutraceuticals, including polyunsaturated fatty acids, flavonoids and other polyphenols, as anti-CVD therapies based on clinical and pre-clinical mechanism-based studies.

Keywords: Atherosclerosis; Cardiovascular disease; Nutraceuticals; Polyphenols; Polyunsaturated fatty acids.

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Figures

Fig. 1
Fig. 1
The actions of nutraceuticals on different stages in the pathogenesis of atherosclerosis. The different steps in the pathogenesis of atherosclerosis (modification of LDL, recruitment of immune cells such as monocytes, their differentiation into macrophages and subsequent transformation to foam cells, apoptosis and necrosis of such foam cells to form lipid-rich necrotic core, inflammasome activation by cholesterol crystals and other factors, stabilization of plaques by extracellular matrix produced by vascular smooth muscle cells and plaque rupture) are shown together with points where some key nutraceuticals mediate their actions. See text for more details.

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