Clinical associations and potential cellular mechanisms linking G6PD deficiency and atherosclerotic cardiovascular disease

Abstract

Glucose 6-phosphate dehydrogenase deficiency (G6PD-d) is the most common enzymopathy in the world, occurring in 5–8% of the global population (half a billion people). Recent epidemiological evidence suggests that G6PD-d may be associated with increased cardiovascular disease (CVD). Atherosclerosis is the dominant cause of CVD, including myocardial infarction, heart failure, stroke, and peripheral artery disease. Atherosclerosis, in turn, is a chronic inflammatory disease, fueled by oxidized lipids and influenced by various immune and nonimmune cells including vascular endothelial and smooth muscle cells, monocytes and macrophages, T cells, B cells, and red blood cells. Here, we review the existing epidemiological evidence supporting a role for G6PD-d in CVD in humans and explore the data on potential cellular mechanisms by which G6PD-d may exacerbate atherosclerosis.