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Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
Clinical associations and potential cellular mechanisms linking G6PD deficiency and atherosclerotic cardiovascular
Patrick H Andrews1, James C Zimring1,2, Coleen A McNamara1,3
1Beirne B. Carter Center for Immunology Research, Charlottesville, VA 22903 USA.
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.
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