Figure 1.

Effects of estrogens and androgen signaling on multiple cellular processes implicated in the regulation of cardiovascular calcification. Note that estrogen can bind to estrogen receptors (ER, resulting in nuclear translation), G-protein coupled estrogen receptors (GPER, eliciting cytosolic signaling), and estrogen binding proteins (EBPs, eliciting cytosolic signaling) to exert a variety of effects—both positive and negative—on molecules influencing ectopic calcification. In general, androgens bind to androgen receptors (AR) and have a smaller number of signal transducing elements compared to estrogens. Abbreviations and impact on calcification: RANKL, receptor activator of nuclear factor κB ligand (promotes calcification); PPAR γ, peroxisome proliferator-activated receptor-γ (prevents calcification); NFκB, nuclear factor κ B (promotes inflammation/calcification); NADPH oxidase, nicotinamide adenine dinucleotide phosphate oxidase (increases oxidative stress/calcification); SOD, superoxide dismutase (reduces oxidative stress/calcification); O₂•⁻, superoxide anion (increases calcification); p53, tumor protein 53 (promotes inflammation/calcification).