Modulation of neointimal lesion formation by endogenous androgens is independent of vascular androgen receptor.

摘要: Low androgen levels have been linked with an increased risk of cardiovascular disease in men. Previous studies sug- gested that androgens directly inhibit atherosclerotic lesion formation although the underlying mechanisms for this remain unclear. This study addressed hypothesis endogenous arterial remodelling by a direct action on receptor (AR) vascular wall. Methods and results We studied series novel mouse lines cell-specific deletion AR either endothelium or smooth muscle cells both cell types. Findings were compared model global deficiency wild-type mice (castrated). characterized phenotype, pharmacology histology, assessed neoin- timal following injury to femoral artery. Cell-specific did not alter body weight, circulating testosterone seminal vesicle but caused limited alterations contractility blood pressure. Neointimal was unaltered selective from endothelium, muscle, Castration neointimal volume (Sham vs. Castration: 2.4 × 10 7 + 4.5 6 3.9 4.9 mm 3 , P ¼ 0.04, n 9-10). Conclusion Vascular had no effect formation, while low systemic ad- versely affect size. These findings suggest cardio-protective effects are mediated outside vasculature AR-independent mechanisms.