Fig 6.

Schematic representation for possible mechanisms underlying the protective role of ALA against vascular calcification. In normal conditions, Gas6/Axl interaction and sequential Akt activation are involved in maintenance of VSMC survival in an autocrine mode. During Pi-induced calcification, VSMCs display a considerable decrease in survival because of down-regulation of Gas6/Axl/Akt signalling and an increase in mitochondria-mediated apoptosis. This apoptosis is thought to cause mitochondria perturbation by insulting accumulated oxidants. ALA may protect against aortic calcification at least in part by rescuing Gas6–Axl survival pathway and by inhibiting mitochondrial-mediated apoptosis in VSMCs through improvement of mitochondria function by its antioxidant potential. The dashed line indicates an unresolved issue to be determined.