PROS1 and hyperphosphatemia: Elastin fragmentation precedes AC, and calcium deposits can also result in damage to elastin fibers in smooth muscle cells.[31] [32] Microcalcifications have been shown to co-localize with aortic elastin degradation in the aortas of humans and mice.[31] [32] In addition to the biomechanical effects of AC, inflammation, WSS, oxidative stress, hyperphosphatemia, and elastolysis further serve as stimuli that promote vascular bone morphogenic protein signaling and matrix remodeling.[33]