CAC paracrine effect over ECFC in response to atherosclerotic factors. The current figure shows a schematic overview of the processes taking place in response to the direct contact of CAC with the atherosclerotic plaque secretome (AP). (A) The secretome of CAC induce () ECFC angiogenesis and migration. (B) Incubation of CAC with atherosclerotic factors (Cathepsin-D, MMP9 and other proteases) promotes the rupture and degradation of ECM proteins. Further incubation of ECFC with the CAC released factors (fibulins, endostatin, restin, thrombospondins, LTBP1, etc.) inhibits the paracrine effect of CAC, since angiogenesis and migration of ECFC decreases () compared to ECFC stimulated with the secretome of control CAC (not affected by AP factors). Curved arrows represent the release of factors by CAC, the AP arteries or CAC after incubation with AP secretome. Straight arrows indicate the direction of the effect of the factors released by CAC control (A), AP or CAC+AP (B).