Figure 2.

Role of Mstn and Act-A in vascular lesions: (A) In VSMCs, uremia, oxidative stress, and inflammation are some of the possible triggers of Mstn and Act-A expression, which could contribute to the atherosclerotic process. Mstn has a salient role in VSMC phenotypic modification, inducing cytoskeleton remodeling, migration, and inflammatory and pro-fibrotic molecule expression. On the other hand, Act-A is more involved with VSMC transformation into osteoblast-like cells responsible for medial calcification; (B) In atherosclerotic lesions, Mstn and Act-A infiltrating positive cells (monocytes, macrophages) are present. At that level, Mstn and Act-A may modulate inflammatory response and cell migratory capability. Abbreviations: Act-A = activin-A; Mstn = myostatin; VSMCs = vascular smooth muscle cells.