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Endothelial dysfunction marks the early stages of atherosclerosis where oxidative stress enhances endothelium cell permeability, LDL oxidation, monocyte adherence, platelet activation, vascular inflammation, as well as proliferation and infiltration of vascular smooth muscle cells (VSMCs) from media to arterial intima ( -/- mice model showed a reduction in the expression levels of antioxidant enzymes [NAD(P)H dehydrogenase, NQO1, catalase and GPX1], increased macrophage migration, production of pro-inflammatory cytokines, and atherosclerotic lesions (Song et al., 2015)
doi: 10.3390/diagnostics14080848
By enhancing fibroblast migration to injury sites, BPC-157 accelerates the production of new structural material needed for tissue repair
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