YY‐11, a camel milk‐derived peptide, inhibits TGF‐β‐mediated atherogenic signaling in human vascular smooth muscle cells

Abstract

Cardiovascular diseases (CVDs) combined are the major cause of death, accounting for almost 70% of all mortality worldwide (Organization, 2017). The underlying pathology of most CVD is the complex chronic inflammatory condition of atherosclerosis (Libby, 2006;Liu et al., 2014;Xu et al., 2014). Atherosclerosis occurs in medium to large vessels and commences with the trapping of lipoproteins in the vessel wall by modified proteoglycans with hyperelongated glycosaminoglycan (GAG) chains (Nigro et al., 2006;Williams & Tabas, 1995). The process is amenable to therapeutic intervention at several steps as, for example, pharmacologically blocking the GAG elongation process inhibits lipid deposition in an animal model of atherosclerosis (Ballinger et al., 2010;Getachew et al., 2010).