Complement and Complement Regulatory Proteins as Potential Molecular Targets for Vascular Diseases
Juan Acosta, Xuebin Qin and Jose Halperin
Affiliation: Harvard Medical School, 1 Kendall Square, Bldg. 600, 3rd Floor, Cambridge, MA 02139, USA.
Keywords: Proteins, mechanismspecific, vasculitis, thrombosis, MAC complexes
By-products of complement activation and complement regulatory proteins are increasingly recognized to play an important pathogenic role in a variety of vascular diseases including atherosclerosis, ischemia and reperfusion injury, hyperacute graft rejection, vasculitis, and the vascular complications of human diabetes. “Self” damage by autologous complement is mediated by activation products of the complement cascades or by direct insertion of the membrane attack complex (MAC) into cell membranes. Specifically, insertion of MAC complexes into endothelial cells results in the release of an array of growth factors and cytokines that induces proliferation, inflammation and thrombosis in the vascular wall. This paper reviews complement and complement regulatory proteins with specific focus on the vasculature and vascular diseases; it highlights complement and its regulators as potential targets for the rational design of mechanismspecific drugs for the treatment of some of the most prevalent human diseases.
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