A Potential Therapeutic Target for Influenza A-Induced Cardiovascular Disease

Le had previously demonstrated using murine models that MAGI1 is required for the regulation of EC activation. Using MAGI1-depleted ECs and MAGI1 overexpression studies in ECs, Le found MAGI1 to inhibit interferon signaling which in turn promoted IAV infection. Interestingly, treatment of ECs with oxidized low-density lipoprotein led to an increase in MAGI1 expression and IAV infection suggesting MAGI1 to be a part of the mechanistic link between serum lipid levels and post IAV-infection patient prognosis. “We have found that MAGI1 is involved in IAV infection of endothelial cells. Previously, we reported the crucial role of MAGI1 in endothelial cell activation and subsequent atherogenesis. In the current report, we found that IAV infection increases MAGI1 expression and enhances virus infection by inhibiting various anti-virus responses,” said Le. “These data suggest the crucial role of MAGI1 in inhibiting IAV-mediated anti-viral responses, and the induction of MAGI1 by oxidized LDL and influenza A virus infection itself can accelerate further virus infection and promote severe endothelial cell activation. Thus, MAGI1 as a promoter of both endothelial cell activation and virus infection, is a potential therapeutic target for influenza virus infection.” Further studies will improve our understanding of MAGI1 function in vascular biology and IAV-induced cardiovascular disease as well as the potential of MAGI1 to be a therapeutic target.