Age‐dependent Decline in Angiogenesis and Repair from Influenza

Abstract

Aging is associated with impaired repair of lung injury, while influenza and pneumonia are one of the leading causes of death in aged adults. Angiogenesis – the formation of new capillaries –plays key roles in repair from injury. Angiogenesis is impaired in aging animals. Thus, in order to develop more efficient strategies for lung injury in aged people, we need to understand the mechanism by which aging inhibits angiogenesis and how the signaling contributes to impairment of repair from injury. It has been reported that angiopoietin like4 (ANGPTL4) contributes to influenza infection. However, it remains unknown whether ANGPTL4 mediates age-dependent impairment of repair from influenza infection. Here we find that the levels of ANGPTL4 are higher in aged endothelial cells (ECs) compared to young ECs. Survival rate of PR8 influenza infection is lower in aged mice. The mRNA levels of ANGPTL4 peak at 7 days post influenza infection (dpi) in young mice, while the levels remain high at 14 dpi in aged mouse lungs. These results suggestthat repair from influenza infection is inhibited in aged lung through ANGPTL4. Modulation of ANGPTL4 may reverse the impairment of angiogenesis and improves recovery from influenza infection in aged lungs.