Multiple organ dysfunction syndrome (
MODS) remains a great challenge in
critical care because of its common occurrence, high cost of care, and high mortality. Vascular endothelial injury is the initiation step in the development of
MODS, and EPCs are essential for the process of organ repair. It is unclear whether and how
caveolin-1 (Cav-1) in EPCs contributes to the pathogenesis of
MODS. The present study is aimed at investigating the potential role of Cav-1 in EPCs during
MODS. We established a
MODS model in pigs, isolated and characterized EPCs from the
MODS model, and tracked Cav-1 expression and various in vitro behaviors of EPCs from the
MODS model. Then, we knockdown Cav-1 expression with
siRNA or induce Cav-1 expression with proinflammatory factors to evaluate potential effects on EPCs. Our results suggest that Cav-1 expression correlated with
EPC functions during
MODS and Cav-1 regulates the function of endothelial progenitor cells via PI3K/Akt/eNOS signaling during
MODS. Thus, Cav-1 in EPCs could be an attractive target for the treatment of
MODS.