The increase of HIF-1α can also downregulate the expression of Bcl-2, an antiapoptotic protein, which in turn induces apoptosis of human umbilical vein endothelial cells during hypoxia [46], whereas the inhibition of HIF-1α expression can reduce cleaved caspase-3 expression in the rat model of hemorrhagic shock and alleviate the acute lung injury in rats [47]. The gene discussed is BCL2; the disease is Shock.