Fig. 1

There are three major possible mechanisms of ALI complicated by AAD. (1) AngII could trigger overexpression of MCP-1 in PMVECs by activating NF-κB signaling pathway. MCP-1 plays a great role in the recruitment of macrophages in lung tissues, and MMP-9 derived from macrophages could induce the degradation of extracellular matrix and vascular basilar membrane; (2) AngII could induce the apoptosis of PMVECs through activating the caspase-3, up-regulating the expression of Bax and down-regulating the expression of Bcl-2; (3) AngII could trigger endothelial barrier injury, which may be related to the dephosphorylation of Y685-VE-cadherin and the endothelial skeletal rearrangement. AngII angiotensin II, MCP-1, monocyte chemoattractant protein-1, PMVECs pulmonary microvascular endothelial cells, MMP-9, matrix metalloproteinase 9