Cell-Specific Dual Role of Caveolin-1 in Pulmonary Hypertension

Figure 2

This figure depicts the proposed model of PH (#1). Injury to EC results in progressive loss of endothelial caveolin-1, loss of vasodilators, and the activation of proliferative and anti-apoptotic pathways leading to PH. EC disruption is progressive resulting in further loss of multiple proteins and possibly the loss of EC. Extensive damage/loss of EC exposes SMC to direct shear stress leading to enhanced expression of caveolin-1 which participates in further cell proliferation and cell migration resulting in neointima formation. Newly formed EC in neointima express increased eNOS; possibly low caveolin-1 expression in these cells may in part be responsible for the observed dysfunctional eNOS. The resulting oxidant/nitration injury further influences PH adversely.