Combination of Dichloroacetate and Atorvastatin Regulates Excessive Proliferation and Oxidative Stress in Pulmonary Arterial Hypertension Development via p38 Signaling

Figure 8

A schematic showing the proposed mechanism of dichloroacetate- and atorvastatin-related phenotype regulation. DCA inconsiderably increased apoptosis and oxidative stress and decreased proliferation and ΔΨ_m (MMP) in a p38 activation-dependent manner. By contrast, ATO markedly upregulated the p38 signal pathway and oxidative stress, resulting in profound apoptosis. Slightly reduced proliferation and MMP when DCA and ATO combination treatment could achieve more therapeutic targets and only cause moderate ROS damage.