In line with these findings, the pulmonary artery obtained from rats with flow-induced pulmonary hypertension showed reduced expressions of α-SMA and SM-MHC-II, suggesting VSMC de-differentiates from the contractile phenotype to the synthetic phenotype in response to increased blood flow after creation of the aortocaval fistula. Here, ACTA1 is linked to pulmonary arterial hypertension.