Here, increased H19 levels were shown to mediate the therapeutic effect of melatonin in this PAH rat model by sponging miR-675-3p, thereby releasing its inhibition on IGF1R, and by inhibiting miR-200a, leading to the de-repression of PDCD4, which promoted apoptosis and suppressed proliferation of human and rat PASMCs, in vitro (Figure 3F) [105]. This evidence concerns the gene H19 and pulmonary arterial hypertension.