In this study, we obtained the following main findings: (1) IL-17 induced RVH even under normoxia; (2) The expression of IL-17 in RV tissues during the chronic hypoxia exposure was upregulated in a time-dependent manner; (3) IL-17 further aggravated hypoxia-induced right ventricular hypertrophy; (4) IL-17 might participate in RVH through STAT3 activation; and (5) IL-17 induced cardiomyocyte injury and further aggravated hypoxia-induced cardiomyocyte injury by activating STAT3. Here, IL17A is linked to Right ventricular hypertrophy.