The overexpression of tomoregulin-1 significantly reduced the increase of LVPWD, LVPWS, LVAWS and LVAWD (Fig. 5), decreased the degree of cardiac hypertrophy (Fig. 5), and reduced collagen accumulation in the interstitial space (Fig. 6), which collectively contribute to the slowed progression of cardiac hypertrophy, whereas knockdown of tomoregulin-1 expression exacerbated phenotypes of cardiac hypertrophy induced by TAC. The gene discussed is TMEFF1; the disease is persistent truncus arteriosus.