In a rabbit model ofisoprenaline-induced AF, Su et al. [27] observed high levels ofangiotensin-2, HIF-1α, transforming growth factor-β(TGF-β), and MMP-9 expression, while also noting a positive correlationbetween HIF-1α levels and the degree of myocardial fibrosis.Accordingly, the inhibition of HIF-1α expression resulted incorresponding decreases in TGF-β and MMP-9 expression, reducing thedegree of myocardial fibrosis and thereby supporting the ability ofHIF-1α to induce AF in part through the upregulation of MMP-9 andTGF-β. This evidence concerns the gene HIF1A and atrial fibrillation.