Furthermore, we found that the following the mechanisms were involved: 1) inhibition of atrial sympathetic hyperinnervation with TH, GAP43 and NGF reduction; 2) inhibition of atrial myocyte apoptosis and fibrosis via the down-regulation of apoptosis- and fibrosis-related proteins, including cleaved caspase-9, AIF, BAX, α-SMA and TGF-β1 in chronic OSA canines; and 3) alleviation of atrial metabolic remodeling caused by OSA through the Sirt1-AMPK pathway. The gene discussed is ACTA1; the disease is obstructive sleep apnea syndrome.