Furthermore, LDN markedly attenuated Ang II-induced left atrial remodeling, inflammation and oxidative stress as well as the activation of multiple signals (AKT, ERK1/2, HIF-1α, TGF-β/smad2/3, and CX43) in the atria, suggesting that LDN inhibited AF possibly through blood pressure-dependent and blood pressure-independent manners. The gene discussed is SMAD2; the disease is atrial fibrillation.